<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">David G. Blauvelt</style></author><author><style face="normal" font="default" size="100%">Sato, Tomokazu F</style></author><author><style face="normal" font="default" size="100%">Wienisch, Martin</style></author><author><style face="normal" font="default" size="100%">Murthy, Venkatesh N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Distinct spatiotemporal activity in principal neurons of the mouse olfactory bulb in anesthetized and awake states.</style></title><secondary-title><style face="normal" font="default" size="100%">Front Neural Circuits</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Front Neural Circuits</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">46</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The acquisition of olfactory information and its early processing in mammals are modulated by brain states through sniffing behavior and neural feedback. We imaged the spatiotemporal pattern of odor-evoked activity in a population of output neurons (mitral/tufted cells, MTCs) in the olfactory bulb (OB) of head-restrained mice expressing a genetically-encoded calcium indicator. The temporal dynamics of MTC population activity were relatively simple in anesthetized animals, but were highly variable in awake animals. However, the apparently irregular activity in awake animals could be predicted well using sniff timing measured externally, or inferred through fluctuations in the global responses of MTC population even without explicit knowledge of sniff times. The overall spatial pattern of activity was conserved across states, but odor responses had a diffuse spatial component in anesthetized mice that was less prominent during wakefulness. Multi-photon microscopy indicated that MTC lateral dendrites were the likely source of spatially disperse responses in the anesthetized animal. Our data demonstrate that the temporal and spatial dynamics of MTCs can be significantly modulated by behavioral state, and that the ensemble activity of MTCs can provide information about sniff timing to downstream circuits to help decode odor responses.</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23543674?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Foivos Markopoulos</style></author><author><style face="normal" font="default" size="100%">Rokni, Dan</style></author><author><style face="normal" font="default" size="100%">Gire, David H</style></author><author><style face="normal" font="default" size="100%">Murthy, Venkatesh N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Functional properties of cortical feedback projections to the olfactory bulb.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuron</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Neuron</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Dec 20</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">76</style></volume><pages><style face="normal" font="default" size="100%">1175-88</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Sensory perception is not a simple feed-forward process, and higher brain areas can actively modulate information processing in &quot;lower&quot; areas. We used optogenetic methods to examine how cortical feedback projections affect circuits in the first olfactory processing stage, the olfactory bulb. Selective activation of back projections from the anterior olfactory nucleus/cortex (AON) revealed functional glutamatergic synaptic connections on several types of bulbar interneurons. Unexpectedly, AON axons also directly depolarized mitral cells (MCs), enough to elicit spikes reliably in a time window of a few milliseconds. MCs received strong disynaptic inhibition, a third of which arises in the glomerular layer. Activating feedback axons in vivo suppressed spontaneous as well as odor-evoked activity of MCs, sometimes preceded by a temporally precise increase in firing probability. Our study indicates that cortical feedback can shape the activity of bulbar output neurons by enabling precisely timed spikes and enforcing broad inhibition to suppress background activity.</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23259952?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sato, Tomokazu .</style></author><author><style face="normal" font="default" size="100%">Murthy, Venkatesh N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Light-emitting diodes for biological microscopy.</style></title><secondary-title><style face="normal" font="default" size="100%">Cold Spring Harb Protoc</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cold Spring Harb Protoc</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">2012</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Various technological advances have made imaging an increasingly useful tool in the life sciences. Imaging techniques that move away from the limitations of wide-field microscopy have allowed deeper, higher-resolution imaging of thick biological tissue. Even within wide-field microscopy, advancements such as structured and sheet illumination, as well as improvements of biological probes, have led to better visualization of cells and their subcellular structures. The illumination source for wide-field microscopy, however, has remained relatively unchanged for decades, relying mainly on xenon, mercury, and halogen lamps. Light-emitting diodes (LEDs) have existed for more than 80 years, but their spectral range and output light flux have only recently become large enough for use in biological applications. This article presents the basic information necessary to build and to use an LED-based illumination source for microscopy. It also provides some useful resources about LED advancements. Although commercial LED-based illuminators for microscopy are available, custom-built illumination systems can incorporate the latest LED chips into microscopes more quickly and inexpensively than is possible through the retail market.</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23209140?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Hagiwara, Akari</style></author><author><style face="normal" font="default" size="100%">Pal, Sumon K</style></author><author><style face="normal" font="default" size="100%">Sato, Tomokazu F</style></author><author><style face="normal" font="default" size="100%">Wienisch, Martin</style></author><author><style face="normal" font="default" size="100%">Murthy, Venkatesh N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Optophysiological analysis of associational circuits in the olfactory cortex.</style></title><secondary-title><style face="normal" font="default" size="100%">Front Neural Circuits</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Front Neural Circuits</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">18</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Primary olfactory cortical areas receive direct input from the olfactory bulb, but also have extensive associational connections that have been mainly studied with classical anatomical methods. Here, we shed light on the functional properties of associational connections in the anterior and posterior piriform cortices (aPC and pPC) using optophysiological methods. We found that the aPC receives dense functional connections from the anterior olfactory nucleus (AON), a major hub in olfactory cortical circuits. The local recurrent connectivity within the aPC, long invoked in cortical autoassociative models, is sparse and weak. By contrast, the pPC receives negligible input from the AON, but has dense connections from the aPC as well as more local recurrent connections than the aPC. Finally, there are negligible functional connections from the pPC to aPC. Our study provides a circuit basis for a more sensory role for the aPC in odor processing and an associative role for the pPC.</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22529781?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Lau, C G</style></author><author><style face="normal" font="default" size="100%">Murthy, Venkatesh N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Activity-dependent regulation of inhibition via GAD67</style></title><secondary-title><style face="normal" font="default" size="100%">J. Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2012</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.jneurosci.org/content/32/25/8521.abstract</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">32</style></volume><pages><style face="normal" font="default" size="100%">8521-8531</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Alterations in network activity trigger compensatory changes in excitation and inhibition that restore neuronal firing rate to an optimal range. One example of such synaptic homeostasis is the downregulation of inhibitory transmission by chronic inactivity, in part, through the reduction of vesicular transmitter content. The enzyme glutamic acid decarboxylase 67 (GAD67) is critical for GABA synthesis, but its involvement in homeostatic plasticity is unclear. We explored the role of GAD67 in activity-dependent synaptic plasticity using a mouse line (&lt;i&gt;Gad1–/–&lt;/i&gt;) in which GAD67 expression is disrupted by genomic insertion of the green fluorescent protein (GFP). Homozygous deletion of &lt;i&gt;Gad1&lt;/i&gt; significantly reduced miniature inhibitory postsynaptic current (mIPSC) amplitudes and GABA levels in cultured hippocampal neurons. The fractional block of mIPSC amplitude by a low affinity, competitive GABAA receptor antagonist was higher in GAD67-lacking neurons, suggesting that GABA concentration in the synaptic cleft is lower in knockout animals. Chronic suppression of activity by the application of tetrodotoxin (TTX) reduced mIPSC amplitudes and the levels of GAD67 and GABA. Moreover, TTX reduced GFP levels in interneurons, suggesting that GAD67 gene expression is a key regulatory target of activity. These &lt;i&gt;in vitro&lt;/i&gt; experiments were corroborated by &lt;i&gt;in vivo&lt;/i&gt; studies in which olfactory deprivation reduced mIPSC amplitudes and GFP levels in glomerular neurons in the olfactory bulb. Importantly, TTX-induced downregulation of mIPSC was attenuated in &lt;i&gt;Gad1–/–&lt;/i&gt; neurons. Altogether, these findings indicate that activity-driven expression of GAD67 critically controls GABA synthesis and, thus, vesicular filling of the transmitter. &lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">25</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>5</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Wienisch, Martin</style></author><author><style face="normal" font="default" size="100%">David G. Blauvelt</style></author><author><style face="normal" font="default" size="100%">Sato, Tomokazu F</style></author><author><style face="normal" font="default" size="100%">Murthy, Venkatesh N</style></author></authors><secondary-authors><author><style face="normal" font="default" size="100%">Tommaso Fellin</style></author><author><style face="normal" font="default" size="100%">Michael Halassa</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Two-Photon Imaging of Neural Activity in Awake, Head-Restrained Mice</style></title><secondary-title><style face="normal" font="default" size="100%">Neuronal Network Analysis : Concepts and Experimental Approaches</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2012</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.springerprotocols.com/Abstract/doi/10.1007/7657_2011_18#</style></url></web-urls></urls><publisher><style face="normal" font="default" size="100%">Humana Press (Springer Protocols) </style></publisher><pages><style face="normal" font="default" size="100%">pp 45-60</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Two-photon microscopy has become an invaluable tool for visualizing the activity of neuronal populations at cellular resolution in vivo. Imaging typically requires restraining the head of the animal underneath the objective of a dedicated optical setup and experiments are therefore often performed under anesthesia. Here, we describe a method that allows imaging in awake mice with minimal motion artifacts and without the need for extensive training of the animal. We detail the necessary surgical procedures to chronically implant a small, lightweight headplate and to create a clear window for imaging. The design of a simple apparatus capable of stably accommodating the headplate while the mouse is positioned on a wheel with spring suspension is presented. When used in combination with a multiphoton microscope, this approach greatly facilitates optical recordings in nonanesthetized animals and opens the door to many projects that can bridge the gap between neural activity and behavior. &lt;/p&gt;
</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Isogai, Y.</style></author><author><style face="normal" font="default" size="100%">Si, S.</style></author><author><style face="normal" font="default" size="100%">Pont-Lezica, L.</style></author><author><style face="normal" font="default" size="100%">Tan, T.</style></author><author><style face="normal" font="default" size="100%">Kapoor, V.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Dulac, C</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Molecular organization of vomeronasal chemoreception</style></title><secondary-title><style face="normal" font="default" size="100%">Nature</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.nature.com/nature/journal/vaop/ncurrent/full/nature10437.html</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">doi:10.1038/nature10437</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The vomeronasal organ (VNO) has a key role in mediating the social and defensive responses of many terrestrial vertebrates to species- and sex-specific chemosignals1. More than 250 putative pheromone receptors have been identified in the mouse VNO2, 3, but the nature of the signals detected by individual VNO receptors has not yet been elucidated. To gain insight into the molecular logic of VNO detection leading to mating, aggression or defensive responses, we sought to uncover the response profiles of individual vomeronasal receptors to a wide range of animal cues. Here we describe the repertoire of behaviourally and physiologically relevant stimuli detected by a large number of individual vomeronasal receptors in mice, and define a global map of vomeronasal signal detection. We demonstrate that the two classes (V1R and V2R) of vomeronasal receptors use fundamentally different strategies to encode chemosensory information, and that distinct receptor subfamilies have evolved towards the specific recognition of certain animal groups or chemical structures. The association of large subsets of vomeronasal receptors with cognate, ethologically and physiologically relevant stimuli establishes the molecular foundation of vomeronasal information coding, and opens new avenues for further investigating the neural mechanisms underlying behaviour specificity.&lt;/p&gt;
</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Olfactory maps in the brain</style></title><secondary-title><style face="normal" font="default" size="100%">Annu Rev Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=21692659</style></url></web-urls></urls><edition><style face="normal" font="default" size="100%">2011/06/23</style></edition><volume><style face="normal" font="default" size="100%">34</style></volume><pages><style face="normal" font="default" size="100%">233-58</style></pages><isbn><style face="normal" font="default" size="100%">1545-4126 (Electronic)0147-006X (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The responses of neural elements in many sensory areas of the brain vary systematically with their physical position, leading to a topographic representation of the outside world. Sensory representation in the olfactory system has been harder to decipher, in part because it is difficult to find appropriate metrics to characterize odor space and to sample this space densely. Recent experiments have shown that the arrangement of glomeruli, the elementary units of processing, is relatively invariant across individuals in a species, yet it is flexible enough to accommodate new sensors that might be added. Evidence supports the existence of coarse spatial domains carved out on a genetic or functional basis, but a systematic organization of odor responses or neural circuits on a local scale is not evident. Experiments and theory that relate the properties of odorant receptors to the detailed wiring diagram of the downstream olfactory circuits and to behaviors they trigger may reveal the design principles that have emerged during evolution.&lt;/p&gt;
</style></abstract><accession-num><style face="normal" font="default" size="100%">21692659</style></accession-num><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138; email: vnmurthy@fas.harvard.edu.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dietz, Shelby B</style></author><author><style face="normal" font="default" size="100%">Foivos Markopoulos</style></author><author><style face="normal" font="default" size="100%">Murthy, Venkatesh N</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Postnatal development of dendrodendritic inhibition in the mammalian olfactory bulb</style></title><secondary-title><style face="normal" font="default" size="100%">Frontiers in Cellular Neuroscience</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.frontiersin.org/cellular_neuroscience/10.3389/fncel.2011.00010/abstract</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">5</style></volume><pages><style face="normal" font="default" size="100%">10</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The mitral-granule cell (MC-GC) reciprocal synapse is an important source of auto- and lateral inhibition in the olfactory bulb (OB), and this local inhibition is critical for odor discrimination. We may gain insight into the role of MC autoinhibition in olfaction by correlating the functional development of the autoinhibition with the postnatal development of olfactory function. We have studied the functional development of the MC-GC reciprocal synapse using whole-cell patch-clamp recordings from MCs and GCs in acute olfactory bulb slices from 3- to 30-day old rats. The magnitude of dendrodendritic inhibition (DDI) measured by depolarizing a single MC and recording recurrent inhibition in the same cell increased up to the fifteenth day of life (P15), but dropped between P15 and P30. The initial increase and later decrease in DDI was echoed by a similar increase and decrease in the frequency of miniature inhibitory postsynaptic currents (mIPSCs), suggesting an accompanying modulation in the number of synapses available to participate in DDI. The late decrease in DDI could also result, in part, from a decrease in GC excitability as well as an increase in relative contribution of N-methyl D-aspartate (NMDA) receptors to gamma-amino butyric acid (GABA) release from GC synapses. Changes in release probability of GABAergic synapses are unlikely to account for the late reduction in DDI, although they might contribute to the early increase during development. Our results demonstrate that the functional MC-GC circuit evolves over development in a complex manner that may include both construction and elimination of synapses.&lt;/p&gt;
</style></abstract><notes><style face="normal" font="default" size="100%">&lt;p&gt;n/a&lt;/p&gt;
</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Petzold, G. C.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Role of astrocytes in neurovascular coupling</style></title><secondary-title><style face="normal" font="default" size="100%">Neuron</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.cell.com/neuron/abstract/S0896-6273(11)00723-9</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">71</style></volume><pages><style face="normal" font="default" size="100%">782-797</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Neural activity is intimately tied to blood flow in the brain. This coupling is specific enough in space and time that modern imaging methods use local hemodynamics as a measure of brain activity. In this review, we discuss recent evidence indicating that neuronal activity is coupled to local blood flow changes through an intermediary, the astrocyte. We highlight unresolved issues regarding the role of astrocytes and propose ways to address them using novel techniques. Our focus is on cellular level analysis in vivo, but we also relate mechanistic insights gained from ex vivo experiments to native tissue. We also review some strategies to harness advances in optical and genetic methods to study neurovascular coupling in the intact brain.&lt;/p&gt;
</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dhawale, A. K.</style></author><author><style face="normal" font="default" size="100%">Hagiwara, A.</style></author><author><style face="normal" font="default" size="100%">Bhalla, U. S.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.*</style></author><author><style face="normal" font="default" size="100%">Albeanu, D. F.*</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Non-redundant odor coding by sister mitral cells revealed by light addressable glomeruli in the mouse</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Nov</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=20953197</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">11</style></number><edition><style face="normal" font="default" size="100%">2010/10/19</style></edition><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">1404-12.</style></pages><isbn><style face="normal" font="default" size="100%">1546-1726 (Electronic)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Sensory inputs frequently converge on the brain in a spatially organized manner, often with overlapping inputs to multiple target neurons. Whether the responses of target neurons with common inputs become decorrelated depends on the contribution of local circuit interactions. We addressed this issue in the olfactory system using newly generated transgenic mice that express channelrhodopsin-2 in all of the olfactory sensory neurons. By selectively stimulating individual glomeruli with light, we identified mitral/tufted cells that receive common input (sister cells). Sister cells had highly correlated responses to odors, as measured by average spike rates, but their spike timing in relation to respiration was differentially altered. In contrast, non-sister cells correlated poorly on both of these measures. We suggest that sister mitral/tufted cells carry two different channels of information: average activity representing shared glomerular input and phase-specific information that refines odor representations and is substantially independent for sister cells.</style></abstract><accession-num><style face="normal" font="default" size="100%">20953197</style></accession-num><auth-address><style face="normal" font="default" size="100%">Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Qing, Q.</style></author><author><style face="normal" font="default" size="100%">Pal, S. K.</style></author><author><style face="normal" font="default" size="100%">Tian, B.</style></author><author><style face="normal" font="default" size="100%">Duan, X.</style></author><author><style face="normal" font="default" size="100%">Timko, B. P.</style></author><author><style face="normal" font="default" size="100%">Cohen-Karni, T.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Lieber, C. M.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Nanowire transistor arrays for mapping neural circuits in acute brain slices</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Feb 2</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=20133836</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5</style></number><edition><style face="normal" font="default" size="100%">2010/02/06</style></edition><volume><style face="normal" font="default" size="100%">107</style></volume><pages><style face="normal" font="default" size="100%">1882-7</style></pages><isbn><style face="normal" font="default" size="100%">1091-6490 (Electronic)0027-8424 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Revealing the functional connectivity in natural neuronal networks is central to understanding circuits in the brain. Here, we show that silicon nanowire field-effect transistor (Si NWFET) arrays fabricated on transparent substrates can be reliably interfaced to acute brain slices. NWFET arrays were readily designed to record across a wide range of length scales, while the transparent device chips enabled imaging of individual cell bodies and identification of areas of healthy neurons at both upper and lower tissue surfaces. Simultaneous NWFET and patch clamp studies enabled unambiguous identification of action potential signals, with additional features detected at earlier times by the nanodevices. NWFET recording at different positions in the absence and presence of synaptic and ion-channel blockers enabled assignment of these features to presynaptic firing and postsynaptic depolarization from regions either close to somata or abundant in dendritic projections. In all cases, the NWFET signal amplitudes were from 0.3-3 mV. In contrast to conventional multielectrode array measurements, the small active surface of the NWFET devices, approximately 0.06 microm(2), provides highly localized multiplexed measurements of neuronal activities with demonstrated sub-millisecond temporal resolution and, significantly, better than 30 microm spatial resolution. In addition, multiplexed mapping with 2D NWFET arrays revealed spatially heterogeneous functional connectivity in the olfactory cortex with a resolution surpassing substantially previous electrical recording techniques. Our demonstration of simultaneous high temporal and spatial resolution recording, as well as mapping of functional connectivity, suggest that NWFETs can become a powerful platform for studying neural circuits in the brain.</style></abstract><accession-num><style face="normal" font="default" size="100%">20133836</style></accession-num><custom2><style face="normal" font="default" size="100%">2808222</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Chemistry and Chemical Biology, Center for Brain Science, School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Petzold, G. C.</style></author><author><style face="normal" font="default" size="100%">Hagiwara, A.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Serotonergic modulation of odor input to the mammalian olfactory bulb</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jun</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=19430472</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6</style></number><edition><style face="normal" font="default" size="100%">2009/05/12</style></edition><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">784-91</style></pages><isbn><style face="normal" font="default" size="100%">1546-1726 (Electronic)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Centrifugal serotonergic fibers innervate the olfactory bulb, but the importance of these projections for olfactory processing is unclear. We examined serotonergic modulation of sensory input to olfactory glomeruli using mice that express synaptopHluorin in olfactory receptor neurons (ORN). Odor-evoked synaptic input to glomeruli was attenuated by increased serotonin signaling through serotonin 2C (5-HT2C) receptors and amplified by decreased serotonergic activity. Intravital multiphoton calcium imaging revealed that 5-HT2C receptor activation amplified odor-evoked activity in a subset of juxtaglomerular cells and attenuated glutamate release from ORN terminals via GABA(B) receptors. Endogenous serotonin released by electrical stimulation of the dorsal raphe nucleus attenuated odor-evoked responses without detectable bias in glomerular position or odor identity. Weaker glomerular responses, however, were less sensitive to raphe stimulation than strong responses. Our data indicate that the serotonergic system regulates odor inputs in the olfactory bulb and suggest that behavioral states may alter odor processing at the earliest stages.</style></abstract><accession-num><style face="normal" font="default" size="100%">19430472</style></accession-num><notes><style face="normal" font="default" size="100%">Petzold, Gabor CHagiwara, AkariMurthy, Venkatesh NResearch Support, Non-U.S. Gov'tUnited StatesNature neuroscienceNat Neurosci. 2009 Jun;12(6):784-91. Epub 2009 May 10.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, Massachusetts, USA. gabor.petzold@charite.de</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Soucy, E. R.</style></author><author><style face="normal" font="default" size="100%">Albeanu, D. F.</style></author><author><style face="normal" font="default" size="100%">Fantana, A. L.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Meister, M.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Precision and diversity in an odor map on the olfactory bulb</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Feb</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=19151709</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">2</style></number><edition><style face="normal" font="default" size="100%">2009/01/20</style></edition><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">210-20</style></pages><isbn><style face="normal" font="default" size="100%">1546-1726 (Electronic)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We explored the map of odor space created by glomeruli on the olfactory bulb of both rat and mouse. Identified glomeruli could be matched across animals by their response profile to hundreds of odors. Their layout in different individuals varied by only approximately 1 glomerular spacing, corresponding to a precision of 1 part in 1,000. Across species, mouse and rat share many glomeruli with apparently identical odor tuning, arranged in a similar layout. In mapping the position of a glomerulus to its odor tuning, we found only a coarse relationship with a precision of approximately 5 spacings. No chemotopic order was apparent on a finer scale and nearby glomeruli were almost as diverse in their odor sensitivity as distant ones. This local diversity of sensory tuning stands in marked distinction from other brain maps. Given the reliable placement of the glomeruli, it represents a feature, not a flaw, of the olfactory bulb.</style></abstract><accession-num><style face="normal" font="default" size="100%">19151709</style></accession-num><notes><style face="normal" font="default" size="100%">Soucy, Edward RAlbeanu, Dinu FFantana, Antoniu LMurthy, Venkatesh NMeister, MarkusUnited StatesNature neuroscienceNat Neurosci. 2009 Feb;12(2):210-20. Epub 2009 Jan 18.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, 52 Oxford Street, Cambridge, Massachusetts 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Petzold, G. C.</style></author><author><style face="normal" font="default" size="100%">Albeanu, D. F.</style></author><author><style face="normal" font="default" size="100%">Sato, T. F.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Coupling of neural activity to blood flow in olfactory glomeruli is mediated by astrocytic pathways</style></title><secondary-title><style face="normal" font="default" size="100%">Neuron</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jun 26</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=18579080</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6</style></number><edition><style face="normal" font="default" size="100%">2008/06/27</style></edition><volume><style face="normal" font="default" size="100%">58</style></volume><pages><style face="normal" font="default" size="100%">897-910</style></pages><isbn><style face="normal" font="default" size="100%">1097-4199 (Electronic)0896-6273 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Functional neuroimaging uses activity-dependent changes in cerebral blood flow to map brain activity, but the contributions of presynaptic and postsynaptic activity are incompletely understood, as are the underlying cellular pathways. Using intravital multiphoton microscopy, we measured presynaptic activity, postsynaptic neuronal and astrocytic calcium responses, and erythrocyte velocity and flux in olfactory glomeruli during odor stimulation in mice. Odor-evoked functional hyperemia in glomerular capillaries was highly correlated with glutamate release, but did not require local postsynaptic activity. Odor stimulation induced calcium transients in astrocyte endfeet and an associated dilation of upstream arterioles. Calcium elevations in astrocytes and functional hyperemia depended on astrocytic metabotropic glutamate receptor 5 and cyclooxygenase activation. Astrocytic glutamate transporters also contributed to functional hyperemia through mechanisms independent of calcium rises and cyclooxygenase activation. These local pathways initiated by glutamate account for a large part of the coupling between synaptic activity and functional hyperemia in the olfactory bulb.</style></abstract><accession-num><style face="normal" font="default" size="100%">18579080</style></accession-num><notes><style face="normal" font="default" size="100%">Petzold, Gabor CAlbeanu, Dinu FSato, Tomokazu FMurthy, Venkatesh NT32 GM008313-23/GM/NIGMS NIH HHS/United StatesComparative StudyResearch Support, Non-U.S. Gov'tUnited StatesNeuronNeuron. 2008 Jun 26;58(6):897-910.</style></notes><custom2><style face="normal" font="default" size="100%">2922004</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Albeanu, D. F.</style></author><author><style face="normal" font="default" size="100%">Soucy, E.</style></author><author><style face="normal" font="default" size="100%">Sato, T. F.</style></author><author><style face="normal" font="default" size="100%">Meister, M.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">LED arrays as cost effective and efficient light sources for widefield microscopy</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2008</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=18478056</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5</style></number><edition><style face="normal" font="default" size="100%">2008/05/15</style></edition><volume><style face="normal" font="default" size="100%">3</style></volume><pages><style face="normal" font="default" size="100%">e2146</style></pages><isbn><style face="normal" font="default" size="100%">1932-6203 (Electronic)1932-6203 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">New developments in fluorophores as well as in detection methods have fueled the rapid growth of optical imaging in the life sciences. Commercial widefield microscopes generally use arc lamps, excitation/emission filters and shutters for fluorescence imaging. These components can be expensive, difficult to maintain and preclude stable illumination. Here, we describe methods to construct inexpensive and easy-to-use light sources for optical microscopy using light-emitting diodes (LEDs). We also provide examples of its applicability to biological fluorescence imaging.</style></abstract><accession-num><style face="normal" font="default" size="100%">18478056</style></accession-num><notes><style face="normal" font="default" size="100%">Albeanu, Dinu FSoucy, EdwardSato, Tomokazu FMeister, MarkusMurthy, Venkatesh NResearch Support, Non-U.S. Gov'tUnited StatesPloS onePLoS One. 2008 May 14;3(5):e2146.</style></notes><custom2><style face="normal" font="default" size="100%">2361193</style></custom2><auth-address><style face="normal" font="default" size="100%">Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, United States of America.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Tyler, W. J.</style></author><author><style face="normal" font="default" size="100%">Petzold, G. C.</style></author><author><style face="normal" font="default" size="100%">Pal, S. K.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Experience-dependent modification of primary sensory synapses in the mammalian olfactory bulb</style></title><secondary-title><style face="normal" font="default" size="100%">J Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2007</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Aug 29</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17728456</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">35</style></number><edition><style face="normal" font="default" size="100%">2007/08/31</style></edition><volume><style face="normal" font="default" size="100%">27</style></volume><pages><style face="normal" font="default" size="100%">9427-38</style></pages><isbn><style face="normal" font="default" size="100%">1529-2401 (Electronic)0270-6474 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Experience-dependent changes in neural circuits have traditionally been investigated several synapses downstream of sensory input. Whether experience can alter the strength of primary sensory synapses remains mostly unknown. To address this issue, we investigated the consequences of odor deprivation on synapses made by olfactory sensory axons in the olfactory bulb of rats. Odor deprivation triggered an increase in the probability of glutamate release from olfactory sensory neuron synapses. Deprivation also increased the amplitude of quantal synaptic currents mediated by AMPA- and NMDA-type glutamate receptors, as well as the abundance of these receptors in the glomerular region. Our results demonstrate that sensory experience is capable of modulating synaptic strength at the earliest stages of information transfer between the environment and an organism. Such compensatory experience-dependent changes may represent a mechanism of sensory gain control.</style></abstract><accession-num><style face="normal" font="default" size="100%">17728456</style></accession-num><notes><style face="normal" font="default" size="100%">Tyler, William JPetzold, Gabor CPal, Sumon KMurthy, Venkatesh NNS050976/NS/NINDS NIH HHS/United StatesResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tUnited StatesThe Journal of neuroscience : the official journal of the Society for NeuroscienceJ Neurosci. 2007 Aug 29;27(35):9427-38.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138, USA. wtyler@asu.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Newton, A. J.</style></author><author><style face="normal" font="default" size="100%">Kirchhausen, T.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Inhibition of dynamin completely blocks compensatory synaptic vesicle endocytosis</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Nov 21</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17093049</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">47</style></number><edition><style face="normal" font="default" size="100%">2006/11/10</style></edition><volume><style face="normal" font="default" size="100%">103</style></volume><pages><style face="normal" font="default" size="100%">17955-60</style></pages><isbn><style face="normal" font="default" size="100%">0027-8424 (Print)0027-8424 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The ability of synapses to sustain signal propagation relies on rapid recycling of transmitter-containing presynaptic vesicles. Clathrin- and dynamin-mediated retrieval of vesicular membrane has an undisputed role in synaptic vesicle recycling. There is also evidence for other modes of vesicle retrieval, including bulk retrieval and the so-called kiss-and-run recycling. Whether dynamin in required for these other modes of synaptic vesicle endocytosis remains unclear. Here, we have tested the role of dynamin in synaptic vesicle endocytosis by using a small molecule called dynasore, which rapidly inhibits the GTPase activity of dynamin with high specificity. Endocytosis after sustained or brief stimuli was completely and reversibly blocked by dynasore in cultured hippocampal neurons expressing the fluorescent tracer synaptopHluorin. By contrast, dynasore had no effect on exocytosis. In the presence of dynasore, low-frequency stimulation led to sustained accumulation of synaptopHluorin and other vesicular proteins on the surface membrane at a rate predicted from net exocytosis. These vesicular components remained on surface membranes even after the stimulus was terminated, suggesting that all endocytic events rely on dynamin during low-frequency activity as well as in the period after it. Ultrastructural analysis revealed a reduction in the density of synaptic vesicles and the presence of endocytic structures only at synapses that were stimulated in the presence of dynasore. In sum, our data indicate that dynamin is essential for all forms of compensatory synaptic vesicle endocytosis including any kiss-and-run events.</style></abstract><accession-num><style face="normal" font="default" size="100%">17093049</style></accession-num><notes><style face="normal" font="default" size="100%">Newton, A JamilaKirchhausen, TomMurthy, Venkatesh NGM075252/GM/NIGMS NIH HHS/United StatesNS39059/NS/NINDS NIH HHS/United StatesResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.United StatesProceedings of the National Academy of Sciences of the United States of AmericaProc Natl Acad Sci U S A. 2006 Nov 21;103(47):17955-60. Epub 2006 Nov 8.</style></notes><custom2><style face="normal" font="default" size="100%">1693854</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Hartman, K. N.</style></author><author><style face="normal" font="default" size="100%">Pal, S. K.</style></author><author><style face="normal" font="default" size="100%">Burrone, J.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Activity-dependent regulation of inhibitory synaptic transmission in hippocampal neurons</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">May</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=16582905</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5</style></number><edition><style face="normal" font="default" size="100%">2006/04/04</style></edition><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">642-9</style></pages><isbn><style face="normal" font="default" size="100%">1097-6256 (Print)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Neural activity regulates the number and properties of GABAergic synapses in the brain, but the mechanisms underlying these changes are unclear. We found that blocking spike activity globally in developing hippocampal neurons from rats reduced the density of GABAergic terminals as well as the frequency and amplitude of miniature inhibitory postsynaptic currents (mIPSCs). Chronic inactivity later in development led to a reduction in the mIPSC amplitude, without any change in GABAergic synapse density. By contrast, hyperpolarizing or abolishing spike activity in single neurons did not alter GABAergic synaptic inputs. Suppressing activity in individual presynaptic GABAergic neurons also failed to decrease synaptic output. Our results indicate that GABAergic synapses are regulated by the level of activity in surrounding neurons. Notably, we found that the expression of GABAergic plasticity involves changes in the amount of neurotransmitter in individual vesicles.</style></abstract><accession-num><style face="normal" font="default" size="100%">16582905</style></accession-num><notes><style face="normal" font="default" size="100%">Hartman, Kenichi NPal, Sumon KBurrone, JuanMurthy, Venkatesh NComparative StudyResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.United StatesNature neuroscienceNat Neurosci. 2006 May;9(5):642-9. Epub 2006 Apr 2.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Burrone, J.</style></author><author><style face="normal" font="default" size="100%">Li, Z.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Studying vesicle cycling in presynaptic terminals using the genetically encoded probe synaptopHluorin</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Protoc</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2006</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=17406557</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6</style></number><edition><style face="normal" font="default" size="100%">2007/04/05</style></edition><volume><style face="normal" font="default" size="100%">1</style></volume><pages><style face="normal" font="default" size="100%">2970-8</style></pages><isbn><style face="normal" font="default" size="100%">1750-2799 (Electronic)1750-2799 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Genetically encoded fluorescent probes have become indispensable tools in the biological sciences. Studies of synaptic vesicle recycling have been facilitated by a group of GFP-derived probes called pHluorins. These probes exploit changes in pH that accompany exocytosis and recapture of synaptic vesicles. Here we describe how these synaptic tracers can be used in rodent hippocampal neurons to monitor the synaptic vesicle cycle in real time and to obtain mechanistic insights about it. Synapses can be observed in living samples using a wide-field fluorescence microscope and a cooled charge-coupled device camera. A simple specimen chamber allows electrical stimulation of synapses to evoke exocytosis in a precisely controlled manner. We present protocols to measure various parameters of the synaptic vesicle cycle. This technique can be easily adapted to study different classes of synapses from wild-type and mutant mice. Once cultured neurons expressing synaptopHluorin are available, the whole procedure should take about 2 h.</style></abstract><accession-num><style face="normal" font="default" size="100%">17406557</style></accession-num><notes><style face="normal" font="default" size="100%">Burrone, JuanLi, ZhiyingMurthy, Venkatesh NEnglandNature protocolsNat Protoc. 2006;1(6):2970-8.</style></notes><auth-address><style face="normal" font="default" size="100%">MRC Center for Developmental Neurobiology, King's College London, London SE1 1UL, UK.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Star, E. N.</style></author><author><style face="normal" font="default" size="100%">Newton, A. J.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Real-time imaging of Rab3a and Rab5a reveals differential roles in presynaptic function</style></title><secondary-title><style face="normal" font="default" size="100%">J Physiol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Nov 15</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=16141272</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">Pt 1</style></number><edition><style face="normal" font="default" size="100%">2005/09/06</style></edition><volume><style face="normal" font="default" size="100%">569</style></volume><pages><style face="normal" font="default" size="100%">103-17</style></pages><isbn><style face="normal" font="default" size="100%">0022-3751 (Print)0022-3751 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We investigated the roles of two Rab-family proteins, Rab3a and Rab5a, in hippocampal synaptic transmission using real-time fluorescence imaging. During synaptic activity, Rab3a dissociated from synaptic vesicles and dispersed into neighbouring axonal regions. Dispersion required calcium-dependent exocytosis and was complete before the entire vesicle pool turned over. In contrast, even prolonged synaptic activity produced limited dispersion of Rab5a. A GTPase-deficient mutant, Rab3a (Q81L), dispersed more slowly than wild-type Rab3a, and decreased the rate of exocytosis and the size of the recycling pool of vesicles. While overexpression of Rab3a did not affect vesicle recycling, overexpression of Rab5a reduced the recycling pool size by 50%. We propose that while Rab3a preferentially associates with recycling synaptic vesicles and modulates their trafficking, Rab5a is largely excluded from recycling vesicles.</style></abstract><accession-num><style face="normal" font="default" size="100%">16141272</style></accession-num><notes><style face="normal" font="default" size="100%">Star, Erin NNewton, A JamilaMurthy, Venkatesh NComparative StudyResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.EnglandThe Journal of physiologyJ Physiol. 2005 Nov 15;569(Pt 1):103-17. Epub 2005 Sep 1.</style></notes><custom2><style face="normal" font="default" size="100%">1464220</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dietz, S. B.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Contrasting short-term plasticity at two sides of the mitral-granule reciprocal synapse in the mammalian olfactory bulb</style></title><secondary-title><style face="normal" font="default" size="100%">J Physiol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Dec 1</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=16166156</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">Pt 2</style></number><edition><style face="normal" font="default" size="100%">2005/09/17</style></edition><volume><style face="normal" font="default" size="100%">569</style></volume><pages><style face="normal" font="default" size="100%">475-88</style></pages><isbn><style face="normal" font="default" size="100%">0022-3751 (Print)0022-3751 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The mitral-granule reciprocal synapse shapes the response of the olfactory bulb to odour stimuli by mediating lateral and reciprocal inhibition. We investigated the short-term plasticity of both the mitral-to-granule excitatory synapse and the granule-to-mitral inhibitory synapse in rat olfactory bulb slices, using whole-cell patch clamp recordings. The granule-to-mitral inhibitory synapse invariably exhibited paired-pulse depression at interstimulus intervals of less than a second, while the mitral-to-granule excitatory synapse showed heterogeneous responses, which on average yielded a moderate facilitation. Trains of stimuli led to a much greater depression at the granule-to-mitral synapse than at the mitral-to-granule synapse. Since mitral cells commonly respond to odours by burst firing with each inhalation cycle, we used bursts of stimuli to study recovery from depression. We found that recovery from depression induced by fast trains of stimuli was more rapid at the mitral-to-granule synapse than at the granule-to-mitral synapse. In addition, depression was enhanced by higher calcium concentrations, suggesting at least partial contribution of presynaptic mechanisms to short-term depression. The observed short-term plasticity could enable mitral cells to overcome autoinhibition and increase action potential propagation along lateral dendrites by burst firing.</style></abstract><accession-num><style face="normal" font="default" size="100%">16166156</style></accession-num><notes><style face="normal" font="default" size="100%">Dietz, Shelby BMurthy, Venkatesh NResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.EnglandThe Journal of physiologyJ Physiol. 2005 Dec 1;569(Pt 2):475-88. Epub 2005 Sep 15.</style></notes><custom2><style face="normal" font="default" size="100%">1464232</style></custom2><auth-address><style face="normal" font="default" size="100%">Graduate Program in Neuroscience, Harvard Medical School, Boston, MA, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Li, Z.</style></author><author><style face="normal" font="default" size="100%">Burrone, J.</style></author><author><style face="normal" font="default" size="100%">Tyler, W. J.</style></author><author><style face="normal" font="default" size="100%">Hartman, K. N.</style></author><author><style face="normal" font="default" size="100%">Albeanu, D. F.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic vesicle recycling studied in transgenic mice expressing synaptopHluorin</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Apr 26</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15837917</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">17</style></number><edition><style face="normal" font="default" size="100%">2005/04/20</style></edition><volume><style face="normal" font="default" size="100%">102</style></volume><pages><style face="normal" font="default" size="100%">6131-6</style></pages><isbn><style face="normal" font="default" size="100%">0027-8424 (Print)0027-8424 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Synaptic vesicles are recycled locally within presynaptic specializations. We examined how vesicles are reused after endocytosis, using transgenic mice expressing the genetically encoded fluorescent indicator synaptopHluorin in subsets of neurons. At both excitatory and inhibitory synapses in cultured hippocampal neurons, newly endocytosed vesicles did not preferentially enter the releasable pool of vesicles. Rather, they entered the reserve pool first and subsequently the readily releasable pool over a period of several minutes. All vesicles in the recycling pool could be accessed by spaced stimuli, arguing against preferential local reuse of the readily releasable vesicles. Interestingly, nearly half the vesicles at excitatory synapses, and a third at inhibitory synapses, could not be recruited for release even by sustained stimuli. We conclude that, at presynaptic terminals in the hippocampus, most vesicles vacate release sites after exocytosis and are replaced by existing vesicles from the reserve pool, placing constraints on kiss-and-run recycling.</style></abstract><accession-num><style face="normal" font="default" size="100%">15837917</style></accession-num><notes><style face="normal" font="default" size="100%">Li, ZhiyingBurrone, JuanTyler, William JHartman, Kenichi NAlbeanu, Dinu FMurthy, Venkatesh NResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.United StatesProceedings of the National Academy of Sciences of the United States of AmericaProc Natl Acad Sci U S A. 2005 Apr 26;102(17):6131-6. Epub 2005 Apr 18.</style></notes><custom2><style face="normal" font="default" size="100%">1087931</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Tyler, W. J.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic vesicles</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Biol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2004</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Apr 20</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=15084295</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">8</style></number><edition><style face="normal" font="default" size="100%">2004/04/16</style></edition><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">R294-7</style></pages><isbn><style face="normal" font="default" size="100%">0960-9822 (Print)0960-9822 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><accession-num><style face="normal" font="default" size="100%">15084295</style></accession-num><notes><style face="normal" font="default" size="100%">Tyler, William JMurthy, Venkatesh NEnglandCurrent biology : CBCurr Biol. 2004 Apr 20;14(8):R294-7.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Burrone, J.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic gain control and homeostasis</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Opin Neurobiol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2003</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Oct</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=14630218</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5</style></number><edition><style face="normal" font="default" size="100%">2003/11/25</style></edition><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">560-7</style></pages><isbn><style face="normal" font="default" size="100%">0959-4388 (Print)0959-4388 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Chronic changes in activity can induce neurons to alter the strength of all their synapses in unison. Although the specific changes that occur appear to vary depending on the experimental preparation, their net effect is to counter the experimentally induced modification of activity. Such adaptive, cell-wide changes in synaptic strength serve to stabilize neuronal activity and are collectively referred to as homeostatic synaptic plasticity. Recent studies have shed light on what triggers homeostatic synaptic plasticity, whether or not it is distinct from other forms of synaptic plasticity and whether or not it occurs in the intact brain.</style></abstract><accession-num><style face="normal" font="default" size="100%">14630218</style></accession-num><notes><style face="normal" font="default" size="100%">Burrone, JuanMurthy, Venkatesh NResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.ReviewEnglandCurrent opinion in neurobiologyCurr Opin Neurobiol. 2003 Oct;13(5):560-7.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular &amp; Cellular Biology, 16 Divinity Avenue, Harvard University, Cambridge, MA 02138, USA. jburrone@mcb.harvard.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Samuel, A. D.</style></author><author><style face="normal" font="default" size="100%">Silva, R. A.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic activity of the AFD neuron in Caenorhabditis elegans correlates with thermotactic memory</style></title><secondary-title><style face="normal" font="default" size="100%">J Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2003</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan 15</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12533596</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">2</style></number><edition><style face="normal" font="default" size="100%">2003/01/21</style></edition><volume><style face="normal" font="default" size="100%">23</style></volume><pages><style face="normal" font="default" size="100%">373-6</style></pages><isbn><style face="normal" font="default" size="100%">1529-2401 (Electronic)0270-6474 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Thermotactic behavior in Caenorhabditis elegans is sensitive to both a worm's ambient temperature (T(amb)) and its memory of the temperature of its cultivation (T(cult)). The AFD neuron is part of a neural circuit that underlies thermotactic behavior. By monitoring the fluorescence of pH-sensitive green fluorescent protein localized to synaptic vesicles, we measured the rate of the synaptic release of AFD in worms cultivated at temperatures between 15 and 25 degrees C, and subjected to fixed, ambient temperatures in the same range. We found that the rate of AFD synaptic release is high if either T(amb) &gt; T(cult) or T(amb) &lt; T(cult), but AFD synaptic release is low if T(amb) congruent with T(cult). This suggests that AFD encodes a direct comparison between T(amb) and T(cult).</style></abstract><accession-num><style face="normal" font="default" size="100%">12533596</style></accession-num><notes><style face="normal" font="default" size="100%">Samuel, Aravinthan D TSilva, Ruwan AMurthy, Venkatesh NIn VitroResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.United StatesThe Journal of neuroscience : the official journal of the Society for NeuroscienceJ Neurosci. 2003 Jan 15;23(2):373-6.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">De Camilli, P.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cell biology of the presynaptic terminal</style></title><secondary-title><style face="normal" font="default" size="100%">Annu Rev Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2003</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=14527272</style></url></web-urls></urls><edition><style face="normal" font="default" size="100%">2003/10/07</style></edition><volume><style face="normal" font="default" size="100%">26</style></volume><pages><style face="normal" font="default" size="100%">701-28</style></pages><isbn><style face="normal" font="default" size="100%">0147-006X (Print)0147-006X (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The chemical synapse is a specialized intercellular junction that operates nearly autonomously to allow rapid, specific, and local communication between neurons. Focusing our attention on the presynaptic terminal, we review the current understanding of how synaptic morphology is maintained and then the mechanisms in synaptic vesicle exocytosis and recycling.</style></abstract><accession-num><style face="normal" font="default" size="100%">14527272</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, Venkatesh NDe Camilli, PietroResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.ReviewUnited StatesAnnual review of neuroscienceAnnu Rev Neurosci. 2003;26:701-28.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA. vnmurthy@fas.harvard.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dertinger, S. K.</style></author><author><style face="normal" font="default" size="100%">Jiang, X.</style></author><author><style face="normal" font="default" size="100%">Li, Z.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Whitesides, G. M.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Gradients of substrate-bound laminin orient axonal specification of neurons</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Oct 1</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12237407</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">20</style></number><edition><style face="normal" font="default" size="100%">2002/09/19</style></edition><volume><style face="normal" font="default" size="100%">99</style></volume><pages><style face="normal" font="default" size="100%">12542-7</style></pages><isbn><style face="normal" font="default" size="100%">0027-8424 (Print)0027-8424 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Little is known about the influence of substrate-bound gradients on neuronal development, since it has been difficult to fabricate gradients over the distances typically required for biological studies (a few hundred micrometers). This article demonstrates a generally applicable technique for the fabrication of substrate-bound gradients of proteins with complex shapes, using laminar flows in microchannels. Gradients that range from pure laminin to pure BSA were formed in solution by using a network of microchannels, and these proteins were allowed to adsorb onto a homogeneous layer of poly-l-lysine. Rat hippocampal neurons were cultivated on these substrate-bound gradients. Analysis of optical images of these neurons showed that axon specification is oriented in the direction of increasing surface density of laminin. Linear gradients in laminin adsorbed from a gradient in solution having a slope of nabla [laminin] &gt; about 0.06 microg (ml.microm)(-1) (defined by dividing the change of concentration of laminin in solution over the distance of the gradient) orient axon specification, whereas those with nabla [laminin] &lt; about 0.06 microg (ml.microm)(-1) have no effect.</style></abstract><accession-num><style face="normal" font="default" size="100%">12237407</style></accession-num><notes><style face="normal" font="default" size="100%">Dertinger, Stephan K WJiang, XingyuLi, ZhiyingMurthy, Venkatesh NWhitesides, George MGM 30367/GM/NIGMS NIH HHS/United StatesNS039059/NS/NINDS NIH HHS/United StatesResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.United StatesProceedings of the National Academy of Sciences of the United States of AmericaProc Natl Acad Sci U S A. 2002 Oct 1;99(20):12542-7. Epub 2002 Sep 17.</style></notes><custom2><style face="normal" font="default" size="100%">130496</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Chemistry and Chemical Biology, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Burrone, J.</style></author><author><style face="normal" font="default" size="100%">O'Byrne, M.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Multiple forms of synaptic plasticity triggered by selective suppression of activity in individual neurons</style></title><secondary-title><style face="normal" font="default" size="100%">Nature</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Nov 28</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=12459783</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6914</style></number><edition><style face="normal" font="default" size="100%">2002/12/03</style></edition><volume><style face="normal" font="default" size="100%">420</style></volume><pages><style face="normal" font="default" size="100%">414-8</style></pages><isbn><style face="normal" font="default" size="100%">0028-0836 (Print)0028-0836 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The rules by which neuronal activity causes long-term modification of synapses in the central nervous system are not fully understood. Whereas competitive or correlation-based rules result in local modification of synapses, homeostatic modifications allow neuron-wide changes in synaptic strength, promoting stability. Experimental investigations of these rules at central nervous system synapses have relied generally on manipulating activity in populations of neurons. Here, we investigated the effect of suppressing excitability in single neurons within a network of active hippocampal neurons by overexpressing an inward-rectifier potassium channel. Reducing activity in a neuron before synapse formation leads to a reduction in functional synaptic inputs to that neuron; no such reduction was observed when activity of all neurons was uniformly suppressed. In contrast, suppressing activity in a single neuron after synapses are established results in a homeostatic increase in synaptic input, which restores the activity of the neuron to control levels. Our results highlight the differences between global and selective suppression of activity, as well as those between early and late manipulation of activity.</style></abstract><accession-num><style face="normal" font="default" size="100%">12459783</style></accession-num><notes><style face="normal" font="default" size="100%">Burrone, JuanO'Byrne, MichaelMurthy, Venkatesh NResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.EnglandNatureNature. 2002 Nov 28;420(6914):414-8.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular &amp; Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Star, E. N.</style></author><author><style face="normal" font="default" size="100%">Kwiatkowski, D. J.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Rapid turnover of actin in dendritic spines and its regulation by activity</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Mar</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11850630</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">3</style></number><edition><style face="normal" font="default" size="100%">2002/02/19</style></edition><volume><style face="normal" font="default" size="100%">5</style></volume><pages><style face="normal" font="default" size="100%">239-46</style></pages><isbn><style face="normal" font="default" size="100%">1097-6256 (Print)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Dendritic spines are motile structures that contain high concentrations of filamentous actin. Using hippocampal neurons expressing fluorescent actin and the method of fluorescence recovery after photobleaching, we found that 85 +/- 2% of actin in the spine was dynamic, with a turnover time of 44.2 +/- 4.0 s. The rapid turnover is not compatible with current models invoking a large population of stable filaments and static coupling of filaments to postsynaptic components. Low-frequency stimulation known to induce long-term depression in these neurons stabilized nearly half the dynamic actin in the spine. This effect depended on the activation of N-methyl-D-aspartate (NMDA) receptors and the influx of calcium. In neurons from mice lacking gelsolin, a calcium-dependent actin-binding protein, activity-dependent stabilization of actin was impaired. Our studies provide new information on the kinetics of actin turnover in spines, its regulation by neural activity and the mechanisms involved in this regulation.</style></abstract><accession-num><style face="normal" font="default" size="100%">11850630</style></accession-num><notes><style face="normal" font="default" size="100%">Star, Erin NKwiatkowski, David JMurthy, Venkatesh NResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.United StatesNature neuroscienceNat Neurosci. 2002 Mar;5(3):239-46.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular &amp; Cellular Biology, Harvard University, 16 Divinity Ave., Cambridge, Massachusetts 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zito, K.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Dendritic spines</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Biol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2002</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan 8</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11790313</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">1</style></number><edition><style face="normal" font="default" size="100%">2002/01/16</style></edition><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">R5</style></pages><isbn><style face="normal" font="default" size="100%">0960-9822 (Print)0960-9822 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><accession-num><style face="normal" font="default" size="100%">11790313</style></accession-num><notes><style face="normal" font="default" size="100%">Zito, KarenMurthy, Venkatesh NEnglandCurrent biology : CBCurr Biol. 2002 Jan 8;12(1):R5.</style></notes><auth-address><style face="normal" font="default" size="100%">Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Schikorski, T.</style></author><author><style face="normal" font="default" size="100%">Stevens, C. F.</style></author><author><style face="normal" font="default" size="100%">Zhu, Y.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Inactivity produces increases in neurotransmitter release and synapse size</style></title><secondary-title><style face="normal" font="default" size="100%">Neuron</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Nov 20</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11719207</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">4</style></number><edition><style face="normal" font="default" size="100%">2001/11/24</style></edition><volume><style face="normal" font="default" size="100%">32</style></volume><pages><style face="normal" font="default" size="100%">673-82</style></pages><isbn><style face="normal" font="default" size="100%">0896-6273 (Print)0896-6273 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">When hippocampal synapses in culture are pharmacologically silenced for several days, synaptic strength increases. The structural correlate of this change in strength is an increase in the size of the synapses, with all synaptic components--active zone, postsynaptic density, and bouton--becoming larger. Further, the number of docked vesicles and the total number of vesicles per synapse increases, although the number of docked vesicles per area of active zone is unchanged. In parallel with these anatomical changes, the physiologically measured size of the readily releasable pool (RRP) and the release probability are increased. Ultrastructural analysis of individual synapses in which the RRP was previously measured reveals that, within measurement error, the same number of vesicles are docked as are estimated to be in the RRP.</style></abstract><accession-num><style face="normal" font="default" size="100%">11719207</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NSchikorski, TStevens, C FZhu, YResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.United StatesNeuronNeuron. 2001 Nov 20;32(4):673-82.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Spreading synapsins</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Dec</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11723455</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">12</style></number><edition><style face="normal" font="default" size="100%">2001/11/28</style></edition><volume><style face="normal" font="default" size="100%">4</style></volume><pages><style face="normal" font="default" size="100%">1155-7</style></pages><isbn><style face="normal" font="default" size="100%">1097-6256 (Print)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><accession-num><style face="normal" font="default" size="100%">11723455</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NCommentNewsUnited StatesNature neuroscienceNat Neurosci. 2001 Dec;4(12):1155-7.</style></notes></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Li, Z.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Visualizing postendocytic traffic of synaptic vesicles at hippocampal synapses</style></title><secondary-title><style face="normal" font="default" size="100%">Neuron</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Aug 30</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11545718</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">4</style></number><edition><style face="normal" font="default" size="100%">2001/09/08</style></edition><volume><style face="normal" font="default" size="100%">31</style></volume><pages><style face="normal" font="default" size="100%">593-605</style></pages><isbn><style face="normal" font="default" size="100%">0896-6273 (Print)0896-6273 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We have investigated mechanisms in postendocytic processing of synaptic vesicles at hippocampal synapses, using synaptobrevin/vesicle-associated membrane protein (VAMP) tagged with variants of the green fluorescent protein. Following exocytosis, VAMP is retrieved at synaptic and adjoining axonal regions. Retrieved VAMP-containing vesicles return to synaptic vesicle clusters at a rate slower than endocytosis. Vesicles containing a different protein, synaptophysin, recluster at a similar rate, suggesting common vesicular intermediates for the two proteins. Activity prolongs the time taken by endocytosed vesicles to return to synapses. Exogenous calcium buffers slow endocytosis but have no additional effect on the time course of reclustering. In contrast, the protein kinase inhibitor staurosporine does not affect endocytosis but slows reclustering. Finally, since VAMP can move freely on surface membranes, sustained synaptic activity leads to mixing of this vesicular component between adjacent synapses.</style></abstract><accession-num><style face="normal" font="default" size="100%">11545718</style></accession-num><notes><style face="normal" font="default" size="100%">Li, ZMurthy, V NResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.United StatesNeuronNeuron. 2001 Aug 30;31(4):593-605.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Burrone, J.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic plasticity: rush hour traffic in the AMPA lanes</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Biol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2001</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Apr 3</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11413018</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">7</style></number><edition><style face="normal" font="default" size="100%">2001/06/20</style></edition><volume><style face="normal" font="default" size="100%">11</style></volume><pages><style face="normal" font="default" size="100%">R274-7</style></pages><isbn><style face="normal" font="default" size="100%">0960-9822 (Print)0960-9822 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Recent experiments indicate that modification of synaptic strength may involve rapid regulation of vesicular traffic on the postsynaptic side of the synapse. The specific vesicular trafficking route taken by postsynaptic receptors appears to depend on the stimulus.</style></abstract><accession-num><style face="normal" font="default" size="100%">11413018</style></accession-num><notes><style face="normal" font="default" size="100%">Burrone, JMurthy, V NEnglandCurrent biology : CBCurr Biol. 2001 Apr 3;11(7):R274-7.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular &amp; Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Samuel, A. D.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Hengartner, M. O.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Calcium dynamics during fertilization in C. elegans</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Dev Biol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2001</style></year></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11346453</style></url></web-urls></urls><edition><style face="normal" font="default" size="100%">2001/05/11</style></edition><volume><style face="normal" font="default" size="100%">1</style></volume><pages><style face="normal" font="default" size="100%">8</style></pages><isbn><style face="normal" font="default" size="100%">1471-213X (Electronic)1471-213X (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">BACKGROUND: Of the animals typically used to study fertilization-induced calcium dynamics, none is as accessible to genetics and molecular biology as the model organism Caenorhabditis elegans. Motivated by the experimental possibilities inherent in using such a well-established model organism, we have characterized fertilization-induced calcium dynamics in C. elegans. RESULTS: Owing to the transparency of the nematode, we have been able to study the calcium signal in C. elegans fertilization in vivo by monitoring the fluorescence of calcium indicator dyes that we introduce into the cytosol of oocytes. In C. elegans, fertilization induces a single calcium transient that is initiated soon after oocyte entry into the spermatheca, the compartment that contains sperm. Therefore, it is likely that the calcium transient is initiated by contact with sperm. This calcium elevation spreads throughout the oocyte, and decays monotonically after which the cytosolic calcium concentration returns to that preceding fertilization. Only this single calcium transient is observed. CONCLUSION: Development of a technique to study fertilization induced calcium transients opens several experimental possibilities, e.g., identification of the signaling events intervening sperm binding and calcium elevation, identifying the possible roles of the calcium elevation such as the completion of meiosis, the formation of the eggshell, and the establishing of the embryo's axis of symmetry.</style></abstract><accession-num><style face="normal" font="default" size="100%">11346453</style></accession-num><notes><style face="normal" font="default" size="100%">Samuel, A DMurthy, V NHengartner, M OResearch Support, U.S. Gov't, P.H.S.EnglandBMC developmental biologyBMC Dev Biol. 2001;1:8. Epub 2001 Apr 26.</style></notes><custom2><style face="normal" font="default" size="100%">31342</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, USA. asamuel@fas.harvard.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Fetz, E. E.</style></author><author><style face="normal" font="default" size="100%">Chen, D.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Matsumura, M.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic interactions mediating synchrony and oscillations in primate sensorimotor cortex</style></title><secondary-title><style face="normal" font="default" size="100%">J Physiol Paris</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2000</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Sep-Dec</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=11165903</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">5-6</style></number><edition><style face="normal" font="default" size="100%">2001/02/13</style></edition><volume><style face="normal" font="default" size="100%">94</style></volume><pages><style face="normal" font="default" size="100%">323-31</style></pages><isbn><style face="normal" font="default" size="100%">0928-4257 (Print)0928-4257 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The appearance of oscillatory modes of 'gamma' activity in many cortical areas of different species has generated interest in understanding their underlying mechanisms and possible functions. This paper reviews evidence from studies on primate motor cortex showing that oscillatory activity entrains many neurons during periods of exploratory manipulative behavior. These oscillatory episodes synchronize widely spread neurons in sensorimotor cortex bilaterally, including descending corticospinal neurons, as evidenced by correlated modulations in EMG activity. The resulting neural synchronization involves task-related and -unrelated neurons similarly, suggesting that it is more likely to play some global role in attention than mediating any obvious interactions involved in coordinating movements. Intracellular recordings have elucidated the strength and types of synaptic interactions between motor cortical neurons that are involved in both normal and oscillatory activity. Spike-triggered averages (STAs) of intracellular membrane potentials have revealed serial connections in the form of unitary excitatory and inhibitory post-synaptic potentials (EPSPs and IPSPs). More commonly, STAs showed large synchronous excitatory or inhibitory potentials (ASEPs and ASIPs) beginning before the trigger spike and composed of multiple unitary events. ASEPs involved synchronous activity in a larger and more widespread group of presynaptic neurons than ASIPs. During oscillatory episodes synchronized excitatory and inhibitory synaptic potentials occurred in varying proportions. EPSPs evoked by stimulating neighboring cortical sites during the depolarizing phase of spontaneous oscillations showed evidence of transient potentiation. These observations are consistent with several functional hypotheses, but fit best with a possible role in attention or arousal.</style></abstract><accession-num><style face="normal" font="default" size="100%">11165903</style></accession-num><notes><style face="normal" font="default" size="100%">Fetz, E EChen, DMurthy, V NMatsumura, MNS12542/NS/NINDS NIH HHS/United StatesRR00166/RR/NCRR NIH HHS/United StatesResearch Support, U.S. Gov't, P.H.S.FranceJournal of physiology, ParisJ Physiol Paris. 2000 Sep-Dec;94(5-6):323-31.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Physiology and Biophysics and Regional Primate Research Center, University of Washington, Seattle, WA 98195-7290, USA. fetz@u.washington.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Sejnowski, T. J.</style></author><author><style face="normal" font="default" size="100%">Stevens, C. F.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Dynamics of dendritic calcium transients evoked by quantal release at excitatory hippocampal synapses</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2000</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan 18</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=10639177</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">2</style></number><edition><style face="normal" font="default" size="100%">2000/01/19</style></edition><volume><style face="normal" font="default" size="100%">97</style></volume><pages><style face="normal" font="default" size="100%">901-6</style></pages><isbn><style face="normal" font="default" size="100%">0027-8424 (Print)0027-8424 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Synaptic N-methyl-D-aspartate (NMDA) receptors detect coincident pre- and postsynaptic activity and play a critical role in triggering changes in synaptic strength at central synapses. Despite intensive study of synaptic plasticity, relatively little is known about the magnitude and duration of calcium accumulation caused by unitary events at individual synapses. We used fluorescence imaging to detect NMDA receptor-mediated miniature synaptic calcium transients (MSCTs) caused by spontaneous release of synaptic vesicles in dendrites of cultured hippocampal neurons. MSCTs originated focally in dendritic regions &lt;1 microm in length and decayed with a time constant of 0.35 +/- 0.03 s. Multiple occurrences of MSCTs recorded at single sites had fluctuating amplitudes, with a coefficient of variation of 0.34. From the reduction in the spatial spread of MSCTs with decreasing concentration of indicator dye, we estimated that the dominant endogenous calcium buffer in dendrites is relatively immobile (diffusion coefficient between 10 and 50 microm(2)/s). We conclude that calcium rise caused by spontaneous quantal synaptic NMDA receptor activation (i) is variable, (ii) lasts for a time period briefer than previous measurements indicate, and (iii) is confined by endogenous calcium buffers to local dendritic regions even when synapses are not on spines.</style></abstract><accession-num><style face="normal" font="default" size="100%">10639177</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NSejnowski, T JStevens, C FMH46482/MH/NIMH NIH HHS/United StatesNS12961/NS/NINDS NIH HHS/United StatesResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.United statesProceedings of the National Academy of Sciences of the United States of AmericaProc Natl Acad Sci U S A. 2000 Jan 18;97(2):901-6.</style></notes><custom2><style face="normal" font="default" size="100%">15428</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. vnmurthy@fas.harvard.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Getting the membrane into shape for endocytosis</style></title><secondary-title><style face="normal" font="default" size="100%">Neuron</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Sep</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=10677020</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">1</style></number><edition><style face="normal" font="default" size="100%">2000/02/17</style></edition><volume><style face="normal" font="default" size="100%">24</style></volume><pages><style face="normal" font="default" size="100%">2-4</style></pages><isbn><style face="normal" font="default" size="100%">0896-6273 (Print)0896-6273 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><accession-num><style face="normal" font="default" size="100%">10677020</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NCommentReviewUnited statesNeuronNeuron. 1999 Sep;24(1):2-4.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Optical detection of synaptic vesicle exocytosis and endocytosis</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Opin Neurobiol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jun</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=10395575</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">3</style></number><edition><style face="normal" font="default" size="100%">1999/07/08</style></edition><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">314-20</style></pages><isbn><style face="normal" font="default" size="100%">0959-4388 (Print)0959-4388 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Recent advances in optical methods have catalyzed a detailed study of individual visualized synapses in several model systems. Quantal events at small central synapses, as well as single granule exocytosis in secretory cells, have been detected using quantitative fluorescence imaging. Sensitive detection of exocytosis and endocytosis at individual synapses has advanced our knowledge of synaptic vesicle trafficking.</style></abstract><accession-num><style face="normal" font="default" size="100%">10395575</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NResearch Support, Non-U.S. Gov'tReviewEnglandCurrent opinion in neurobiologyCurr Opin Neurobiol. 1999 Jun;9(3):314-20.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Molecular &amp; Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, Massachusetts 02138, USA. vnmurthy@fas.harvard.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Stevens, C. F.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Reversal of synaptic vesicle docking at central synapses</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Neurosci</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jun</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=10448213</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6</style></number><edition><style face="normal" font="default" size="100%">1999/08/17</style></edition><volume><style face="normal" font="default" size="100%">2</style></volume><pages><style face="normal" font="default" size="100%">503-7</style></pages><isbn><style face="normal" font="default" size="100%">1097-6256 (Print)1097-6256 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We used quantitative fluorescence imaging of vesicles labeled with membrane-soluble dyes to determine rates of undocking and spontaneous exocytosis of vesicles docked to the active zone of hippocampal synapses in culture. Individual vesicles undock about once per two minutes and spontaneously exocytose about once per eight minutes. Thus, not only does undocking occur, but it is over threefold faster than spontaneous fusion.</style></abstract><accession-num><style face="normal" font="default" size="100%">10448213</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NStevens, C FResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.United statesNature neuroscienceNat Neurosci. 1999 Jun;2(6):503-7.</style></notes><auth-address><style face="normal" font="default" size="100%">Howard Hughes Medical Institute, and Molecular Neurobiology Lab, Salk Institute, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zhang, B.</style></author><author><style face="normal" font="default" size="100%">Ganetzky, B.</style></author><author><style face="normal" font="default" size="100%">Bellen, H. J.</style></author><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Tailoring uniform coats for synaptic vesicles during endocytosis</style></title><secondary-title><style face="normal" font="default" size="100%">Neuron</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jul</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=10433253</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">3</style></number><edition><style face="normal" font="default" size="100%">1999/08/05</style></edition><volume><style face="normal" font="default" size="100%">23</style></volume><pages><style face="normal" font="default" size="100%">419-22</style></pages><isbn><style face="normal" font="default" size="100%">0896-6273 (Print)0896-6273 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><accession-num><style face="normal" font="default" size="100%">10433253</style></accession-num><notes><style face="normal" font="default" size="100%">Zhang, BGanetzky, BBellen, H JMurthy, V NReviewUnited statesNeuronNeuron. 1999 Jul;23(3):419-22.</style></notes><auth-address><style face="normal" font="default" size="100%">Department of Human and Molecular Genetics, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA. bxz@bcm.tmc.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic plasticity: step-wise strengthening</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Biol</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">1998</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Sep 10</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=9740794</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">18</style></number><edition><style face="normal" font="default" size="100%">1998/09/19</style></edition><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">R650-3</style></pages><isbn><style face="normal" font="default" size="100%">0960-9822 (Print)0960-9822 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Recent studies suggest that the strength of synapses in the brain may change in a step-wise manner, rather than continuously.</style></abstract><accession-num><style face="normal" font="default" size="100%">9740794</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NReviewEnglandCurrent biology : CBCurr Biol. 1998 Sep 10;8(18):R650-3.</style></notes><auth-address><style face="normal" font="default" size="100%">Molecular Neurobiology Laboratory, Salk Institute, L Jolla, CA 92037, USA. venk@salk.edu</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murthy, V. N.</style></author><author><style face="normal" font="default" size="100%">Stevens, C. F.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Synaptic vesicles retain their identity through the endocytic cycle</style></title><secondary-title><style face="normal" font="default" size="100%">Nature</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">1998</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Apr 2</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Citation&amp;list_uids=9548254</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">6675</style></number><edition><style face="normal" font="default" size="100%">1998/04/21</style></edition><volume><style face="normal" font="default" size="100%">392</style></volume><pages><style face="normal" font="default" size="100%">497-501</style></pages><isbn><style face="normal" font="default" size="100%">0028-0836 (Print)0028-0836 (Linking)</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">After fusion of synaptic vesicles with presynaptic membrane and secretion of the contents of the vesicles into the synaptic cleft (a process known as exocytosis), the vesicular membrane is retrieved by endocytosis (internalization) for re-use. Several issues regarding endocytosis at central synapses are unresolved, including the location of membrane retrieval (relative to the active zone, where exocytosis occurs), the time course of various endocytic steps, and the recycling path taken by newly endocytosed membranes. The classical model of synaptic-vesicle recycling, proposed by analogy to other cellular endocytic pathways, involves retrieval of the membrane, fusion of the membrane with endosome-like compartments and, finally, budding of new synaptic vesicles from endosomes, although the endosomal station may not be obligatory. Here we test the classical model by using the fluorescent membrane dye FM1-43 with quantitative fluorescence microscopy. We find that the amount of dye per vesicle taken up by endocytosis equals the amount of dye a vesicle releases on exocytosis; therefore, we conclude that the internalized vesicles do not, as the classical picture suggests, communicate with intermediate endosome-like compartments during the recycling process.</style></abstract><accession-num><style face="normal" font="default" size="100%">9548254</style></accession-num><notes><style face="normal" font="default" size="100%">Murthy, V NStevens, C FResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.EnglandNatureNature. 1998 Apr 2;392(6675):497-501.</style></notes><auth-address><style face="normal" font="default" size="100%">Howard Hughes Medical Institute and Molecular Neurobiology Laboratory, Salk Institute, La Jolla, California 92037, USA.</style></auth-address></record></records></xml>