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dc.contributor.authorMateo, Celine
dc.contributor.authorAvermann, Michael
dc.contributor.authorGentet, Luc J.
dc.contributor.authorZhang, Feng
dc.contributor.authorDeisseroth, Karl
dc.contributor.authorPetersen, Carl C.H.
dc.date.accessioned2014-12-16T16:38:46Z
dc.date.available2014-12-16T16:38:46Z
dc.date.issued2011-09
dc.date.submitted2011-08
dc.identifier.issn09609822
dc.identifier.issn1879-0445
dc.identifier.urihttp://hdl.handle.net/1721.1/92324
dc.description.abstractBackground Synaptic interactions between excitatory and inhibitory neocortical neurons are important for mammalian sensory perception. Synaptic transmission between identified neurons within neocortical microcircuits has mainly been studied in brain slice preparations in vitro. Here, we investigate brain-state-dependent neocortical synaptic interactions in vivo by combining the specificity of optogenetic stimulation with the precision of whole-cell recordings from postsynaptic excitatory glutamatergic neurons and GFP-labeled inhibitory GABAergic neurons targeted through two-photon microscopy. Results Channelrhodopsin-2 (ChR2) stimulation of excitatory layer 2/3 barrel cortex neurons evoked larger and faster depolarizing postsynaptic potentials and more synaptically driven action potentials in fast-spiking (FS) GABAergic neurons compared to both non-fast-spiking (NFS) GABAergic neurons and postsynaptic excitatory pyramidal neurons located within the same neocortical microcircuit. The number of action potentials evoked in ChR2-expressing neurons showed low trial-to-trial variability, but postsynaptic responses varied strongly with near-linear dependence upon spontaneously driven changes in prestimulus membrane potential. Postsynaptic responses in excitatory neurons had reversal potentials, which were hyperpolarized relative to action potential threshold and were therefore inhibitory. Reversal potentials measured in postsynaptic GABAergic neurons were close to action potential threshold. Postsynaptic inhibitory neurons preferentially fired synaptically driven action potentials from spontaneously depolarized network states, with stronger state-dependent modulation in NFS GABAergic neurons compared to FS GABAergic neurons. Conclusions Inhibitory neurons appear to dominate neocortical microcircuit function, receiving stronger local excitatory synaptic input and firing more action potentials compared to excitatory neurons. In mouse layer 2/3 barrel cortex, we propose that strong state-dependent recruitment of inhibitory neurons drives competition among excitatory neurons enforcing sparse coding.en_US
dc.description.sponsorshipSwiss National Science Foundationen_US
dc.description.sponsorshipHuman Frontier Science Program (Strasbourg, France)en_US
dc.description.sponsorshipSystemsX.ch Initiativeen_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.cub.2011.08.028en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceElsevieren_US
dc.titleIn Vivo Optogenetic Stimulation of Neocortical Excitatory Neurons Drives Brain-State-Dependent Inhibitionen_US
dc.typeArticleen_US
dc.identifier.citationMateo, Celine, Michael Avermann, Luc J. Gentet, Feng Zhang, Karl Deisseroth, and Carl C.H. Petersen. “In Vivo Optogenetic Stimulation of Neocortical Excitatory Neurons Drives Brain-State-Dependent Inhibition.” Current Biology 21, no. 19 (October 2011): 1593–1602. © 2011 Elsevier Ltd.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.mitauthorZhang, Fengen_US
dc.relation.journalCurrent Biologyen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsMateo, Celine; Avermann, Michael; Gentet, Luc J.; Zhang, Feng; Deisseroth, Karl; Petersen, Carl C.H.en_US
dc.identifier.orcidhttps://orcid.org/0000-0003-2782-2509
mit.licensePUBLISHER_POLICYen_US


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