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dc.contributor.authorSagi, Yotam
dc.contributor.authorHeiman, Myriam
dc.contributor.authorPeterson, Jayms D.
dc.contributor.authorMusatov, Sergei
dc.contributor.authorScarduzio, Mariangela
dc.contributor.authorLogan, Stephen M.
dc.contributor.authorKaplitt, Michael G.
dc.contributor.authorSurmeier, Dalton J.
dc.contributor.authorHeintz, Nathaniel
dc.contributor.authorGreengard, Paul
dc.date.accessioned2015-06-15T18:38:09Z
dc.date.available2015-06-15T18:38:09Z
dc.date.issued2014-12
dc.date.submitted2014-09
dc.identifier.issn0027-8424
dc.identifier.issn1091-6490
dc.identifier.urihttp://hdl.handle.net/1721.1/97433
dc.description.abstractRecurrent axon collaterals are a major means of communication between spiny projection neurons (SPNs) in the striatum and profoundly affect the function of the basal ganglia. However, little is known about the molecular and cellular mechanisms that underlie this communication. We show that intrastriatal nitric oxide (NO) signaling elevates the expression of the vesicular GABA transporter (VGAT) within recurrent collaterals of SPNs. Down-regulation of striatal NO signaling resulted in an attenuation of GABAergic signaling in SPN local collaterals, down-regulation of VGAT expression in local processes of SPNs, and impaired motor behavior. PKG1 and cAMP response element-binding protein are involved in the signal transduction that transcriptionally regulates VGAT by NO. These data suggest that transcriptional control of the vesicular GABA transporter by NO regulates GABA transmission and action selection.en_US
dc.description.sponsorshipUnited States Army Medical Research Acquisition Activity (Grant W81XWH-09-1-0108)en_US
dc.language.isoen_US
dc.publisherNational Academy of Sciences (U.S.)en_US
dc.relation.isversionofhttp://dx.doi.org/10.1073/pnas.1420162111en_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.sourceNational Academy of Sciences (U.S.)en_US
dc.titleNitric oxide regulates synaptic transmission between spiny projection neuronsen_US
dc.typeArticleen_US
dc.identifier.citationSagi, Yotam, Myriam Heiman, Jayms D. Peterson, Sergei Musatov, Mariangela Scarduzio, Stephen M. Logan, Michael G. Kaplitt, Dalton J. Surmeier, Nathaniel Heintz, and Paul Greengard. “Nitric Oxide Regulates Synaptic Transmission Between Spiny Projection Neurons.” Proceedings of the National Academy of Sciences 111, no. 49 (November 20, 2014): 17636–17641.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.departmentPicower Institute for Learning and Memoryen_US
dc.contributor.mitauthorHeiman, Myriamen_US
dc.relation.journalProceedings of the National Academy of Sciencesen_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.orderedauthorsSagi, Yotam; Heiman, Myriam; Peterson, Jayms D.; Musatov, Sergei; Scarduzio, Mariangela; Logan, Stephen M.; Kaplitt, Michael G.; Surmeier, Dalton J.; Heintz, Nathaniel; Greengard, Paulen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-6365-8673
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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