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Estradiol attenuates the K + -induced increase in extracellular GABA in rat striatum
dc.contributor.authorHu, Mingen_US
dc.contributor.authorWatson, Christopher J.en_US
dc.contributor.authorKennedy, Robert T.en_US
dc.contributor.authorBecker, Jill B.en_US
dc.date.accessioned2007-03-19T17:26:50Z
dc.date.available2007-03-19T17:26:50Z
dc.date.issued2006-02en_US
dc.identifier.citationHu, Ming; Watson, Chris J.; Kennedy, Robert T.; Becker, Jill B. (2006)."Estradiol attenuates the K + -induced increase in extracellular GABA in rat striatum." Synapse 59(2): 122-124. <http://hdl.handle.net/2027.42/49529>en_US
dc.identifier.issn0887-4476en_US
dc.identifier.issn1098-2396en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/49529
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16320305&dopt=citationen_US
dc.description.abstractEstradiol acts rapidly and directly to inhibit L-type Ca 2+ current in medium spiny neurons from striatum. Since medium spiny neurons contain Γ-aminobutyric acid (GABA), we hypothesized that estradiol inhibition of Ca 2+ channel current in the cell body would result in decreased GABA release. In this study, we examined the effect of estradiol on the concentration of GABA, taurine, and glutamate in dialysate from striatum. In support of our hypothesis, the K + -evoked increase in GABA, but not taurine or glutamate, was significantly attenuated 30 min after treatment with estradiol. Synapse 59: 122–124, 2006. © 2005 Wiley-Liss, Inc.en_US
dc.format.extent138007 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleEstradiol attenuates the K + -induced increase in extracellular GABA in rat striatumen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumPsychology Department, University of Michigan, Ann Arbor, Michigan 48109 ; M.H. and C.J.W. contributed equally to the work in this paper.en_US
dc.contributor.affiliationumDepartment of Chemistry, University of Michigan, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationumDepartment of Chemistry, University of Michigan, Ann Arbor, Michigan 48109 ; Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109 ; Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationumPsychology Department, University of Michigan, Ann Arbor, Michigan 48109 ; Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109 ; Reproductive Sciences Program, University of Michigan Medical School, Ann Arbor, Michigan 48109 ; 4040 East Hall, 530 Church St., Ann Arbor, MI 48109-1043en_US
dc.identifier.pmid16320305en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/49529/1/20221_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/syn.20221en_US
dc.identifier.sourceSynapseen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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