Ethanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling

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dc.contributor.advisorMorrisett, Richard A.
dc.contributor.committeeMemberHarris, Adron R
dc.contributor.committeeMemberGonzales, Rueben A
dc.contributor.committeeMemberZemelman, Boris
dc.creatorKircher, Daniel M.
dc.creator.orcid0000-0002-5710-1123
dc.date.accessioned2018-03-27T17:29:42Z
dc.date.available2018-03-27T17:29:42Z
dc.date.created2017-12
dc.date.issued2017-12
dc.date.submittedDecember 2017
dc.date.updated2018-03-27T17:29:43Z
dc.description.abstractThe purpose of this study was to determine the effects of ethanol exposure and consumption on the expression of plasticity of D1 dopamine receptor expressing (D1R) medium spiny neurons (MSNs) in the nucleus accumbens (NAc) shell receiving glutamatergic input solely from the ventral hippocampus (vHipp). Drd1a-tdTomato mice on a C57BL/6J background were injected bilaterally in the vHipp with a viral vector in order to express channelrhodopsin (ChR2) in vHipp terminals that synapse onto shell D1R-MSNs. Blue LED light stimulation was used to selectively depolarize ChR2 expressing vHipp terminals in the NAc shell, resulting in light-evoked EPSCs originating from vHipp. In voltage clamp experiments, we found that an induction protocol pairing 1 Hz blue light stimulation with postsynaptic membrane depolarization produced LTD in the vHipp to NAc circuit that is NMDA receptor dependent. In this study we found acute application of ethanol in vitro uniquely alters plasticity in the vHipp to NAc circuit. Low to moderate intoxicating concentration of ethanol blocked light evoked LTD expression which is in contrast to previous observations. Ethanol consumption in rodents impaired vHipp-Shell plasticity as well as resulted in altered glutamatergic signaling, and the insertion of Ca2+ permeable AMPA receptors (CPARs) D1R-MSNs post synaptic membranes. These findings suggest that the vHipp to NAc circuit is highly sensitive to ethanol treatment and may constitute a critical neuroadaptation that leads to the expression of ethanol dependence.
dc.description.departmentPharmaceutical Sciences
dc.format.mimetypeapplication/pdf
dc.identifierdoi:10.15781/T2X63BN9N
dc.identifier.urihttp://hdl.handle.net/2152/63989
dc.language.isoen
dc.subjectElectrophysiology
dc.subjectOptogenetics
dc.subjectNucleus accumbens
dc.subjectNAc
dc.subjectVentral hippocampus
dc.subjectvHipp
dc.subjectAlcohol
dc.subjectEthanol
dc.subjectCIE
dc.subject2BC
dc.subjectEthanol vapor
dc.subjectPlasticity
dc.subjectLTD
dc.subjectNMDAR-LTD
dc.subjectCPAR
dc.subjectGluA2 lacking
dc.titleEthanol experience elicits circuit specific adaptations of ventral hippocampal-accumbens glutamatergic signaling
dc.typeThesis
dc.type.materialtext
thesis.degree.departmentPharmaceutical Sciences
thesis.degree.disciplinePharmaceutical Sciences
thesis.degree.grantorThe University of Texas at Austin
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy

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