Chronic Alcohol Exposure Alters Behavioral and Synaptic Plasticity of the Rodent Prefrontal Cortex

dc.contributor.authorKroener, Svenen_US
dc.contributor.authorMulholland, P. J.en_US
dc.contributor.authorNew, N. N.en_US
dc.contributor.authorGass, J. T.en_US
dc.contributor.authorBecker, H. C.en_US
dc.contributor.authorChandler, L. J.en_US
dc.date.accessioned2013-10-08T19:06:29Z
dc.date.available2013-10-08T19:06:29Z
dc.date.created2012-05-30
dc.description.abstractIn the present study, we used a mouse model of chronic intermittent ethanol (CIE) exposure to examine how CIE alters the plasticity of the medial prefrontal cortex (mPFC). In acute slices obtained either immediately or 1-week after the last episode of alcohol exposure, voltage-clamp recording of excitatory post-synaptic currents (EPSCs) in mPFC layer V pyramidal neurons revealed that CIE exposure resulted in an increase in the NMDA/AMPA current ratio. This increase appeared to result from a selective increase in the NMDA component of the EPSC. Consistent with this, Western blot analysis of the postsynaptic density fraction showed that while there was no change in expression of the AMPA GluR1 subunit, NMDA NR1 and NRB subunits were significantly increased in CIE exposed mice when examined immediately after the last episode of alcohol exposure. Unexpectedly, this increase in NR1 and NR2B was no longer observed after 1-week of withdrawal in spite of a persistent increase in synaptic NMDA currents. Analysis of spines on the basal dendrites of layer V neurons revealed that while the total density of spines was not altered, there was a selective increase in the density of mushroom-type spines following CIE exposure. Examination of NMDA-receptor mediated spike-timing-dependent plasticity (STDP) showed that CIE exposure was associated with altered expression of long-term potentiation (LTP). Lastly, behavioral studies using an attentional set-shifting task that depends upon the mPFC for optimal performance revealed deficits in cognitive flexibility in CIE exposed mice when tested up to 1-week after the last episode of alcohol exposure. Taken together, these observations are consistent with those in human alcoholics showing protracted deficits in executive function, and suggest these deficits may be associated with alterations in synaptic plasticity in the mPFC. © 2012 Kröner et al.en_US
dc.identifier.bibliographicCitationKroener, S., P. J. Mulholland, N. N. New, J. T. Gass, et al. 2012. "Chronic alcohol exposure alters behavioral and synaptic plasticity of the rodent prefrontal cortex." PLOS One 7(5): e37541.en_US
dc.identifier.issn1932-6203en_US
dc.identifier.issue5en_US
dc.identifier.urihttp://hdl.handle.net/10735.1/2874
dc.identifier.volume7en_US
dc.relation.urihttp://dx.doi.org/10.1371/journal.pone.0037541en_US
dc.rightsCC BY 3.0 (Attribution)en_US
dc.rights© 2012 The Authorsen_US
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/en_US
dc.source.journalPLOS Oneen_US
dc.subjectAlcoholismen_US
dc.subjectCognitionen_US
dc.subjectRodentsen_US
dc.titleChronic Alcohol Exposure Alters Behavioral and Synaptic Plasticity of the Rodent Prefrontal Cortexen_US
dc.typeTexten_US
dc.type.genrearticleen_US

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