Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens

It is widely accepted that long-lasting changes of synaptic strength in the nucleus accumbens, a brain region involved in drug reward, mediate acute and chronic effects of alcohol. However, our understanding of the mechanisms underlying the effects of alcohol on synaptic plasticity is limited by the...

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Main Authors: Gilles Erwann Martin, Xincai eJi, Sucharita eSaha
Format: Article
Language:English
Published: Frontiers Media S.A. 2015-07-01
Series:Frontiers in Synaptic Neuroscience
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fnsyn.2015.00012/full
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author Gilles Erwann Martin
Xincai eJi
Sucharita eSaha
author_facet Gilles Erwann Martin
Xincai eJi
Sucharita eSaha
author_sort Gilles Erwann Martin
collection DOAJ
description It is widely accepted that long-lasting changes of synaptic strength in the nucleus accumbens, a brain region involved in drug reward, mediate acute and chronic effects of alcohol. However, our understanding of the mechanisms underlying the effects of alcohol on synaptic plasticity is limited by the fact that the nucleus accumbens receives glutamatergic inputs from distinct brain regions (e.g. the prefrontal cortex, the amygdala and the hippocampus), each region providing different information (e.g. spatial, emotional and cognitive). Combining whole-cell patch-clamp recordings and the optogenetic technique, we examined synaptic plasticity, and its regulation by alcohol, at cortical, hippocampal and amygdala inputs in fresh slices of mouse tissue. We showed that the origin of synaptic inputs determines the basic properties of glutamatergic synaptic transmission, the expression of spike-timing dependent long-term depression (tLTD) and long-term potentiation (tLTP) and their regulation by alcohol. While we observed both tLTP and tLTD at amygadala and hippocampal synapses, we showed that cortical inputs only undergo tLTD. Functionally, we provide evidence that acute EtOH has little effects on higher order information coming from the prefrontal cortex (PFCx), while severely impacting the ability of emotional and contextual information to induce long-lasting changes of synaptic strength.
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spelling doaj.art-c38a7bcb01f14bfbb0427f4e69f2c0252022-12-21T19:50:56ZengFrontiers Media S.A.Frontiers in Synaptic Neuroscience1663-35632015-07-01710.3389/fnsyn.2015.00012150247Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbensGilles Erwann Martin0Xincai eJi1Sucharita eSaha2University of Massachusetts Medical SchoolUniversity of Massachusetts Medical SchoolUniversity of Massachusetts Medical SchoolIt is widely accepted that long-lasting changes of synaptic strength in the nucleus accumbens, a brain region involved in drug reward, mediate acute and chronic effects of alcohol. However, our understanding of the mechanisms underlying the effects of alcohol on synaptic plasticity is limited by the fact that the nucleus accumbens receives glutamatergic inputs from distinct brain regions (e.g. the prefrontal cortex, the amygdala and the hippocampus), each region providing different information (e.g. spatial, emotional and cognitive). Combining whole-cell patch-clamp recordings and the optogenetic technique, we examined synaptic plasticity, and its regulation by alcohol, at cortical, hippocampal and amygdala inputs in fresh slices of mouse tissue. We showed that the origin of synaptic inputs determines the basic properties of glutamatergic synaptic transmission, the expression of spike-timing dependent long-term depression (tLTD) and long-term potentiation (tLTP) and their regulation by alcohol. While we observed both tLTP and tLTD at amygadala and hippocampal synapses, we showed that cortical inputs only undergo tLTD. Functionally, we provide evidence that acute EtOH has little effects on higher order information coming from the prefrontal cortex (PFCx), while severely impacting the ability of emotional and contextual information to induce long-lasting changes of synaptic strength.http://journal.frontiersin.org/Journal/10.3389/fnsyn.2015.00012/fullElectrophysiologysynaptic plasticityalcoholdrug addictionoptogeneticsAccumbens
spellingShingle Gilles Erwann Martin
Xincai eJi
Sucharita eSaha
Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens
Frontiers in Synaptic Neuroscience
Electrophysiology
synaptic plasticity
alcohol
drug addiction
optogenetics
Accumbens
title Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens
title_full Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens
title_fullStr Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens
title_full_unstemmed Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens
title_short Role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens
title_sort role of the origin of glutamatergic synaptic inputs in controlling synaptic plasticity and its modulation by alcohol in mice nucleus accumbens
topic Electrophysiology
synaptic plasticity
alcohol
drug addiction
optogenetics
Accumbens
url http://journal.frontiersin.org/Journal/10.3389/fnsyn.2015.00012/full
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