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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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2015-07-01
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Series: | Frontiers in Synaptic Neuroscience |
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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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id | doaj.art-c38a7bcb01f14bfbb0427f4e69f2c025 |
institution | Directory Open Access Journal |
issn | 1663-3563 |
language | English |
last_indexed | 2024-12-20T06:00:36Z |
publishDate | 2015-07-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Synaptic Neuroscience |
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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