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dc.contributor.authorKolpakova, Jenya
dc.contributor.authorvan der Vinne, Vincent
dc.contributor.authorGiménez-Gómez, Pablo
dc.contributor.authorLe, Timmy
dc.contributor.authorMartin, Gilles E
dc.date.accessioned2023-02-14T19:40:21Z
dc.date.available2023-02-14T19:40:21Z
dc.date.issued2022-12-15
dc.identifier.citationKolpakova J, van der Vinne V, Gimenez-Gomez P, Le T, Martin GE. Binge alcohol drinking alters the differential control of cholinergic interneurons over nucleus accumbens D1 and D2 medium spiny neurons. Front Cell Neurosci. 2022 Dec 15;16:1010121. doi: 10.3389/fncel.2022.1010121. PMID: 36589290; PMCID: PMC9797504.en_US
dc.identifier.issn1662-5102
dc.identifier.doi10.3389/fncel.2022.1010121en_US
dc.identifier.pmid36589290
dc.identifier.urihttp://hdl.handle.net/20.500.14038/51692
dc.description.abstractAnimals studies support the notion that striatal cholinergic interneurons (ChIs) play a central role in basal ganglia function by regulating associative learning, reward processing, and motor control. In the nucleus accumbens (NAc), a brain region that mediates rewarding properties of substance abuse, acetylcholine regulates glutamatergic, dopaminergic, and GABAergic neurotransmission in naïve mice. However, it is unclear how ChIs orchestrate the control of these neurotransmitters/modulators to determine the synaptic excitability of medium spiny neurons (MSNs), the only projecting neurons that translate accumbens electrical activity into behavior. Also unknown is the impact of binge alcohol drinking on the regulation of dopamine D1- and D2 receptor-expressing MSNs (D1- and D2-MSNs, respectively) by ChIs. To investigate this question, we optogenetically stimulated ChIs while recording evoked and spontaneous excitatory postsynaptic currents (sEPSCs) in nucleus accumbens core D1- and D2-MSN of ChAT.ChR2.eYFPxDrd1.tdtomato mice. In alcohol-naïve mice, we found that stimulating NAc ChIs decreased sEPSCs frequency in both D1- and D2-MSNs, presumably through a presynaptic mechanism. Interestingly, ChI stimulation decreased MSN synaptic excitability through different mechanisms in D1- vs. D2-MSNs. While decrease of ChI-mediated sEPSCs frequency in D1-MSNs was mediated by dopamine, the same effect in D2-MSNs resulted from a direct control of glutamate release by ChIs. Interestingly, after 2 weeks of binge alcohol drinking, optogenetic stimulation of ChIs enhanced glutamate release in D1-MSNs, while its effect on D2-MSNs remained unchanged. Taken together, these data suggest that cholinergic interneurons could be a key target for regulation of NAc circuitry and for alcohol consumption.en_US
dc.language.isoenen_US
dc.relation.ispartofFrontiers in Cellular Neuroscienceen_US
dc.relation.urlhttps://doi.org/10.3389/fncel.2022.1010121en_US
dc.rights© 2022 Kolpakova, van der Vinne, Gimenez-Gomez, Le and Martin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these termsen_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectcholinergic interneuronen_US
dc.subjectdopamineen_US
dc.subjectglutamatergic synaptic transmissionen_US
dc.subjectnucleus accumbensen_US
dc.subjectoptogeneticen_US
dc.titleBinge alcohol drinking alters the differential control of cholinergic interneurons over nucleus accumbens D1 and D2 medium spiny neuronsen_US
dc.typeJournal Articleen_US
dc.source.journaltitleFrontiers in cellular neuroscience
dc.source.volume16
dc.source.beginpage1010121
dc.source.endpage
dc.source.countrySwitzerland
dc.identifier.journalFrontiers in cellular neuroscience
refterms.dateFOA2023-02-14T19:40:22Z
dc.contributor.departmentBrudnick Neuropsychiatric Research Instituteen_US
dc.contributor.departmentMorningside Graduate School of Biomedical Sciencesen_US
dc.contributor.departmentNeurobiologyen_US
dc.contributor.departmentMorningside Graduate School of Biomedical Sciences, Neuroscience Program
dc.contributor.departmentMartin Lab
dc.contributor.studentJenya Kolpakova
dc.contributor.studentTimmy Le
dc.description.thesisprogramNeuroscience


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© 2022 Kolpakova, van der Vinne,
Gimenez-Gomez, Le and Martin. This
is an open-access article distributed
under the terms of the Creative
Commons Attribution License (CC BY).
The use, distribution or reproduction in
other forums is permitted, provided
the original author(s) and the copyright
owner(s) are credited and that the
original publication in this journal is
cited, in accordance with accepted
academic practice. No use, distribution
or reproduction is permitted which
does not comply with these terms
Except where otherwise noted, this item's license is described as © 2022 Kolpakova, van der Vinne, Gimenez-Gomez, Le and Martin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms