Cholinergic interneurons mediate cocaine extinction in male mice through plasticity across medium spiny neuron subtypes.
CP: Neuroscience
acetylcholine
cocaine
nucleus accumbens
plasticity
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
31 05 2022
31 05 2022
Historique:
received:
24
08
2021
revised:
07
03
2022
accepted:
05
05
2022
entrez:
1
6
2022
pubmed:
2
6
2022
medline:
7
6
2022
Statut:
ppublish
Résumé
Cholinergic interneurons (ChINs) in the nucleus accumbens (NAc) have been implicated in the extinction of drug associations, as well as related plasticity in medium spiny neurons (MSNs). However, since most previous work relied on artificial manipulations, whether endogenous acetylcholine signaling relates to drug associations is unclear. Moreover, despite great interest in the opposing effects of dopamine on MSN subtypes, whether ChIN-mediated effects vary by MSN subtype is also unclear. Here, we find that high endogenous acetylcholine event frequency correlates with greater extinction of cocaine-context associations across male mice. Additionally, extinction is associated with a weakening of glutamatergic synapses across MSN subtypes. Manipulating ChIN activity bidirectionally controls both the rate of extinction and the associated plasticity at MSNs. Our findings indicate that NAc ChINs mediate drug-context extinction by reducing glutamatergic synaptic strength across MSN subtypes, and that natural variation in acetylcholine signaling may contribute to individual differences in extinction.
Identifiants
pubmed: 35649378
pii: S2211-1247(22)00649-0
doi: 10.1016/j.celrep.2022.110874
pmc: PMC9196889
mid: NIHMS1812247
pii:
doi:
Substances chimiques
Cholinergic Agents
0
Cocaine
I5Y540LHVR
Acetylcholine
N9YNS0M02X
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
110874Subventions
Organisme : NIDA NIH HHS
ID : DP2 DA035149
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA047869
Pays : United States
Organisme : NINDS NIH HHS
ID : U19 NS104648
Pays : United States
Organisme : NIMH NIH HHS
ID : F32 MH118792
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH106689
Pays : United States
Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare no competing interests.
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