Accumbens D2-MSN hyperactivity drives antipsychotic-induced behavioral supersensitivity.
Journal
Molecular psychiatry
ISSN: 1476-5578
Titre abrégé: Mol Psychiatry
Pays: England
ID NLM: 9607835
Informations de publication
Date de publication:
11 2021
11 2021
Historique:
received:
25
04
2021
accepted:
07
07
2021
revised:
05
07
2021
pubmed:
6
8
2021
medline:
15
3
2022
entrez:
5
8
2021
Statut:
ppublish
Résumé
Antipsychotic-induced dopamine supersensitivity, or behavioral supersensitivity, is a problematic consequence of long-term antipsychotic treatment characterized by the emergence of motor abnormalities, refractory symptoms, and rebound psychosis. The underlying mechanisms are unclear and no approaches exist to prevent or reverse these unwanted effects of antipsychotic treatment. Here we demonstrate that behavioral supersensitivity stems from long-lasting pre, post and perisynaptic plasticity, including insertion of Ca
Identifiants
pubmed: 34349226
doi: 10.1038/s41380-021-01235-6
pii: 10.1038/s41380-021-01235-6
pmc: PMC8760070
doi:
Substances chimiques
Antipsychotic Agents
0
Receptors, Dopamine D1
0
Receptors, Dopamine D2
0
Cocaine
I5Y540LHVR
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
6159-6169Subventions
Organisme : NIDA NIH HHS
ID : F30 DA051159
Pays : United States
Organisme : NIDA NIH HHS
ID : P50 DA046373
Pays : United States
Informations de copyright
© 2021. The Author(s).
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