Chronic nicotine impairs sparse motor learning via striatal fast-spiking parvalbumin interneurons.


Journal

Addiction biology
ISSN: 1369-1600
Titre abrégé: Addict Biol
Pays: United States
ID NLM: 9604935

Informations de publication

Date de publication:
05 2021
Historique:
revised: 09 07 2020
received: 28 03 2020
accepted: 21 07 2020
pubmed: 9 8 2020
medline: 3 11 2021
entrez: 9 8 2020
Statut: ppublish

Résumé

Nicotine can diversely affect neural activity and motor learning in animals. However, the impact of chronic nicotine on striatal activity in vivo and motor learning at long-term sparse timescale remains unknown. Here, we demonstrate that chronic nicotine persistently suppresses the activity of striatal fast-spiking parvalbumin interneurons, which mediate nicotine-induced deficit in sparse motor learning. Six weeks of longitudinal in vivo single-unit recording revealed that mice show reduced activity of fast-spiking interneurons in the dorsal striatum during chronic nicotine exposure and withdrawal. The reduced firing of fast-spiking interneurons was accompanied by spike broadening, diminished striatal delta oscillation power, and reduced sample entropy in local field potential. In addition, chronic nicotine withdrawal impaired motor learning with a weekly sparse training regimen but did not affect general locomotion and anxiety-like behavior. Lastly, the excitatory DREADD hM3Dq-mediated activation of striatal fast-spiking parvalbumin interneurons reversed the chronic nicotine withdrawal-induced deficit in sparse motor learning. Taken together, we identified that chronic nicotine withdrawal impairs sparse motor learning via disruption of activity in striatal fast-spiking parvalbumin interneurons. These findings suggest that sparse motor learning paradigm can reveal the subtle effect of nicotine withdrawal on motor function and that striatal fast-spiking parvalbumin interneurons are a neural substrate of nicotine's effect on motor learning.

Identifiants

pubmed: 32767546
doi: 10.1111/adb.12956
pmc: PMC8243919
doi:

Substances chimiques

Designer Drugs 0
Parvalbumins 0
Nicotine 6M3C89ZY6R

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e12956

Informations de copyright

© 2020 The Authors. Addiction Biology published by John Wiley & Sons Ltd on behalf of Society for the Study of Addiction.

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Auteurs

Baeksun Kim (B)

Convergence Research Center for Diagnosis, Treatment and Care System of Dementia (DTC), Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Division of Bio-Medical Science and Technology, KIST School, Korea University of Science and Technology (UST), Seoul, Republic of Korea.

Heh-In Im (HI)

Convergence Research Center for Diagnosis, Treatment and Care System of Dementia (DTC), Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Division of Bio-Medical Science and Technology, KIST School, Korea University of Science and Technology (UST), Seoul, Republic of Korea.
Center for Neuroscience, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.

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