Impact of acute and chronic nicotine administration on midbrain dopaminergic neuron activity and related behaviours in TRPV1 knock-out juvenile mice.


Journal

The European journal of neuroscience
ISSN: 1460-9568
Titre abrégé: Eur J Neurosci
Pays: France
ID NLM: 8918110

Informations de publication

Date de publication:
02 2022
Historique:
revised: 16 12 2021
received: 27 09 2021
accepted: 17 12 2021
pubmed: 24 12 2021
medline: 12 4 2022
entrez: 23 12 2021
Statut: ppublish

Résumé

The addictive properties of nicotine, the main alkaloid in tobacco and tobacco-derived products, largely depend on its action on the activity of midbrain dopamine (DA) neurons. The transient receptor potential vanilloid 1 (TRPV1) channel has also been examined as an emerging contributor to addiction-related symptoms due to its ability to modulate midbrain neurons. Thus, the objective of our study was to explore the role of TRPV1 receptors (TRPV1Rs) on nicotine-induced behaviours and associated response of DA neuron activity. Both wild type juvenile mice and juvenile mice with invalidation of the TRPV1R gene were exposed to acute or chronic nicotine 0.3 mg/kg administration. We analysed locomotor activity in response to the drug. In addition, we performed cell-attached and whole-cell recordings from ventral tegmental area (VTA) neurons after nicotine exposure. Our results showed that the genetic deletion of TRPV1Rs reduced nicotine-induced locomotor sensitization. In addition, it provided evidence in support of TRPV1Rs being regulators of inhibitory synaptic transmission in the VTA. However, TRPV1Rs did not seem to modulate either nicotine-induced conditioning place preference or nicotine-evoked electrical activity of DA neurons. In conclusion, TRPV1Rs modulate nicotine-induced psychomotor sensitization in mice independently of a control on VTA DA neuron activity. Thus, TRPV1R control may depend on another key player of the mesolimbic circuit.

Identifiants

pubmed: 34939238
doi: 10.1111/ejn.15577
doi:

Substances chimiques

TRPV Cation Channels 0
TRPV1 protein, mouse 0
Nicotine 6M3C89ZY6R

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

697-713

Informations de copyright

© 2021 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.

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Auteurs

Anne-Emilie Allain (AE)

INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.
PHYCELL Platform INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.

Oceane Aribo (O)

INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.

Maria-Carmen Medrano (MC)

INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.

Marie-Line Fournier (ML)

INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.

Sandrine S Bertrand (SS)

INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.
PHYCELL Platform INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.

Stephanie Caille (S)

INCIA, UMR 5287, Univ. Bordeaux, CNRS, Bordeaux, France.

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