Decreased Ventral Tegmental Area CB1R Signaling Reduces Sign Tracking and Shifts Cue-Outcome Dynamics in Rat Nucleus Accumbens.
Pavlovian
dopamine
endocannabinoids
optogenetics
pharmacology
photometry
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN: 1529-2401
Titre abrégé: J Neurosci
Pays: United States
ID NLM: 8102140
Informations de publication
Date de publication:
21 06 2023
21 06 2023
Historique:
received:
21
07
2022
revised:
10
05
2023
accepted:
15
05
2023
pmc-release:
21
12
2023
medline:
23
6
2023
pubmed:
20
5
2023
entrez:
19
5
2023
Statut:
ppublish
Résumé
Sign-tracking (ST) rats show enhanced cue sensitivity before drug experience that predicts greater discrete cue-induced drug seeking compared with goal-tracking or intermediate rats. Cue-evoked dopamine in the nucleus accumbens (NAc) is a neurobiological signature of sign-tracking behaviors. Here, we examine a critical regulator of the dopamine system, endocannabinoids, which bind the cannabinoid receptor-1 (CB1R) in the ventral tegmental area (VTA) to control cue-evoked striatal dopamine levels. We use cell type-specific optogenetics, intra-VTA pharmacology, and fiber photometry to test the hypothesis that VTA CB1R receptor signaling regulates NAc dopamine levels to control sign tracking. We trained male and female rats in a Pavlovian lever autoshaping (PLA) task to determine their tracking groups before testing the effect of VTA → NAc dopamine inhibition. We found that this circuit is critical for mediating the vigor of the ST response. Upstream of this circuit, intra-VTA infusions of rimonabant, a CB1R inverse agonist, during PLA decrease lever and increase food cup approach in sign-trackers. Using fiber photometry to measure fluorescent signals from a dopamine sensor, GRAB
Identifiants
pubmed: 37208179
pii: JNEUROSCI.1486-22.2023
doi: 10.1523/JNEUROSCI.1486-22.2023
pmc: PMC10286939
doi:
Substances chimiques
Dopamine
VTD58H1Z2X
Endocannabinoids
0
Rimonabant
RML78EN3XE
Polyesters
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
4684-4696Subventions
Organisme : NIDA NIH HHS
ID : F31 DA050367
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA043533
Pays : United States
Informations de copyright
Copyright © 2023 the authors.
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