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Ventral arkypallidal neurons inhibit accumbal firing to promote reward consumption.

The shell of the nucleus accumbens (NAcSh) and ventral pallidum (VP) are critical for reward processing, although how coordinated activity within these nuclei orchestrates reward valuation and consumption remains unclear. Inhibition of NAcSh firing is necessary for reward consumption, but the source...

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Detalles Bibliográficos
Autores principales: Vachez, Yvan M., Tooley, Jessica R., Abiraman, Kavitha, Matikainen-Ankney, Bridget, Casey, Eric, Earnest, Tom, Ramos, Leana M., Silberberg, Hanna, Godynyuk, Elizabeth, Uddin, Olivia, Marconi, Lauren, Le Pichon, Claire E., Creed, Meaghan C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7933121/
https://www.ncbi.nlm.nih.gov/pubmed/33495635
http://dx.doi.org/10.1038/s41593-020-00772-7
Descripción
Sumario:The shell of the nucleus accumbens (NAcSh) and ventral pallidum (VP) are critical for reward processing, although how coordinated activity within these nuclei orchestrates reward valuation and consumption remains unclear. Inhibition of NAcSh firing is necessary for reward consumption, but the source of this inhibition remains unknown. Here, we report that a subpopulation of VP neurons, the ventral arkypallidal (vArky) neurons, project back to the NAcSh, where they inhibit NAcSh neurons in vivo in mice. Consistent with this pathway driving reward consumption via inhibition of the NAcSh, calcium activity of vArky neurons scaled with reward palatability and predicted the subsequent drinking behavior during a free-access paradigm, which was dissociable from reward seeking. Activation of the VP to NAchSh pathway increased on-going reward consumption while amplifying hedonic reactions to reward. Our results establish a pivotal role of vArky neurons in promoting reward consumption, through modulating NAcSh firing in a value-dependent manner.