Manipulations of central amygdala neurotensin neurons alter the consumption of ethanol and sweet fluids in mice

María Luisa Torruella-Suárez, Jessica R. Vandenberg, Elizabeth S. Cogan, Gregory J. Tipton, Adonay Teklezghi, Kedar Dange, Gunjan K. Patel, Jenna A. McHenry, J. Andrew Hardaway, Pranish A. Kantak, Nicole A. Crowley, Jeffrey F. DiBerto, Sara P. Faccidomo, Clyde W. Hodge, Garret D. Stuber, Zoé A. McElligott

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

The central nucleus of the amygdala plays a significant role in alcohol use and other affective disorders; however, the genetically-defined neuronal subtypes and projections that govern these behaviors are not well known. Here we show that neurotensin neurons in the central nucleus of the amygdala of male mice are activated by in vivo ethanol consumption and that genetic ablation of these neurons decreases ethanol consumption and preference in non-ethanol-dependent animals. This ablation did not impact preference for sucrose, saccharin, or quinine. We found that the most robust projection of the central amygdala neurotensin neurons was to the parabrachial nucleus, a brain region known to be important in feeding behaviors, conditioned taste aversion, and alarm. Optogenetic stimulation of projections from these neurons to the parabrachial nucleus is reinforcing, and increases ethanol drinking as well as consumption of sucrose and saccharin solutions. These data suggest that this central amygdala to parabrachial nucleus projection influences the expression of reward-related phenotypes and is a novel circuit promoting consumption of ethanol and palatable fluids.

Original languageEnglish (US)
Pages (from-to)632-647
Number of pages16
JournalJournal of Neuroscience
Volume40
Issue number3
DOIs
StatePublished - Jan 15 2020

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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