Inactivation of a CRF-dependent amygdalofugal pathway reverses addiction-like behaviors in alcohol-dependent rats

Giordano de Guglielmo, Marsida Kallupi, Matthew B. Pomrenze, Elena Crawford, Sierra Simpson, Paul Schweitzer, George F. Koob, Robert O. Messing and Olivier George ()
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Giordano de Guglielmo: The Scripps Research Institute
Marsida Kallupi: The Scripps Research Institute
Matthew B. Pomrenze: The University of Texas at Austin
Elena Crawford: The Scripps Research Institute
Sierra Simpson: The Scripps Research Institute
Paul Schweitzer: The Scripps Research Institute
George F. Koob: National Institutes of Health
Robert O. Messing: The University of Texas at Austin
Olivier George: The Scripps Research Institute

Nature Communications, 2019, vol. 10, issue 1, 1-11

Abstract: Abstract The activation of a neuronal ensemble in the central nucleus of the amygdala (CeA) during alcohol withdrawal has been hypothesized to induce high levels of alcohol drinking in dependent rats. In the present study we describe that the CeA neuronal ensemble that is activated by withdrawal from chronic alcohol exposure contains ~80% corticotropin-releasing factor (CRF) neurons and that the optogenetic inactivation of these CeA CRF+ neurons prevents recruitment of the neuronal ensemble, decreases the escalation of alcohol drinking, and decreases the intensity of somatic signs of withdrawal. Optogenetic dissection of the downstream neuronal pathways demonstrates that the reversal of addiction-like behaviors is observed after the inhibition of CeA CRF projections to the bed nucleus of the stria terminalis (BNST) and that inhibition of the CRFCeA-BNST pathway is mediated by inhibition of the CRF-CRF1 system and inhibition of BNST cell firing. These results suggest that the CRFCeA-BNST pathway could be targeted for the treatment of excessive drinking in alcohol use disorder.

Date: 2019
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DOI: 10.1038/s41467-019-09183-0

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