Anti-relapse neurons in the infralimbic cortex of rats drive relapse-suppression by drug omission cues

Amanda Laque, Genna De Ness, Grant E. Wagner, Hermina Nedelescu, Ayla Carroll, Debbie Watry, Tony Kerr, Eisuke Koya, Bruce T. Hope, Friedbert Weiss (), Greg I. Elmer () and Nobuyoshi Suto ()
Additional contact information
Amanda Laque: The Scripps Research Institute
Genna De Ness: The Scripps Research Institute
Grant E. Wagner: The Scripps Research Institute
Hermina Nedelescu: The Scripps Research Institute
Ayla Carroll: The Scripps Research Institute
Debbie Watry: The Scripps Research Institute
Tony Kerr: The Scripps Research Institute
Eisuke Koya: University of Sussex
Bruce T. Hope: National Institute on Drug Abuse, NIH/DHHS
Friedbert Weiss: The Scripps Research Institute
Greg I. Elmer: University of Maryland School of Medicine
Nobuyoshi Suto: The Scripps Research Institute

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract Drug addiction is a chronic relapsing disorder of compulsive drug use. Studies of the neurobehavioral factors that promote drug relapse have yet to produce an effective treatment. Here we take a different approach and examine the factors that suppress—rather than promote—relapse. Adapting Pavlovian procedures to suppress operant drug response, we determined the anti-relapse action of environmental cues that signal drug omission (unavailability) in rats. Under laboratory conditions linked to compulsive drug use and heightened relapse risk, drug omission cues suppressed three major modes of relapse-promotion (drug-predictive cues, stress, and drug exposure) for cocaine and alcohol. This relapse-suppression is, in part, driven by omission cue-reactive neurons, which constitute small subsets of glutamatergic and GABAergic cells, in the infralimbic cortex. Future studies of such neural activity-based cellular units (neuronal ensembles/memory engram cells) for relapse-suppression can be used to identify alternate targets for addiction medicine through functional characterization of anti-relapse mechanisms.

Date: 2019
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DOI: 10.1038/s41467-019-11799-1

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