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A persistent alcohol cue memory trace drives relapse to alcohol seeking after prolonged abstinence.

Science advances (2020-06-05)
Esther Visser, Mariana R Matos, Rolinka J van der Loo, Nathan J Marchant, Taco J de Vries, August B Smit, Michel C van den Oever
ABSTRACT

Alcohol use disorder is characterized by a high risk of relapse during periods of abstinence. Relapse is often triggered by retrieval of persistent alcohol memories upon exposure to alcohol-associated environmental cues, but little is known about the neuronal circuitry that supports the long-term storage of alcohol cue associations. We found that a small ensemble of neurons in the medial prefrontal cortex (mPFC) of mice was activated during cue-paired alcohol self-administration (SA) and that selective suppression of these neurons 1 month later attenuated cue-induced relapse to alcohol seeking. Inhibition of alcohol seeking was specific to these neurons as suppression of a non-alcohol-related or sucrose SA-activated mPFC ensemble did not affect relapse behavior. Hence, the mPFC neuronal ensemble activated during cue-paired alcohol consumption functions as a lasting memory trace that mediates cue-evoked relapse long after cessation of alcohol intake, thereby providing a potential target for treatment of alcohol relapse vulnerability.

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Sigma-Aldrich
4-idrossitamoxifene, ≥70% Z isomer (remainder primarily E-isomer)
Sigma-Aldrich
TWEEN® 80, viscous liquid
Sigma-Aldrich
TWEEN® 80, viscous liquid