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Nat Neurosci. 2013 Aug;16(8):1111-7. doi: 10.1038/nn.3439. Epub 2013 Jun 23.

Disruption of alcohol-related memories by mTORC1 inhibition prevents relapse.

Author information

1
The Ernest Gallo Research Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.

Abstract

Relapse to alcohol abuse is an important clinical issue that is frequently caused by cue-induced drug craving. Therefore, disruption of the memory for the cue-alcohol association is expected to prevent relapse. It is increasingly accepted that memories become labile and erasable soon after their reactivation through retrieval during a memory reconsolidation process that depends on protein synthesis. Here we show that reconsolidation of alcohol-related memories triggered by the sensory properties of alcohol itself (odor and taste) activates mammalian target of rapamycin complex 1 (mTORC1) in select amygdalar and cortical regions in rats, resulting in increased levels of several synaptic proteins. Furthermore, systemic or central amygdalar inhibition of mTORC1 during reconsolidation disrupts alcohol-associated memories, leading to a long-lasting suppression of relapse. Our findings provide evidence that the mTORC1 pathway and its downstream substrates are crucial in alcohol-related memory reconsolidation and highlight this pathway as a therapeutic target to prevent relapse.

PMID:
23792945
PMCID:
PMC3725202
DOI:
10.1038/nn.3439
[Indexed for MEDLINE]
Free PMC Article

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