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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
de Guglielmo G,Kallupi M,Pomrenze MB,Crawford E,Simpson S,Schweitzer P,Koob GF,Messing RO,George Odoi
10.1038/s41467-019-09183-0subject
Has Abstractpub_date
2019-03-18 00:00:00pages
1238issue
1issn
2041-1723pii
10.1038/s41467-019-09183-0journal_volume
10pub_type
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