Blockade of alcohol escalation and "relapse" drinking by pharmacological FAAH inhibition in male and female C57BL/6J mice.

ABSTRACT:

Background

Anandamide (AEA)-dependent signaling is regulated by the catabolic enzyme fatty acid amide hydrolase (FAAH). Several lines of evidence have demonstrated that FAAH and AEA are involved in the behavioral effects of alcohol. Therefore, we investigated whether a selective FAAH inhibitor, URB597 (cyclohexylcarbamic acid 3'-[aminocarbonyl]-[1,1'-biphenyl]-3-yl ester), altered alcohol intake in mice in a voluntary alcohol drinking model.

Methods

Mice, subjected to 3 weeks of chronic intermittent access (IA) in a two-bottle choice paradigm with 24-h access every other day, developed rapid escalation of alcohol intake and high preference. We evaluated the pharmacological effects of URB597 after both acute (1-day) withdrawal from chronic IA and 1-week withdrawal using the a

SUBMITTER: Zhou Y 

PROVIDER: S-EPMC5693682 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature