Ethanol ‐induced alterations in endocannabinoids and relevant neurotransmitters in the nucleus accumbens of fatty acid amide hydrolase knockout mice

Extracellular endocannabinoids and neurotransmitters were measured by in vivo microdialysis in the nucleus accumbens (NAc) of fatty acid amide hydrolase knockout (FAAH KO) and wild ‐type (WT) mice during an ethanol challenge in EtOH‐naive and repeated (r) EtOH–treated mice. EtOH challenge caused a sustained increase in 2‐arachidonoylglycerol (2‐AG) levels in EtOH‐naive WT mice but not in FAAH KO mice. In contrast, 2‐AG levels were decreased following EtOH challen ge in (r)EtOH‐treated mice in both genotypes. AbstractDeletion of fatty acid amide hydrolase (FAAH), enzyme responsible for degrading endocannabinoids, increases alcohol consumption and preference. However, there is a lack of data on neurochemical events in mice exposed to alcohol in the absence of FAAH. Extracellular levels of endocannabinoids and relevant neurotransmitters were measured by in vivo microdialysis in the nucleus accumbens (NAc) of FAAH knockout (KO) and wild ‐type (WT) mice during an ethanol (EtOH; 2 g/kg, ip) challenge in EtOH‐naive and repeated (r) EtOH–treated mice. In both genotypes, EtOH treatment caused no changes in baseline endocannabinoid levels, although FAAH KO mice displayed higher baselineN‐arachidonoylethanolamine levels than WT mice. EtOH challenge caused a sustained increase in 2‐arachidonoylglycerol (2‐AG) levels in EtOH‐naive WT mice but not in FAAH KO mice. In contrast, 2‐AG levels were decreased following EtOH challenge in (r)EtOH‐treated mice in ...
Source: Addiction Biology - Category: Addiction Authors: Tags: ORIGINAL ARTICLE Source Type: research