Acute alcohol exposure in rats (8% ethanol in the liquid diet for a period of 24 h)
is associated with a decrease in the levels of endocannabinoids (anandamide and 2-arachidonoyl-glycerol)
as well as in various N-acylethanolamines, in different brain regions. In the present
study, we wanted to further explore: (i) whether these decreases might be caused by
an increase in fatty acid amide hydrolase (FAAH), the enzyme involved in the degradation
of N-acylethanolamines including anandamide, and (ii) whether the changes in endocannabinoid
levels are accompanied by parallel changes in the major cannabinoid receptor type,
the CB(1) receptor, activated by these ligands in the brain. Our data proved that
FAAH activity did not increase in any of the four regions analyzed, even it was reduced
in the hypothalamus and the prefrontal cortex. Paradoxically, FAAH levels increased
in the hypothalamus and, to a lesser extent, in the prefrontal cortex and the amygdala,
but not in the caudate-putamen. By contrast, the levels of CB(1) receptors were markedly
reduced in the amygdala and prefrontal cortex of these rats, although no changes were
seen in the hypothalamus and the caudate-putamen. These results suggest that reductions
in the levels of endocannabinoids and related N-acylethanolamines caused by acute
alcohol exposure are not originated by an enhanced degradation by FAAH enzyme, but
they are associated with low levels of the receptors activated by these ligands, although
this parallelism did not occur in all brain regions analyzed. In any case, these observations
would support the notion of a general reduction in the activity of the cannabinoid
signaling system by acute alcohol exposure.