Neuropeptide Y (NPY) acts as an endogenous anxiolytic, and, like endocannabinoids, plays an important role in the regulation of neuronal excitability during ethanol withdrawal (Rubio et al., 2011). Since acetaldehyde is considered a mediator of ethanol central effects, this research aims at investigating, following intoxication and during withdrawal, the effects of acetaldehyde on NPY expression in brain areas particularly vulnerable to alcohol, and the influence of cannabinoid system on it. Rats underwent acetaldehyde intoxication (450mg/kg, i.g., 4 times daily for 4 days); AM281, a CB1 selective antagonist (2,5 mg/kg, i.p.) was administered during abstinence. Immunohistochemical analysis on NPY expression was performed at 1h, 16h, 72h after the last acetaldehyde administration, in NAcc and hippocampus. NPY expression in NAcc and hippocampus (p<0.01) was reduced compared to CTR at 1h; NPY density increased at 16h (hippocampus: p<0.01; p<0.0001; NAcc p<0.01), with respect to 1h levels; at 72h a further increase in NPY was observed with respect to 16 h (p<0.01). In CTR group, AM281 increased NPY density with respect to vehicle at 16h (hippocampus p<0.01; NAcc p<0.001) and 72h (hippocampus p<0.01; NAcc p<0.01). In ACD group, AM281 increased NPY expression at 16h in hippocampus (p<0.001) and NAcc (p<0.001), compared to vehicle; no significant differences were observed at 72 h. This study shows for the first time the effect of ACD intoxication and withdrawal on NPY levels in discrete brain regions and suggests the involvement of cannabinoid system on ACD-induced neuronal modification in acute and late withdrawal.
|Number of pages||0|
|Publication status||Published - 2014|