Rico_2007_Toxicol.Lett_174_25

Alcohol abuse is a health problem throughout the world and alcohol consumption is linked to the occurrence of several pathological conditions. Acute ethanol administration exerts a variety of actions on the central nervous system (CNS). Zebrafish has been used as an attractive model system to investigate behavioral and neurochemical changes promoted by alcohol intoxication. Here we investigated the in vitro and in vivo effects promoted by ethanol and its metabolites on zebrafish brain acetylcholinesterase (AChE). There was a significant increase of AChE (33%) activity after acute 1% ethanol exposure. However, ethanol in vitro did not alter AChE activity. Acetaldehyde, the first metabolite of alcohol metabolism, promoted a dose-dependent decrease (15%, 27.5% and 46.5%) at 0.25%, 0.5% and 1%, respectively. Acetate, a product of acetaldehyde degradation, did not change AChE activity. Furthermore, the acute ethanol exposure was able to inhibit AChE transcripts at 0.5% and 1%. These findings suggest that the alterations on zebrafish AChE could reveal molecular mechanisms related to cholinergic signaling in alcoholism.