Ethanol intoxication fails to affect sprouting induced by entorhinal cortex lesions.

Abstract After unilateral entorhinal cortex lesions, acute ethanol exposure (mean daily intake=16.3±0.3 g/kg for 15 days) of juvenile rats failed to alter lesion-induced axonal sprouting in the dentate gyrus. The distribution of acetylcholinesterase in the dentate gyrus was identified histochemically as an indicator of axonal sprouting. Comparisons between operated and intact sides were based on qualitative observations and quantitative morphometry techniques using a computerized image analyser to evaluate the widths of the bands of the molecular layer. Whether ethanol-exposed or not, rats with unilateral entorhinal cortex lesions exhibited substantial qualitative and quantitative evidence of axonal sprouting. These results indicate that a 15-day post-operative ethanol exposure had no effect on axonal sprouting in juvenile rats and thus qualify previous findings about ethanol-mediated effects on axonal sprouting.