Sprouting responsiveness in the dentate gyrus is reduced by ethanol administered following but not preceding an entorhinal lesion.
We examined the effect of ethanol on lesion-induced sprouting in the molecular layer of the dentate gyrus. Adult rats were fed a liquid diet containing either ethanol or sucrose for 14 days before and 9 days following unilateral entorhinal cortex lesions. One group was provided the ethanol diet ad libitum during both the pre- and postlesion period. Three other groups were pair-fed to the latter group; one consumed ethanol prelesion, one postlesion, and one did not receive ethanol. Sections through the rostral hippocampus were stained for histochemical localization of acetylcholinesterase. Following the entorhinal lesion the pale-staining commissural/associational zone ipsilateral to the lesion typically expands and exhibits decreased acetylcholinesterase staining. When ethanol was administered after the lesion, expansion of the commissural/associational zone was significantly diminished compared with the two groups that received the control diet after the lesion. Ethanol administered for 2 weeks before the lesion had no measurable effect on commissural/associational zone expansion. These findings imply that, at least for short-term exposure, ethanol reduces the sprouting responsiveness of systems in the dentate gyrus only during the postlesion period when sprouting normally occurs.
D000110:Acetylcholinesterase / Q000032:analysis; D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology*; D000431:Ethanol / Q000494:pharmacology*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D006651:Histocytochemistry; D008032:Limbic System / Q000502:physiology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D000431:Ethanol; D000110:Acetylcholinesterase