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Time Course and Reversibility of Ethanol's Suppressive Effects on Axon Sprouting in the Dentate Gyrus of the Adult Rat
Author(s) -
Lind Marcia D.,
Goodlett Charles R.,
West James R.
Publication year - 1988
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1988.tb00222.x
Subject(s) - dentate gyrus , acetylcholinesterase , entorhinal cortex , hippocampal formation , axon , lesion , aché , axon terminal , hippocampus , chemistry , sprouting , ethanol , commissure , endocrinology , rhinencephalon , medicine , anatomy , biology , pathology , biochemistry , enzyme , botany
Ethanol was administered chronically to adult rats in a liquid diet for 14 days preceding and for 5,7,8,9, or 10 days following the unilateral destruction of the entorhinal cortex. Control groups received a diet of lab chow and water and were sacrificed at comparable survival times. An additional experimental group was given ethanol until 9 days after the lesion, then switched to lab chow and water and sacrificed 1 day later. Coronal sections through the dorsal hippocampal formation were stained and analyzed histochemically for the localization of acetylcholinesterase (AChE). Quantitative measurements of the histochemical patterns in the molecular layer of the dentate gyrus were obtained. Ethanol exposure inhibited the withdrawal of the acetylcholinesterase‐stained septohippocampal fibers and limited the typical lesion‐induced expansion of the pale‐staining commissural/associational zone in the molecular layer of the denervated dentate gyrus. However, abstinence from ethanol for just 24 h released the inhibitory effect on the acetylcholinesterase‐staining fibers, resulting in a significant expansion of the commissural/associational zone.