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Long Lasting Changes in Gerbil Brain after Chronic Ethanol Exposure: A Quantitative Study of the Glial Cell Marker S‐100 and DNA
Author(s) -
Rosengren Lars E.,
Wronski Andrzej,
Briving Carin,
Haglid Kenneth G.
Publication year - 1985
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.1530-0277.1985.tb05528.x
Subject(s) - cerebellar vermis , cerebellum , brainstem , cerebral cortex , endocrinology , medicine , cerebellar cortex , muscle hypertrophy , chemistry , biology , anatomy , pathology
Glial S‐100 protein, soluble protein, and DNA were quantitatively studied in brains of gerbils chronically exposed to ethanol in a nutritionally complete fluid diet Eight different brain areas were studied. After exposure to ethanol for 3 months followed by a 4‐month post‐treatment ethanol‐free period, increased amounts of S‐100 protein per wet weight were found in the frontal cerebral cortex, the sensory‐motor cerebral cortex, the posterior cerebellar vermis, and the brainstem. The increase of S‐100 in the posterior cerebellar vermis was paralleled by an increase in DNA per wet weight, which was also increased in the anterior cerebellar vermis. However, a decreased content of DNA was observed in the frontal cerebral cortex, despite the increase of S‐100 protein, suggesting a cell loss affecting cells other than astroglial in this area. In the cerebellar vermis, elevated concentrations of soluble proteins per wet weight were found, whereas a decreased amount was found in the anterior cerebellar hemispheres. It is suggested that the S‐100 protein acts as a marker for astroglial cell volume and that a concomitant increase of S‐100 protein and DNA might indicate an increase in the number of astroglial cells. Thus, our results obtained after ethanol exposure and subsequent ethanol abstinence are compatible with changes consisting of astroglial hypertrophy in the cortex areas and brainstem, as well as astroglial hypertrophy and/or proliferation in the posterior cerebellar vermis, a dear sign of the preceding noxae.