AIMS: The number of cerebellar microglia after 5(1)/2 months of continuous or intermittent ethanol exposure was studied using the optical dissector method. METHODS: Male Wistar rats were divided into three groups: an intermittently ethanol-exposed group, a continuously ethanol-exposed group and a control group (n = 6 in each group). The intermittently treated rats had two ethanol-withdrawal periods per week throughout the experiment. The number of microglia was measured in the anterior (folium II) and the posterior (folium X) cerebellar vermis. Tomato (Lycopersicon esculentum) lectin was used to stain the cerebellar microglia. RESULTS: The volumes of folia II and X were similar in all the groups. The number of microglia increased in the molecular layer of folium II in the intermittently ethanol-exposed group compared with the continuously exposed and control groups. In the granular layer, there were no differences between the groups in the number of microglia. CONCLUSIONS: The results suggest that the number of cerebellar microglia increases in the anterior vermis before any ethanol-induced cerebellar atrophy is discernible. Repeated ethanol withdrawals seem to be more essential in inducing microgliosis than ethanol intoxication per se.
AIMS: The number of cerebellar microglia after 5(1)/2 months of continuous or intermittent ethanol exposure was studied using the optical dissector method. METHODS: Male Wistar rats were divided into three groups: an intermittently ethanol-exposed group, a continuously ethanol-exposed group and a control group (n = 6 in each group). The intermittently treated rats had two ethanol-withdrawal periods per week throughout the experiment. The number of microglia was measured in the anterior (folium II) and the posterior (folium X) cerebellar vermis. Tomato (Lycopersicon esculentum) lectin was used to stain the cerebellar microglia. RESULTS: The volumes of folia II and X were similar in all the groups. The number of microglia increased in the molecular layer of folium II in the intermittently ethanol-exposed group compared with the continuously exposed and control groups. In the granular layer, there were no differences between the groups in the number of microglia. CONCLUSIONS: The results suggest that the number of cerebellar microglia increases in the anterior vermis before any ethanol-induced cerebellar atrophy is discernible. Repeated ethanol withdrawals seem to be more essential in inducing microgliosis than ethanol intoxication per se.
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