Neither chronic exposure to ethanol nor aging affects type I or type II corticosteroid receptors in rat hippocampus

Abstract

Both chronic exposure to ethanol and aging are reported to result in a loss of hippocampal pyramidal neurons and an elevation in plasma corticosteroid concentration. Aging has also been reported to result in a reduction in corticosterone receptors and corticosterone-concentrating cells in the hippocampus. Since these aging-associated effects have been hypothesized to be due to the cumulative exposure to corticosteroids over the life span, in the present studies, we investigated the hypothesis that corticosteroids play a similar role in the loss of hippocampal neurons during chronic ethanol ingestion. In contrast to our expectations, when a liquid diet containing either ethanol or sucrose was administered to male Long-Evans rats for 20–24 weeks, a period of treatment found previously to result in hippocampal neuronal loss, there were no ethanol-associated effects on the specific binding of [ 3H]-aldosterone to Type I or of [ 3H]dexamethasone to Type II receptors in cytosol derived from either whole hippocampus or dorsal versus ventral hippocampus. Allowing the rats to withdraw from the chronic ethanol exposure for 12 weeks also failed to reveal any ethanol-associated effects on corticosteroid receptor concentrations in the hippocampus. The basal morning concentrations of corticosterone in blood plasma were not affected by any of these treatments. In view of these null findings we next investigated the effects of aging on hippocampal corticosteroid receptors in male Long-Evans and Fischer 344 rats. Again we were surprised to find no aging-associated reductions in [ 3H]aldosterone-Type I, [ 3H]corticosterone-Type I or [ 3H]dexamethasone-Type II receptor concentrations in whole hippocampal cytosol, despite the fact that plasma concentrations of CORT were clearly elevated in the aged Long-Evans rats. Our results, therefore, do not support the hypothesis that corticosteroids play a significant role in the loss of hippocampal neurons associated with chronic ethanol ingestion or aging.