Effects of alcohol on the hypothalamo-hypophysial axis : a specific look at LHRH release

Abstract

Effects of acute and chronic ethanol (ETOH) administration on hypothalamic LHRH and plasma LH levels were examined in castrate and intact male rats. Two acute studies utilizing I.P. injections of ETOH (1.0-1.5 g/kg) or saline were conducted. The first study involved the injection of rats every 4 hours for 2 days, while the second study maintained a 6 hour injection sequence for 8 days. In a third experiment ETOH was chronically administered to rats via the Bio-Serve alcohol liquid diet. A Bio-Serve non-alcohol diet was given to all controls. After completing acute and chronic injection regimens, some of the animals from each group were decapitated, brains removed, and the hypothalamus with median eminence (ME), subjected to acetic acid extraction and LHRH quantitated via RIA. Brains from other animals were removed following cardiac perfusion with 10% phosphate buffered formalin. Blocks containing the hypothalamus with ME were then post fixed in Bouin's solution and processed for immunocytochemistry (ICC). RIA data for both acute and chronic studies showed that hypothalamic LHRH was inversely correlated with plasma LH. In response to castration, both saline and ETOH treated rats showed a decrease in LHRH content with a concomitant increase in LH. The acute studies revealed that ETOH treated animals retained significantly greater concentrations of LHRH, and showed significantly lower LH levels when compared to saline treated controls. Likewise, ETOH treated intact animals showed significant increases in LHRH content, with LH levels remaining significantly lower than the saline treated intact controls. In the chronic study the same pattern was observed, although the differences were not significant. Differences visualized immunocytochemically, in both acute and chronic studies, were consistent with the data obtained using RIA. Thus, these data support the hypothesis that acute administration of ETOH diminishes or possibly inhibits LHRH release, and hence provides an explanation for depressed LH levels observed in humans and ETOH treated rats. These data also suggest that either the mode of ETOH action with respect to LH release is different following chronic vs acute ETOH administration, or that chronic ETOH feeding to rats is not an adequate model for studying the effects of ETOH on the hypothalamo-hypophysial-LH axis.