Abstract

Two experiments investigated short-term food deprivation effects on neuroendocrine processes influenced by estrogen. These studies were prompted by prior work indicating that food deprivation increased the number of immunocytochemically identified cells containing estradiol receptors in the medial preoptic area of ovariectomized female hamsters. Presumably, this is one way that changes in metabolic fuel availability might alter the responsiveness of one or more systems to estradiol. The purpose of this study was to investigate two effects of estradiol that might be affected by food deprivation; these were 1) the positive feedback effects of estradiol on the luteinizing hormone (LH) surge, and 2) the facilitating effects of estradiol on locomotor activity. In Experiment 1, ovariectomized hamsters were administered estradiol, before or after 48 h of food deprivation. Two days after hormone treatment, blood was obtained by cardiac puncture, once in the morning (1100 h) and twice during the afternoon (1600–1800 h). These times were chosen to best characterize the magnitude of the LH surge. Food deprivation enhanced the amplitude of the LH surge in response to estradiol when this treatment preceded, but not when it followed, the administration of estradiol. However, there was variability in the dose of estradiol at which this effect of food deprivation occurred. In Experiment 2, the locomotor (running wheel) activity of two groups of gonadally intact female hamsters was quantified; one group was tested during the early (days l + 2; low estradiol) part of the estrous cycle, and the other group was tested during the late (days 3 + 4; high estradiol) part of the estrous cycle. In both groups, testing was performed first under ad lib feeding conditions and again during 48 h of food deprivation. On average, the days 3 + 4 group was more active than the days 1 + 2 group, reflecting their differing levels of endogenous estradiol. Food deprivation significantly increased locomotor activity, independently of the stage of the estrous cycle during which it was imposed. These results are discussed in terms of the influence that altered estradiol receptor expression in the medial preoptic area might play in generating the effects we observed following short-term food deprivation.

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