Food restriction attenuates the hormonal and neuronal responses to the positive feedback effects of estradiol to prolong lactational diestrus in rats.

摘要

Food restriction prolongs lactational infertility in rats. The experiments presented in this thesis were done to investigate the possibility that this effect is due to an attenuated response to the positive feedback effects of estradiol (E2) that stimulate the surge in luteinizing hormone (LH) release. Furthermore, the hypothesis that the hypothalamus is one site affected by food restriction in attenuating E2 induced LH surges was examined. The first series of experiments examined the ability of E2 to induce LH surges in both ad lib fed and food restricted dams at different times of lactation. Results were that on day 20 postpartum (pp) ad lib fed dams showed LH surges after E2 treatment, but food restricted dams did not. Ovariectomy (OVX) or RU486 treatment restored the ability of E2 to induce LH surges in food restricted dams, and chronic progesterone (P) reduced E2-induced LH surges in ad lib fed OVX dams. The second series of experiments showed that food restricted dams had less Fos-like immunoreactive (FOS-ir) cells in the anteroventral preoptic area (AVPV) than ad lib fed dams on day 20 pp. These effects were reflected in a reduced ability of E2 to induce P receptor (PR) immunoreactivity, but not in the number of E2 receptors (ERα) in the AVPV. As with the LH surge, the effects of food restriction on E2 induction of PRs were mediated by P. Results suggest that the lactational diestrus is prolonged by a decrease in sensitivity to E2 in the AVPV, and this effect is mediated by the high levels of P in food restricted dams.