The effects of adrenalectomy and corticosterone replacement on maternal behavior in the postpartum rat
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l25Plasma corticosterone concentrations were measured following adrenalectomy of pregnant rats on the last day of gestation. Plasma corticosterone concentrations decreased 40 and 60 min after adrenalectomy by 36 and 32‰, respectively, and regained the preoperative concentration 2 h following operation. When the fetuses were injected with an inhibitor of 11²-steroid hydroxylase (Su4885) plasma corticosterone concentrations decreased 40, 60 and 120 min following adrenalectomy by 63, 67 and 71‰, respectively. The results strongly suggest that the fetal adrenal glands are the source of plasma corticosterone in adrenalectomized pregnant rats.(Endocrinology96: 1297, 1975)
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In this study, we explored the influence of corticosterone, the major glucocorticoid in the rat, on the locomotor response to cocaine. In particular, in a first series of experiments, we determined the effects of suppressing endogenous glucocorticoids by adrenalectomy on a full dose-response curve of cocaine-induced locomotion and the influence, on this behavioral response, of different corticosterone concentrations, by implanting different corticosterone pellets in adrenalectomized rats. Adrenalectomy decreased the locomotor response to cocaine, inducing a vertical shift in the dose-response curve, and corticosterone dose-dependently reversed the decrease induced by adrenalectomy. The effects of adrenalectomy were fully replicated by the acute central infusion of corticosteroid receptor antagonists, and the action of glucocorticoids did not seem to depend on nonspecific effects such as a general alteration of motor responses or drug metabolism. Thus, neither adrenalectomy, corticosterone receptor antagonists nor corticosterone replacement modified saline-induced locomotion and the administration of corticosterone did not increase locomotion. Furthermore, adrenalectomy slightly increased brain concentrations of cocaine, an effect that cannot account for the decrease in drug-induced locomotion it induced. In a second series of experiments, we tested whether corticosterone levels at the time of adrenalectomy could influence the outcome of this surgical procedure on the locomotor response to cocaine. We thus adrenalectomized rats under different conditions resulting in different levels of the hormone. Corticosterone levels at the moment of adrenalectomy had dose-dependent long-term facilitatory effects on the response to the drug. These findings underline a facilitatory role of glucocorticoids in the behavioral effects of psychostimulant drugs.
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Testicular metabolism was examined after adult rats were adrenalectom-ized and/or treated with corticosterone (0.7S, 1.5, and 3.0 mg/day) for 5 days. The weight and DNA and RNA concentrations of testes were not affected by either adrenalectomy or corticosterone replacement but corticosterone (3.0 mg) reduced (p<0.05) testis protein and prevented the loss of testis carbohydrate noted after adrenalectomy. Anaerobic glucose catabolism (cell-free preparations) increased 12% (p<0.05) after adrenalectomy and decreased 13% (p<0.05) after corticosterone (3.0 mg) therapy but neither of these treatments affected aerobic glucose catabolism. Corticosterone (3.0 mg) depressed (p<0.05) the oxidation of glucose-1-14C and glucose-6-14C to 14CO2; whereas adrenalectomy showed a tendency to increase the activity of 14CO2. Testosterone synthesis dropped (p<0.05) after corticosterone (3.0 mg) therapy but was not altered by adrenalectomy. The results suggest that adrenalectomy modifies testicular glucose ca-tabolism and that corticosterone may affect the testis by reducing glucose utilization and testosterone synthesis.
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The food intake of sham-operated and adrenalectomized rats was measured in 12-h intervals with animals housed in either alternating periods of 12:12 light-dark or in continuous light. The food intake with alternating light and dark was unaffected by adrenalectomy. The maintenance of a constant infusion of corticosterone in adrenalectomized rats also did not disturb the pattern of food intake. In continuous light, food intake was not significantly different in each 12-h period of the daily cycle. Neither adrenalectomy nor the injection of corticosterone, 240 micrograms/day, altered the average 12-h food intake in rats in constant light. The weight of interscapular brown adipose was smaller in adrenalectomized animals, but the protein content was unaffected. Adrenalectomy significantly increased the specific binding of the purine nucleotide GDP to mitochondria from brown adipose tissue. This specific binding was restored to normal by either corticosterone infusion or injection. We conclude that light is the principal entrainer for the average food intake during 12-h periods and that within the framework of these experiments corticosterone plays an insignificant role in controlling food intake. However, adrenalectomy did significantly increase the purine nucleotide binding to mitochondria from brown adipose tissue.
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