Vasopressin-Related Peptides Increase the Hippocampal Corticosterone Receptor Capacity of Diabetes Insipidus (Brattleboro) Rats*

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Abstract
The binding of [3H]corticosterone to receptors in cytosol of several brain regions and of [3H]dexamethasone to receptors in pituitary cytosol was measured after chronic treatment of homozygous diabetes insipidus rats (Ho-Di) with various neuropeptides. All rats were adrenalectomized 24 h before sacrifice for depletion of endogenous adrenal hormones and at that time administration of the peptides was discontinued. At sacrifice the rats were perfused with saline to remove plasma transcortin from the tissues. The apparent maximal binding capacity for corticosterone and dexamethasone was significantly lower in hippocampus and anterior pituitary (36.8% and 39.2%, respectively) of Ho-Di rats than of homozygous nondiabetic rats (Ho- No) of the same strain. In contrast, the neurointermediate pituitary lobe of Ho-Di rats had more than twice as many (211%) binding sites, whereas neither receptor capacity in hypothalamus and septum nor plasma transcortin in these rats were significantly different from those in Ho-No rats. Treatment of Ho-Di rats with arginine-vasopressin, des-glycinamide arginine vasopressin, or 1-desamino-8-D-arginine-vasopressin daily for 1 week resulted in an elevation of receptor capacity in hippocampus and anterior pituitary near the level observed in nondiabetic controls. No effects on the other brain regions, the neurointermediate pituitary lobe, and on plasma transcortin were observed with these peptide treatments. Administration of oxytocin and ACTH-(4–10) did not affect receptor binding. It is concluded that in the Ho-Di Brattleboro rat the glucocorticoid receptor system in the hippocampus and in the anterior pituitary is selectively affected by neuropeptides related to vasopressin.