Corticosteroid receptor plasticity and recovery of a deficient hippocampus-associated behavior after unilateral (dorsal) hippocampectomy.
Unilateral ablation of the right dorsal hippocampus (HCX) produced changes in maximal corticosteroid binding capacity (Bmax) in the contralateral hippocampal lobe of the rat with time. The mechanism by which this time course of changes was produced seemed to involve the pituitary-adrenal system, since a certain difference in corticosteroid receptor binding pattern was noted between chronic adrenalectomized (ADX) rats and rats which remained intact during postlesion survival. In the presence of endogenous adrenal hormones the HCX-induced changes in corticosteroid receptor binding relative to that observed in rats with the overlying neocortex ablated (control) were the following: a 26% decrease at 5 days after HCX; an increase the following 3 weeks with a maximum of 46% at 20 days postsurgery; and recovery towards control values after longer survival times. After discrimination of corticosteroid binding into two corticosterone (CORT) binding receptor populations, e.g. glucocorticoid receptors (GR) and mineralocorticoid-like or CORT receptors (CR), the lesion-induced effect was more pronounced in GR than in CR. A 72% increase over controls was measured at 20 days postsurgery. In the absence of the adrenals, however, the Bmax of corticosteroid binding was not decreased at 5 days after HCX. The relative increase in Bmax reached a maximum of 39% over control levels at 30 days postsurgery and recovery towards control values after longer survival did not occur. The increase in corticosteroid receptor capacity after HCX, therefore, is transient in the presence of adrenocortical secretion and permanent in its absence.(ABSTRACT TRUNCATED AT 250 WORDS)
D000315:Adrenalectomy; D000818:Animals; D003345:Corticosterone / Q000378:metabolism; D007839:Functional Laterality / Q000502:physiology*; D006624:Hippocampus / Q000378:metabolism* / Q000502:physiology; D008297:Male; D009409:Nerve Crush; D009473:Neuronal Plasticity; D051381:Rats; D011919:Rats, Inbred Strains; D011965:Receptors, Glucocorticoid / Q000032:analysis* / Q000502:physiology; D011987:Receptors, Steroid; D012193:Reversal Learning / Q000502:physiology*
D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; C024357:corticosterone receptor; D003345:Corticosterone