Immunocytochemical localization of luteinizing hormone-releasing hormone in male and female rat brains. Quantitative studies on the effect of gonadal steroids.

Abstract

The peroxidase-antiperoxidase immunocytochemical method was used to determine quantitatively the effects of gonadal steroids on the immunoreactive luteinizing hormone-releasing hormone (LHRH) content in the brain of male and female rats. In the male rat, gonadectomy decreased both the number of cell bodies and optical density of staining in cell bodies containing immunoreactive LHRH; decreased the percentage of area covered by LHRH fibers in the middle and caudal aspects of the median eminence (ME) but not the organum vasculosum lamina terminalis (OVLT), and decreased the number of LHRH fibers localized in the midbrain central gray (MCG). Since others have shown previously that gonadectomy increases the LHRH content of portal blood in the male rat, the results suggest that the decreased somal accumulation of LHRH and decreased LHRH content in fibers in the ME and MCG measured in the present study following loss of testicular steroids reflect increased LHRH release from the ME and MCG into the portal blood and brain, respectively. Estrogen replacement in the gonadectomized female rat increased the optical density of staining in cell bodies but not the number of cell bodies containing immunoreactive LHRH, increased the percentage of area containing LHRH fibers in the caudal aspect of the ME but not the OVLT, and decreased the number of fibers containing LHRH in the MCG. Since others have shown previously that estrogen replacement to gonadectomized female rats decreases LHRH release into portal blood, the present results suggest that the estrogen-induced increases in somal accumulation of LHRH and increases in LHRH content in fibers in the ME reflect a decreased LHRH release from the ME into the portal blood. By analogous reasoning, the decreased LHRH fiber content measured in the MCG following estrogen replacement to gonadectomized females reflects an increased LHRH release into the MCG. This inference is consistent with a postulated role for LHRH in this brain site in the facilitation of lordotic responsiveness.