Steroid regulation of LHRH in rat brain: Glucocorticoids and androgens
Description
Luteinizing hormone releasing hormone (LHRH), a decapeptide, is synthesized in the central nervous system, released into the portal blood, and transported to the anterior pituitary, where it regulates the secretion of luteinizing hormone (LW) and follicle-stimulating hormone (FSH). Therefore, LHRH is a key integrator between the neural and endocrine systems and plays a pivotal role in promoting reproductive functions. The synthesis and secretion of LHRH are under the exquisite control of different neurotransmitters and steroid hormones, including glucocorticoids and androgens. In this dissertation, the effect of glucocorticoid treatment on the content of LHRH neurons was examined first. It was shown in male, but not in female rats, that corticosterone treatment not only increased the number of detectable LHRH neurons in the region around the organum vasculosum of the lamina terminalis (OVLT), but also increased the average size of the neurons in this region. Double-labeling immunocytochemistry demonstrated that LHRH neurons do not have androgen receptors. Further studies revealed that a certain number of tyrosine hydroxylase (TH) neurons in the hypothalamic periventricular nucleus and P-endorphin neurons in the arcuate nucleus colocalize with androgen receptors, suggesting that both TH neurons and P-endorphin neurons might be involved in the mediation of the effects of androgens on LHRH neurons. Androgenic-anabolic steroid (AAS) treatment increased the colocalization rate of TH neurons with androgen receptors in the periventricular nucleus. In the arcuate nucleus, the colocalization of TH neurons with androgen receptors was significantly greater in the dorsomedial than in ventrolateral portions of the nucleus. Finally, it was demonstrated that about 70% of somatostatin neurons in the periventricular nucleus contain androgen receptors. This result provides an anatomical basis for the possible direct action of androgens on these somostatin neurons. Contrary to what was expected, AAS treatment had no effect on the colocalization rate, suggesting that a subpopulation of somatostatin neurons may not express androgen receptors at all