Effects of castration or testosterone implants upon pituitary function in hypogonadal mice bearing normal foetal preoptic area grafts.

Abstract

Grafts of normal mouse preoptic area (POA) tissue into the third ventricle of gonadotrophin-releasing hormone (GnRH)-deficient hypogonadal (hpg) mice resulted in an elevation of pituitary GnRH receptors, an increased synthesis of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) by the pituitary gland, an elevation of gonadal LH receptors and in the stimulation of steroidogenesis and spermatogenesis in the testis. In normal mice both castration or the subcutaneous implantation of testosterone capsules for 10 days reduced GnRH receptors, pituitary LH and FSH content, and the latter treatment also caused a 50% reduction in testicular LH receptors. In hpg mice bearing POA grafts testosterone implants failed to affect any of the above parameters, and castration failed to affect pituitary gonadotrophin hormone content, although there was a slight reduction in pituitary GnRH receptors after castration. These experiments suggest that neither the pituitary gonadotroph, nor the GnRH neurone represent major sites for the direct negative feedback of testosterone upon gonadotrophic hormone secretion in male mice.