Evidence that the posterior pituitary plays a role in neuropeptide Y and luteinizing hormone-releasing hormone-stimulated gonadotropin secretion in vitro.

Abstract

Neuropeptide Y (NPY) has been shown to increase gonadotropin secretion directly at the level of the anterior pituitary (AP) in both the absence and the presence of luteinizing hormone-releasing hormone (LHRH). This is interesting because high-affinity 125I-NPY-binding sites have not been found in the AP. However, high-affinity 125I-NPY-binding sites have been localized in the posterior pituitary (PP), and it has been shown that removal of the PP alters luteinizing hormone (LH) secretion in vivo. The following studies were conducted to determine if gonadotropin responsiveness to either NPY alone or to NPY in combination with LHRH was significantly different in AP cells cultured in the presence compared with the absence of PP cells. The studies indicated that NPY-induced LH secretion was significantly greater in the presence of PP cells, while follicle-stimulating hormone (FSH) secretion was not significantly affected. LHRH-induced LH secretion was also significantly greater in the presence of PP cells; however, LHRH-induced FSH secretion was significantly decreased. NPY potentiated LHRH-induced LH secretion in AP cells cultured in both the presence and the absence of PP cells; however, the degree of potentiation was not significantly different whether PP cells were present or absent. These results indicate that the PP may play a role in the responsiveness of the AP to NPY and to LHRH but plays no apparent role in NPY potentiation of LHRH responsiveness.