Neuropeptide Y (NPY) acts at the hypothalamus to stimulate LH secretion through increased I.HRH secretion. NPY is also cosecreted into the portal system in a pulsatile manner with LHRH and may act at the anterior pituitary. to increase LH secretion through potentiation of LHRH responsiveness and possibly through direct stimulation; however, controversy exists concerning this direct action of NPY at the pituitary. Utilizing dispersed anterior pituitary. monolayer cell cultures, the first goal of this study was to determine the effects of vehicle, 10-10 MLHRH, 10-7 MNPY, 10-6 MNPY, 10-10MLHPH + 10-7 MNPY, and 10-10 MLHRH + 10-6 MNPY on LH and FSH responsiveness. Under these conditions, 10-6 MNPY alone significantly stimulated LH secretion (630% above basal) and both 10-7 MNPY and 10-6 MNPY significantly potentiated LHRH-induced LH secretion (195 and 244% above LHRH alone, respectively). Neither 10-7 MNPY nor 10-6 MNPY alone stimulated FSH secretion; however, both 10-7 M and 10-6 MNPY significantly potentiated LHRH-induced FSH secretion (130 and 135% above LHRH alone, respectively). The second goal of this study was to determine whether the gonadal steroid conditions prevailing prior to the preovulatory gonadotropin surge play a role in modulating NPY responsiveness; this experiment utilized anterior pituitary (AP) halves from immature ovariectomized estrogen + progesterone (E + P) primed female rats to determine the role of gonadal steroids in the LH and FSH response to vehicle, 10-8 M LHRH, 10-7 MNPY, 10-6 M NPY, 10-8 M LHRH + 10-7 M NPY. 10-8 M LHRH + 10-6 MNPY. Under these conditions, data indicated that NPY alone did not significantly stimulate LH secretion in this animal model. However. LHRH-induced LH release was potentiated by 10-6 MNPY in vehicle, estrogen (E). and estrogen + progesterone primed groups (240.160 and 200% above LHRH alone, respectively), while 10-7 MNPY potentiated LHRH-induced LH release only in the estrogen and estrogen + progesterone-primed groups (150 and 170% greater than LHRH alone, respectively). Estrogen + progesterone did not significantly increase the magnitude of NPY potentiation above that observed in the estrogen only group. NPY alone did not stimulate FSH secretion in any group. Neither estrogen alone nor estrogen + progesterone had any effect on FSH responsiveness to NPY or LHRH alone: neither estrogen alone nor estrogen + progesterone potentiated LHRH-induced FSH secretion. These studies demonstrated that in dispersed AP cell cultures derived from intact random cycle rats, NPY was capable of acting either alone to stimulate LH secretion or in combination with LHRH to potentiate both LH and FSH secretion. When the immature ovariectomized E + P-primcd rat model was employed, these studies demonstrated that estrogen alone in the absence of progesteron (P) was sufficient to maximize LH responsiveness to NPY + LHRH. thereby indicating that P probably acts at the hypothalamus in vivo to induce the gonadotropin surge observed in this model. The data support the hypothesis that NPY is a physiologically significant modulator of gonadotropin secretion.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrine and Autonomic Systems
- Cellular and Molecular Neuroscience