Evidence for α 1 -Adrenergic Involvement in Neuropeptide Y-Stimulated GnRH Release in Female Rabbits

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Both neuropeptide Y (NPY) and norepinephrine stimulate gonadotropin-releasing hormone (GnRH) secretion in intact or ovariectomized (OVx) estradiol-treated rabbits. The mechanism by which NPY stimulates GnRH is currently unknown. We have tested the hypothesis that NPY increases GnRH release via an α-adrenergic pathway. Adult female rabbits were OVx and had Silastic capsules containing 17β-estradiol inserted subcutaneously that maintained plasma estradiol levels similar to those in ovarian intact rabbits. One week later, push-pull (PP) perfusion cannulae, with tips positioned in the mediobasal hypothalamus (MBH), and jugular vein catheters were placed in all does. Blood and PP perfusate samples were obtained every 20 min during 7 h perfusion of the MBH with Krebs-Ringer phosphate buffer (KRP). Intrahypothalamic treatment with NPY (n = 5), prazosin (αi-adrenergic antagonist; n = 7), yohimbine (α1-adrenergic antagonist; n = 7), NPY plus prazosin (n = 7) or NPY plus yohimbine (n = 6) dissolved in KRP occurred during hours 4 through 6. GnRH in hypothalamic perfusate and luteinizing hormone (LH) and prolactin (PRL) in peripheral plasma were measured by specific radioimmunoassays. As anticipated, NPY alone significantly increased MBH-GnRH secretion (0.93 ± 0.24 vs. 2.46 ± 0.37 pg/ml; p < 0.05). In contrast, NPY infused concomitantly with prazosin did not increase MBH-GnRH release (1.26 ± 0.50 vs. 0.78 ± 0.19 pg/ml; p > 0.05) whereas NPY plus yohimbine did stimulate GnRH secretion (1.15 ± 0.13 vs. 2.65 ± 0.89 pg/ml; p < 0.05). Mean levels of GnRH in does that received NPY plus yohimbine were not different from rabbits receiving NPY alone (2.6 5 ± 0.89 vs. 2.46 ± 0.37 pg/ml; p > 0.05). Prazosin or yohimbine infusion alone did not alter GnRH release. Yohimbine administered either alone (2.19 ± 0.50 vs. 16.35 ± 4.45 ng/ml; p < 0.05) or with NPY (1.04 ± 0.20 vs. 14.18 ± 4.23 ng/ml; p < 0.05) stimulated plasma PRL levels markedly whereas prazosin had no effect on PRL secretion. Plasma LH levels were unchanged by any of the treatments under our experimental conditions. These data suggest that the NPY-stimulated MBH-GnRH release is mediated by or dependent upon α1- but not α2-adrenergic receptor activities. Conversely, PRL release appears to be under inhibitory α2-, but not α1-adrenergic control.

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