Search

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 alpha-adrenergic pathway. Adult female rabbits were OVx and had Silastic capsules containing 17 beta-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 (alpha 1-adrenergic antagonist; n = 7), yohimbine (alpha 2-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 less than 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 greater than 0.05) whereas NPY plus yohimbine did stimulate GnRH secretion (1.15 +/- 0.13 vs. 2.65 +/- 0.89 pg/ml; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The suprachiasmatic nuclei (SCN) have been implicated as neural timers of reproductive events and as possible sites of action for melatonin. We tested the hypothesis that ablation of the SCN (SCNx) would counteract the inhibitory effect of exogenous melatonin in blastocyst implantation in the spotted skunk by removing a possible site of action. Thirty-eight pregnant females with unimplanted blastocysts were treated as follows: 4 served as untreated controls, 6 received empty Silastic capsules, 5 received Silastic capsules containing melatonin, 10 received sham lesions in the SCN, 7 received lesions in the SCN and Silastic capsules containing melatonin, and 6 received lesions in the SCN and empty Silastic capsules. All surgical treatments were completed by February 15. The skunks were subjected to a natural photoperiod, and the duration of preimplantation was measured. The lesions destroyed an average of 87 +/- 10% of the SCN and a small amount of the surrounding hypothalamus. SCNx had no significant effect on duration of preimplantation (200 +/- 25.6 days) when compared to sham SCNx (205 +/- 21.5 days). Melatonin significantly (p less than 0.05) lengthened the duration of preimplantation in both intact (277 +/- 59 days) and SCNx (265 +/- 64.7 days) skunks when compared to all other groups. These data are not consistent with the hypothesis that the SCN are required for melatonin to exert its influence on timing of implantation in the spotted skunk.