Neuropeptide Y levels in microdissected regions of the hypothalamus and in vitro release in response to KCl and prostaglandin E2: effects of castration.
Intracerebroventricular administration of neuropeptide Y (NPY) has been shown to modify LH secretion, with the direction of the response dependent on the steroid background. To study further the role of gonadal steroids in the regulation of NPY secretion, the basal and KCl-evoked release of NPY from the medial basal hypothalamus (MBH) of intact and castrated male rats was assessed twice with the use of an in vitro incubation system. In each experiment, the amounts of NPY released in response to a 15-min pulse of KCl (45 mM) were significantly smaller from the MBH of castrated rats than of intact rats (P less than 0.05). Next, to assess the possible effects of prostaglandin E2 (PGE2), the MBH were exposed in a similar manner to two 15-min pulses, 30 min apart, of 0.568 and 56.8 mumol PGE2. Unlike KCl, PGE2 failed to stimulate NPY release from the MBH of either intact or castrated rats. However, a similar 56.8 mumol concentration of PGE2 was effective in stimulating the release of LHRH. We next examined the effects of castration on NPY levels in several microdissected regions of the hypothalamus. Whereas NPY concentrations were unchanged in the medial preoptic area, paraventricular nucleus and dorsomedial nucleus, NPY levels were significantly decreased in the median eminence, arcuate nucleus, and ventromedial nucleus 2 weeks after castration. These studies show that KCl can stimulate NPY release from the MBH in vitro, like that of LHRH, the KCl-induced NPY response is significantly smaller from the MBH of castrated than intact males, castration can significantly reduce the levels of NPY in the median eminence, arcuate nucleus, and ventromedial nucleus, thereby suggesting that testicular secretions may modulate NPY levels and release from the MBH, and because PGE2 stimulated the release of LHRH but not of NPY, separate regulatory neural events may underlie the secretion of these two neuropeptides.
D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000378:metabolism; D015232:Dinoprostone; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D007033:Hypothalamus, Middle / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008473:Median Eminence / Q000378:metabolism; D009478:Neuropeptide Y / Q000378:metabolism*; D009919:Orchiectomy; D011189:Potassium Chloride / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats; D014018:Tissue Distribution; D014697:Ventromedial Hypothalamic Nucleus / Q000378:metabolism
D009478:Neuropeptide Y; D011458:Prostaglandins E; D007987:Gonadotropin-Releasing Hormone; D011189:Potassium Chloride; D015232:Dinoprostone