A SELECTIVE SEXUALLY DIMORPHIC RESPONSE IN THE MEDIAN-EMINENCE NEUROPEPTIDE-Y

Recent studies show that neuropeptide Y (NPY) is widely distributed in the hypothalamus and that it stimulates luteinizing hormone-releasing hormone (LHRH) release from the medial basal hypothalamus (MBH) of male and female rats. The neuroendocrine factors that regulate NPY neurosecretion in two sexes are not well understood. We have previously observed that orchidectomy (orch) in male rats decreased and testosterone (T) replacement increased NPY levels selectively in the median eminence (ME), arcuate nucleus (ARC) and ventromedial nucleus (VMN) and the KCl-evoked in vitro release of NPY from the MBH was likewise decreased after orch and restored by testosterone replacement. Now we report that these NPY responses are different in female rats following removal of the ovaries. Ovariectomy (ovx) decreased NPY concentrations in the ARC and VMN and not in the ME. Estrogen replacement restored NPY concentrations in the ARC and VMN, however, in the ME NPY concentration decreased significantly. Further, the KCl-evoked NPY release in vitro from either the MBH or ME of intact and ovx rats was similar. In an additional concurrent comparative study in male and female rats, we observed that of the 6 microdissected hypothalamic sites, NPY levels were approximately 50% less in the ME of intact females than in those of intact male rats. Again, in male rats there was a significant decrease in NPY levels in the ME, ARC and VMN after orch, whereas in female rats, NPY levels in the ARC and VMN, but not in the ME decreased after ovx. When the effects on LHRH levels in the ME were evaluated, we observed that unlike the case of ME NPY, LHRH levels decrease in the ME of both sexes in response to gonadectomy. These studies show that despite the widespread distribution and common source of hypothalamic NPY in male and female rats, a sexually dimorphic NPY response is apparent, selectively, in the ME where NPY levels are lower in females than in males and gonadectomy and appropriate steroid-replacement differentially affects NPY levels and release. In view of the observation that the sexually dimorphic response was seen in the ME NPY and not in ME LHRH, and NPY is an important excitatory signal to LHRH neurons in steroid-treated rats, we speculate that the different pattern of gonadotropin secretion seen in male and female rats may be due, in part, to disparate modes of NPY neurosecretion imposed by postnatal androgenization.