Abstract
Neuropeptide Y (NPY) is localized in several hypothalamic sites which are implicated in the control of hypothalamic luteinizing hormone-releasing hormone (LHRH) and pituitary luteinizing hormone (LH) release. We have observed previously that in young rats castration decreases and testosterone (T) replacement restores NPY levels in selected hypothalamic sites. However, in aged male rats, NPY levels were decreased in all hypothalamic sites studied. Since testicular function is diminished in aged rats, we reasoned that decreased T feedback may be responsible for the reduction of NPY in the hypothalamus. Therefore, we compared the effects of castration and T-replacement on NPY levels in microdissected hypothalamic sites of 2.5-month- (young) and 15-month-old (aged) male rats. Serum LH and T levels were markedly reduced in aged as compared to those observed in young rats. In association with the decreased hormone levels, NPY levels were significantly reduced in each of the 7 hypothalamic sites of aged as compared to young rats. Further, in young rats, castration reduced and T-replacement prevented the castration-induced depletion in only 3 sites, viz. the ventromedial hypothalamic nucleus (VMN), arcuate nucleus (ARC) and median eminence (ME). In contrast, castration in aged rats reduced NPY levels not only in the VMN as in young rats, but also in the medial preoptic area (MPOA) and dorsomedial nucleus (DMN). However, the marked reduction in the ME and ARC NPY levels of young rats following castration was not observed in the ME and ARC of aged rats. Furthermore, except in the MPOA, T-replacement in aged rats neither prevented the site-specific castration-induced decrease in NPY nor did it elevate NPY levels in any of the hypothalamic sites to the range seen in intact or castrated T-replaced young rats. Because NPY readily stimulates the release of hypothalamic LHRH and potentiates the action of LHRH on the pituitary on toung rats, these observations are in accord with the view that a gradual age-related diminution in hypothalamic excitatory NPY neuronal function, including the acquisition of refracoriness to T, may adversely affect the LHRH-LH axis leading to reproductive aging in male rats.
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