Facilitatory effects of testosterone on hypothalamic tachykinin levels and release

We have reported earlier that central administration of tachykinins profoundly altered the release of pituitary LH and the direction of the LH response was modulated by gonadal steroids in male rats. To further understand the relationship between androgens and hypothalamic tachykinins, we have examined the effects of castration and of testosterone (T)-replacement on levels of Neurokinin A-like immunoreactivity (NKA-li) in microdissected regions of the rat hypothalamus and on in vitro release of hypothalamic NKA-li. Results showed that castration decreased NKA-li levels specifically in the median eminence (ME) and arcuate (ARC) regions as compared to those in intact rats. T replacement immediately following castration prevented these site-specific decreases in NKA-li. Similarly, basal efflux of NKA-li was significantly reduced from the entire medial basal hypothalamus (including the ME and ARC) and preoptic area (POA) of castrated rats vs. that from the hypothalami of intact and T-replaced castrated rats. These results show that T can modulate levels of NKA-li selectively in sites previously implicated in the control of LH release and since NKA can inhibit LH and hypothalamic LH-releasing hormone (LHRH) release, these observations are in accord with our view that afferents to LHRH neurons are the targets of gonadal steroid feedback on pituitary LH release.