Steroid Modulation of Neuropeptide Y-Induced Luteinizing Hormone Releasing Hormone Release from Median Eminence Fragments from Male Rats

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Abstract
Neuropeptide Y (NPY) has been shown to stimulate hypothalamic release of luteinizing hormone-releasing hormone (LHRH) both in vitro and in vivo. In female rats, NPY facilitation of LHRH release is greatly augmented in advance of preovulatory LHRH surges, likely via the actions of ovarian steroids. However, the role of NPY in regulating LHRH release in male rats and the effects of testicular hormones on LHRH responses to NPY in males are not well understood. The objective of the present studies was to determine whether NPY stimulates LHRH release in vitro from hypothalamic tissue of male rats, and whether these effects could be modulated by testosterone (T). Mediobasal hypothalamic (MBH) or median eminence (ME) fragments from either sham-operated or castrated male rats (7 days) were placed in superfusion chambers and superfused with M199 for a 30-min baseline, 30-min challenge with NPY (10–7M), and a final 30-min challenge with 56 mM KC1. One-milliliter fractions were collected every 10 min and average LHRH release values over the 30-min periods were compared among groups. NPY (10–7M) produced a significant increase in LHRH release from the MBH and ME from intact animals. In contrast, the same dose of NPY did not stimulate LHRH release from tissues from castrated animals; only with a higher dose of NPY (10–6M) were the effects of NPY on LHRH release significant. Potassium challenge (56 mM KCl) significantly stimulated LHRH release from the ME of both intact and castrate male rats suggesting that all tissues were able to respond to a stimulus, and that castration did not alter the responsiveness of the LHRH neuron to a nonspecific secretagogue. To determine the extent to which T regulates the sensitivity of LHRH responses to NPY, male rats were castrated and implanted with T capsules that maintained either low (1.24 ± 0.06 ng/ml) or high (2.17 ± 0.31 ng/ml) physiological plasma levels of T. Treatment with the higher dose of T restored the ability of NPY to stimulate LHRH release from the ME tissues. These results demonstrate that NPY stimulates LHRH release from the hypothalamus in vitro, and that gonadal steroids, in this case T and/or its metabolites, modulate the responsiveness of the LHRH neuron to NPY. Based on these data from intact and castrate-derived tissues, it appears that steroids are necessary to maintain LHRH responsiveness to NPY receptor stimulation.

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