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Do testosterone and estradiol-17 beta enforce inhibition or stimulation of luteinizing hormone-releasing hormone secretion?

The effects of gonadectomy and gonadal steroid replacement on hypothalamic luteinizing hormone-releasing hormone (LHRH) secretion in vivo and in vitroi in the rat are reviewed. The evidence revealed that the part played by testosterone or estradiol-17 beta in regulation of LHRH signals to pituitary gonadotropes is more complex than that which has been surmised from measurements of steroidal effects on luteinizing hormone (LH) release. There is little evidence to date to corroborate the assumptions that the rate of hypothalamic LHRH drive is enhanced to sustain the post-gonadectomy LH response and that gonadal steroids inhibit LHRH secretion in gonadectomized rats. There is a dire need to develop newer techniques not only to characterize the LHRH pulsatility pattern reaching the pituitary gonadotropes on a moment-to-moment basis but also to fully explain the existing evidence that suggests a facilitatory influence of gonadal steroids and invokes participation of newer neural and steroidal and nonsteroidal gonadal factors in regulating the communication between LHRH secreting neurons and pituitary gonadotropes. Plainly, further studies will be necessary to provide a unified view on the exchange of information between the gonads and hypothalamus for control of reproduction.