Effects of 17 beta-estradiol on LH-RH release from rat mediobasal hypothalamic slices

Mediobasal hypothalamic slices of adult ovariectomized (OVX) rats treated or not with 17 beta-estradiol (E2) were superfused in buffered (pH 7.2) Locke medium containing bacitracin. A 6-min pulse of K+ (56 m M) was less effective in releasing luteinizing hormone releasing hormone (LH-RH) from mediobasal hypothalamic slices sampled from OVX rats than from OVX animals treated subcutaneously with either E2 or stilbestrol implants for 5 days; in contrast, the basal release of the neuropeptide was identical in both cases. Direct addition to the superfusion medium of 17 beta-estradiol (10(-10) to 10(-7) M) or stilbestrol (10(-8) M) potentiated the K+-induced LH-RH release from slices of OVX animals. The K+-induced LH-RH release observed after in vivo E2 implantation was not further amplified by in vitro addition of the hormone. Tamoxifen and hydroxytamoxifen, estrogen antagonists, were ineffective by themselves, but reversed the E2 facilitation of K+-evoked LH-RH release. In contrast, 17 alpha-estradiol, progesterone, or cholesterol (10(-8) or 10(-9) M) hat no effect on either basal or stimulated release of the neurohormone. Somatostatin release measured under identical conditions was not affected by castration or by in vitro addition of the steroid.

(1) estradiol appears selectively and specifically involved in the process coupling, nerve endings depolarization, and LH-RH release, and (2) the effect is receptor-mediated and does not appear to require nuclear translocation of the steroid or transcription processes, since it can be readily elicited upon addition of the hormone to nerve endings disconnected from their cell bodies.