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|Title:||Progesterone Action on Hypothalamic Lhrh Neurons: In Vitro and In Vivo Studies|
|Department / Program:||Physiology and Biophysics|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|Subject(s):||Biology, Animal Physiology|
|Abstract:||The present study examined the effect of progesterone (P) on hypothalamic luteinizing hormone-releasing hormone (LHRH) neurons, as estimated by in vitro (superfusion) and in vivo (push-pull perfusion) techniques. The administration of P unequivocally stimulated the release of LHRH from hypothalamic tissue obtained from ovariectomized, estradiol-primed (OVX + E) rats as well as proestrous rats. The salient features of these findings are summarized as follows: (1) P was capable to stimulate LHRH release only when the steroid was delivered in an intermittent mode (10 min-on, 20 min-off; 10 ng/ml). A continuous infusion of P at a similar low concentration (10 ng/ml) was ineffective in modifying the release of LHRH. (2) The estrogen-priming was an obligatory requirement for the in vitro P-stimulated LHRH release and this in vivo priming of E upon the responsiveness of the neural LHRH secretary apparatus appears to be dose-dependent. (3) During the rat estrous cycle, P stimulated LHRH release solely in hypothalamic fragments derived from proestrous, but not from the other stages of the estrous cycle, and (4) It was evident that a prostaglandin E(,2) activity and a cyclic AMP-generating system was involved in the P-stimulated LHRH release.
These observations provide a direct evidence that the facilitatory action of P on the release of luteinizing hormone from the pituitary may be mediated through activation of a neural LHRH apparatus. Furthermore, based upon these data, a hypothesis to delineate the neural sequence of events underlying the P-stimulated LHRH release was proposed: (1) Pulsatile stimulation of P may initially activate norepinephrine (NE) neurons to increase NE tone (presumably pulsatile), (2) NE binds to (alpha)-adrenergic receptor located in the plasma membrane of LHRH neurons and then stimulates the release of prostaglandin E(,2), (3) the enhanced prostaglandin E(,2) activity stimulate adenylate cyclase to increase intracellular cyclic AMP levels, and (4) the increased cyclic AMP levels finally trigger the release of LHRH from the median eminence nerve terminals.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1984.
|Date Available in IDEALS:||2014-12-16|
This item appears in the following Collection(s)
Dissertations and Theses - Molecular and Integrative Physiology
Graduate Dissertations and Theses at Illinois
Graduate Theses and Dissertations at Illinois