Characterization of Luteinizing Hormone - Releasing Hormone (Lhrh) Release From Rat Hypothalamus Using an in Vitro System
Hartter, Daryl Edward
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https://hdl.handle.net/2142/71422
Description
Title
Characterization of Luteinizing Hormone - Releasing Hormone (Lhrh) Release From Rat Hypothalamus Using an in Vitro System
Author(s)
Hartter, Daryl Edward
Issue Date
1983
Department of Study
Physiology and Biophysics
Discipline
Physiology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Animal Physiology
Abstract
The effect of a variety of experimental compounds on the release of immunoreactive luteinizing hormone-releasing hormone (LHRH) from rat hypothalamus was examined using an in vitro superfusion system and sensitive assays for LHRH measurement. High extracellular (60 mM) K('+) ion repeatedly stimulated in vitro LHRH release, an effect attributed to nerve membrane depolarization triggering influx of Na('+) and Ca('++) ions and resulting in exocytosis of LHRH. K('+)-evoked LHRH release was strongly Ca('++)-dependent; however, Na('+) influx was not obligatory in depolarization-induced release. In support of calcium's role in LHRH release, agents permitting influx of Ca('++) (inophore A23187) or increased Ca('++) leakage from intracellular Ca('++) stores (2,4-dinitrophenol) stimulated LHRH release. K('+)-evoked release of LHRH is also thought to involve a microtubular transport mechanism, since colchicine (10('-6) or 10('-5) M) inhibited K('+)-stimulated LHRH output. However, 10('-4) M colchicine dramatically increased LHRH release as well as hypothalamic LHRH content by an unknown mechanism.
The release of LHRH is possibly mediated through adenyl cyclase/cyclic AMP, supported by the finding that adenyl cyclase activators (prostaglandin E, and elevated Mg('++) concentration) and cyclic AMP derivatives stimulated in vitro LHRH release. Employing intermittent delivery of dibutyryl cyclic AMP, mean LHRH release was repeatedly triggered, as assessed by specific assay employing Root anti-LHRH serum. This synchronous LHRH release was Ca('++)-dependent. Intriguingly, cyclic AMP-synchronized LHRH release was not observed when NETT or Chen-Ramirez anti-LHRH sera were used in LHRH measurement, in spite of the fact that spontaneous LHRH release and post-superfusion tissue LHRH content did not differ among the three LHRH assays. These results suggest the existence of immunologically distinct hypothalamic LHRH molecules, a fraction of which are released in response to intermittent cyclic AMP administration and recognized as immunogenic by Root anti-LHRH but to a lesser degree by Nett and Chen-Ramirez LHRH antibodies.
Taken together, these results suggest that Ca('++) ion plays a crucial role in K('+)-stimulated LHRH release from rat hypothalamic fragments superfused in vitro. In addition, it can be postulated that a microtubular transport mechanism is an important component of the LHRH neurosecretory process. . . . (Author's abstract exceeds stipulated maximum length. Discontinued here with permission of author.) UMI
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