{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/71422"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/71422","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Characterization of Luteinizing Hormone - Releasing Hormone (Lhrh) Release From Rat Hypothalamus Using an in Vitro System","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.","abstract_html":"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.","abstract_has_math":false,"creators":["Hartter, Daryl Edward"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Physiology","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2014,"date_issued":"2014-12-16T06:45:42Z","date_published":"2014-12-16T06:45:42Z","updated_at":"2026-07-22T22:26:04Z","subjects":["Biology, Animal Physiology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(UMI)AAI8309952"],"render_values":[{"text":"(UMI)AAI8309952","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/71422","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Hartter, Daryl Edward"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2014-12-16T06:45:42Z","10000-01-01","1983"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Physiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Animal Physiology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/71422","(UMI)AAI8309952"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["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","Made available in DSpace on 2014-12-16T06:45:42Z (GMT). No. of bitstreams: 1 8309952.pdf: 4754267 bytes, checksum: b7a0c606e5f1df68807ba7bc2ebd1fc4 (MD5) Previous issue date: 1983","Embargo set by: Seth Robbins for item 71588 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","128 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1983."]},{"key":"dc:title","label":"Title","values":["Characterization of Luteinizing Hormone - Releasing Hormone (Lhrh) Release From Rat Hypothalamus Using an in Vitro System"]}]}],"canonical_facts":{"dc:creator":["Hartter, Daryl Edward"],"dc:date":["2014-12-16T06:45:42Z","10000-01-01","1983"],"dc:description":["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","Made available in DSpace on 2014-12-16T06:45:42Z (GMT). No. of bitstreams: 1 8309952.pdf: 4754267 bytes, checksum: b7a0c606e5f1df68807ba7bc2ebd1fc4 (MD5) Previous issue date: 1983","Embargo set by: Seth Robbins for item 71588 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","128 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1983."],"dc:identifier":["http://hdl.handle.net/2142/71422","(UMI)AAI8309952"],"dc:subject":["Biology, Animal Physiology"],"dc:title":["Characterization of Luteinizing Hormone - Releasing Hormone (Lhrh) Release From Rat Hypothalamus Using an in Vitro System"],"dc:type":["text"],"thesis:degree_discipline":["Physiology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:26:04Z"}