The role of calcium in gonadotropin releasing hormone-induced luteinizing hormone secretion from the bovine pituitary
dc.contributor.advisor | Amoss, Max S. | |
dc.contributor.committeeMember | Jenkins, William L. | |
dc.contributor.committeeMember | MacKenzie, Duncan S. | |
dc.contributor.committeeMember | McConnell, Stewart | |
dc.creator | Kile, Jay Perry | |
dc.date.accessioned | 2020-09-02T21:04:24Z | |
dc.date.available | 2020-09-02T21:04:24Z | |
dc.date.issued | 1986 | |
dc.description | Typescript (photocopy). | en |
dc.description.abstract | The hypothesis was tested that GnRH acts to release LH by increasing calcium uptake by the gonadotroph which in turn stimulates calcium-calmodulin activity and results in LH release from bovine pituitary cells as it does in the rat. Pituitary glands of calves (4-10 months of age) were enzymatically dispersed (0.2% collagenase) and grown for 5 days to confluency in multiwell plates (3x10^5/well). Cells treated with GnRH (10-1000 ng/ml in Hank's Balanced Salt Solution), Ca++ ionophore A23187 (2.5-10 μM), and ouabain (0.1-1 μM) all produced significant releases of LH. Extracellular Ca++ as low as 46 μM permitted GnRH-induced LH release in a pronounced "all or none" fashion, while thorough washing of the cells with 0.5 mM EGTA in Ca++-free media prevented the action of GnRH. GnRH (100 ng/ml) caused a rapid efflux (15 seconds) of ^45Ca++. Both GnRH-stimulated 45Ca efflux and LH release could be partially blocked by verapamil (10^-5 M). GnRH-induced LH release could also be blocked by nifedipine (10^-7-10^-5 M) and tetrodotoxin (10^-9 10^-7 M), although these agents did not affect 45Ca efflux. The calmodulin antagonists calmidazolium (10^-9-10^-8M) and W7 (10^-6-10^-5 M) were found to block GnRH induced LH release, as well as LH release induced by theophylline (1 mM), KC1 (25 mM), PGE2 (1 μM) and estradiol (25 ng/ml). These data indicated that: (1) calcium is required for GnRH action, but extracellular Ca++ does not regulate LH release; (2) GnRH elevates intracellular Ca++ by opening both voltage sensitive and receptor mediated Ca++ channels; (3) activation of calmodulin is one mechanism involved in GnRH-induced LH release. | en |
dc.format.digitalOrigin | reformatted digital | en |
dc.format.extent | x, 175 leaves | en |
dc.format.medium | electronic | en |
dc.format.mimetype | application/pdf | |
dc.identifier.oclc | 17967716 | |
dc.identifier.uri | https://hdl.handle.net/1969.1/DISSERTATIONS-22005 | |
dc.language.iso | eng | |
dc.publisher.digital | Texas A&M University. Libraries | |
dc.rights | This thesis was part of a retrospective digitization project authorized by the Texas A&M University Libraries. Copyright remains vested with the author(s). It is the user's responsibility to secure permission from the copyright holder(s) for re-use of the work beyond the provision of Fair Use. | en |
dc.rights.uri | http://rightsstatements.org/vocab/InC/1.0/ | |
dc.subject | Major veterinary physiology | en |
dc.subject.classification | 1986 Dissertation K48 | |
dc.subject.lcsh | Luteinizing hormone releasing hormone | en |
dc.subject.lcsh | Gonadotropin | en |
dc.subject.lcsh | Calcium | en |
dc.subject.lcsh | Cattle | en |
dc.subject.lcsh | Physiology | en |
dc.title | The role of calcium in gonadotropin releasing hormone-induced luteinizing hormone secretion from the bovine pituitary | en |
dc.type | Thesis | en |
dc.type.genre | dissertations | en |
dc.type.material | text | en |
thesis.degree.grantor | Texas A&M University | en |
thesis.degree.name | Doctor of Philosophy | en |
thesis.degree.name | Ph. D | en |
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