The functions of somatostatin, norepinephrine and epinephrine in regulation of rhythmic growth hormone secretion were evaluated in male Sprague-Dawley rats. Three experimental strategies were used: (1) the chronic cannulation model to assess the effects of stress, lateral hypothalamic stimulation, monosodium glutamate, and pharmacologic agents on growth hormone dynamics, (2) biochemical mapping of central somatostatinergic pathways involved in growth hormone regulation, and (3) an in vitro perifusion system to study somatostatin release. / It is shown that exictatory and inhibitory neural inputs must be intact to maintain normal rhythmic growth hormone secretion. Growth hormone rises are generated by hypothalamic neurons that liberate a growth hormone releasing factor. These neurons are activated by adrenergic (and probably noradrenergic) inputs. The periventricular and amygdalofugal somatostatinergic systems control ebbs in plasma growth hormone and stress- or lateral hypothalamic stimulation-induced growth hormone suppression. Catecholaminergic regulation of somatostatin release is not defined clearly.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.68669 |
Date | January 1982 |
Creators | Terry, L. Cass. |
Publisher | McGill University |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
Format | application/pdf |
Coverage | Doctor of Philosophy (Department of Medicine) |
Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
Relation | alephsysno: 000157030, proquestno: AAINK60995, Theses scanned by UMI/ProQuest. |
Page generated in 0.0019 seconds