Thyrotrophic Hormone Secretion in Rats After Partial or Total Interruption of Neural Aiferents to the Medial Basal Hypothalamus

Endocrinology ◽  
1967 ◽  
Vol 80 (6) ◽  
pp. 1075-1082 ◽  
Author(s):  
BÉLA HALÁSZ ◽  
WARNER H. FLORSHEIM ◽  
NANCY L. CORCORRAN ◽  
ROGER A. GORSKI
1993 ◽  
Vol 138 (2) ◽  
pp. 225-232 ◽  
Author(s):  
S. Harvey ◽  
R. W. Lea

ABSTRACT Thyrotrophin-releasing hormone (TRH) stimulates GH secretion in domestic fowl by actions at pituitary and central nervous system sites. The possibility that this central action might be mediated by hypothalamic catecholamines or indoleamines was therefore investigated. When TRH was administered into the lateral ventricles of anaesthetized fowl the concentration of 3,4-dihydroxyphenylacetic acid (DOPAC, a metabolite of dopamine (DA)) in the medial basal hypothalamus (MBH) was increased within 20 min. The concentrations of MBH noradrenaline (NA), DA, serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were, however, unaffected by the intracerebroventricular (i.c.v.) administration of TRH, although the MBH concentrations of somatostatin and TRH were concomitantly reduced. A rapid increase in DA release into MBH extracellular fluid and its metabolism to DOPAC was also observed after i.c.v. or i.v. administration of TRH, in birds in which the MBH was perfused in vivo with Ringer's solution. Microdialysate concentrations of NA, 5-HT and 5-HIAA were not, however, affected by central or peripheral injections of TRH. Diminished GH responses to i.v. TRH challenge occurred in birds pretreated with reserpine (a catecholamine depletor), α-methyl-paratyrosine (a DA synthesis inhibitor) and pimozide (a DA receptor antagonist). These results therefore provide evidence for the involvement of a hypothalamic dopaminergic pathway in the induction of GH release following the central or peripheral administration of TRH. In contrast with its inhibitory actions at peripheral sites, DA would appear to have a central stimulatory role in regulating GH release in birds. Journal of Endocrinology (1993) 138, 225–232


1968 ◽  
Vol 41 (1) ◽  
pp. 91-94 ◽  
Author(s):  
K. BROWN-GRANT ◽  
D. J. EL KABIR ◽  
G. FINK

SUMMARY The anterior pituitary content of luteinizing hormone (LH) was greatly reduced 4 hr. after mating in female rabbits; thyrotrophic hormone content was slightly but not significantly reduced. At 24 hr. after mating LH levels were higher than those at 4 hr. but still significantly below control levels; thyrotrophic hormone content was significantly reduced at this time. Since no evidence is available of an increase in thyrotrophic hormone secretion after mating (see Brown-Grant, 1968) it is concluded that the neuroendocrine events concerned in the release of LH in response to coitus in this species also result in a decrease in the synthesis of thyrotrophic hormone.


2002 ◽  
Vol 227 (5) ◽  
pp. 315-320 ◽  
Author(s):  
Gary L. Jackson ◽  
David Kuehl

The objectives of this study were to determine if the c-aminobutyric acid (GABA)B agonist, 3-aminopropyl (methyl) phosphinic acid (SKF97541), would increase luteinizing hormone (LH) secretion when infused by microdialysis into the medial basal hypothalamus (MBH) of the castrated ram, and to determine if the action of SKF97541 would be attenuated by coinfusion of the GABAB antagonist CGP52432. Initial experiments established that infusion of SKF alone, at concentrations as low as 5 μM, increased mean LH, LH pulse amplitude, and in some cases, pulse interval. In the last experiment, animals were treated with artificial cerebrospinal fluid (CSF) alone, SKF alone (30 μM), 3-[[(3, 4-dichlorophenol) methyl] amino] propyl] dieth-oxymethyl) phosphinic acid (CGP) alone (500 μM), or SKF plus CGP. SKF increased both mean LH and LH pulse amplitude as compared with CSF. CGP alone had no significant effect on LH, but it attenuated the effect of SKF on mean LH. These observations indicate that the stimulatory effects of GABAB agonists on LH pulse patterns are mediated through GABAB receptors and provide further evidence that GABAB receptors located in the MBH can regulate pulsatile GnRH-LH release.


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