Involvement of Corticotropin-Releasing Hormone and Endogenous Opioid Peptides in Prolactin-Suppressed Gonadotropin Releasing Hormone Release in vitro

1994 ◽  
Vol 60 (3) ◽  
pp. 291-296 ◽  
Author(s):  
Aldo E. Calogero ◽  
Robertus F.A. Weber ◽  
Francesco Raiti ◽  
Nunziatina Burrello ◽  
Maira Lusia Moncada ◽  
...  
Keyword(s):  
Opioid Peptides ◽  
Gonadotropin Releasing Hormone ◽  
Hormone Release ◽  
Corticotropin Releasing Hormone ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Releasing Hormone ◽  
Release In Vitro

Effects of porcine relaxin on oxytocin release from the neurohypophysis in the anaesthetized lactating rat

1986 ◽  
Vol 109 (3) ◽  
pp. 393-397 ◽  
Author(s):  
K. T. O'Byrne ◽  
L. Eltringham ◽  
G. Clarke ◽  
A. J. S. Summerlee
Keyword(s):  
Opioid Peptides ◽  
Inhibitory Effect ◽  
Opioid Antagonist ◽  
Dependent Manner ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Oxytocin Release ◽  
Relaxin 2

ABSTRACT The effect of relaxin on electrically evoked release of oxytocin from the posterior pituitary was examined by monitoring changes in intramammary pressure in the anaesthetized lactating rat. The amount of oxytocin released by electrical stimulation of the neurohypophysis in vivo was dramatically reduced following i.v. injection of highly purified porcine relaxin (2·5–10 μg/rat). Relaxin inhibited oxytocin release in a dose-dependent manner and the onset of inhibition occurred within 6–10 min and lasted for 10–60 min. No effect on the sensitivity of the mammary gland to exogenous oxytocin was observed after relaxin treatment. During the period of inhibition, i.v. injection of the opioid antagonist naloxone chloride (1 mg/kg) completely and immediately restored electrically evoked oxytocin release. The neurohypophysis is known to contain endogenous opioid peptides, therefore the effect of relaxin on electrically stimulated release of oxytocin from the rat isolated neural lobe in vitro was examined. Relaxin (500–2000 ng/ml) failed to inhibit oxytocin release in vitro. The results suggest that relaxin can inhibit the release of oxytocin from terminals in the neurohypophysis, but by an indirect mechanism. This action appears to be mediated through endogenous opioid peptides whose source is not clear. They are unlikely to be of neurohypophysial origin and may probably come from the adrenal medulla, since acute adrenalectomy negated the inhibitory effect of relaxin on oxytocin release. J. Endocr. (1986) 109, 393–397

Estrogen stimulates gonadotropin-releasing hormone release from rat hypothalamus independently through catecholamine and histamine in vitro

1989 ◽  
Vol 120 (5) ◽  
pp. 644-648 ◽  
Author(s):  
Shirou Ohtsuka ◽  
Takamichi Nishizaki ◽  
Keiichi Tasaka ◽  
Akira Miyake ◽  
Osamu Tanizawa ◽  
...  
Keyword(s):  
Bovine Serum Albumin ◽  
Gonadotropin Releasing Hormone ◽  
Female Rats ◽  
Hormone Release ◽  
Mediobasal Hypothalamus ◽  
Releasing Hormone ◽  
Gnrh Release ◽  
Perifusion System ◽  
Made In

Abstract. Estradiol is known to stimulate gonadotropin-releasing hormone release from the rat mediobasal hypothalamus. Studies were made in an in vitro perifusion system on whether catecholamine and/or histamine was involved in estradiol-induced GnRH release. Normal cycling female rats were decapitated in diestrus II and their medio-basal hypothalami were combined and, perifused with Earl's balanced salt solution containing 0.01% bovine serum albumin bubbled with 95% O2 and 5% CO2. The levels of norepinephrine, dopamine, and histamine and of GnRH in the effluent were measured by HPLC and radioimmunoassay, respectively. Administration of 10−6 mol/l estradiol resulted in releases of norepinephrine, dopamine, histamine and GnRH at levels of 98, 70, 91 and 288%, respectively, of initial values. Administration of 10−6 mol/l norepinephrine or dopamine resulted in no increase in histamine release, and administration of 10−6 mol/l histamine did not increase release of norepinephrine or dopamine. These data suggest that estradiol stimulates the releases of GnRH, catecholamine and histamine from the rat medio-basal hypothalamus, and that it increases GnRH release independently through catecholamine and histamine. As we found previously that norepinephrine or histamine stimulates GnRH release from the mediobasal hypothalamus, we conclude that estradiol stimulates releases of norepinephrine and histamine, resulting in GnRH release from the medio-basal hypothalamus.

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