The effect of the blockade of α-melanocyte-stimulating hormone on LH release in the rat

1993 ◽  
Vol 137 (2) ◽  
pp. 197-202 ◽  
Author(s):  
C. Caballero ◽  
M. E. Celis

ABSTRACT We have investigated the effect of blocking α-MSH on the release of LH in rats at pro-oestrus. Continuous infusion of Pro-Leu-Gly-NH2 (PLG; 0·2 μg/h), from the afternoon of dioestrus-2 until the day of oestrus, inhibited LH at pro-oestrus and the next ovulation on the day of oestrus. Plasma α-MSH levels decreased significantly in rats treated with PLG. This inhibitory effect on LH release was not observed in rats treated with a continuous infusion of a diluted antiserum against α-MSH (0·5 μl/h, diluted 1/10) from the afternoon of dioestrus-2 until the day of oestrus. On the contrary, the administration of undiluted antiserum against α-MSH (0·5 μl/h) blocked LH release and ovulation. The release of α-MSH into the blood was also significantly blocked by this treatment. When serum levels of progesterone were measured at 12.00 and 14.00 h in rats in which α-MSH release was blocked by PLG or concentrated antiserum, a significant decrease was observed when compared with the levels of progesterone in control rats. These results show that the blockade of α-MSH inhibits LH release and the next ovulation in rats treated with PLG or with concentrated antiserum against α-MSH, through a blockade of progesterone of adrenal origin. Journal of Endocrinology (1993) 137, 197–202

1987 ◽  
Vol 114 (1) ◽  
pp. 84-89
Author(s):  
P. Negri-Cesi ◽  
F. Celotti ◽  
R. C. Melcangi ◽  
M. Zanisi ◽  
M. Motta

Abstract. The aim of the present experiments was to analyze whether the inhibitory effect exerted by testosterone on FSH release might be mediated by the intracerebral transformation of the hormone into oestrogenic metabolites. Advantage has been taken of the availability of the potent antioestrogen tamoxifen. Two series of experiments have been performed. In the first one, adult male rats have been castrated and submitted, beginning immediately after surgery, to a 6-day treatment with testosterone propionate (2 mg/rat/day), tamoxifen (50 or 200 μg/rat/day) or testosterone propionate (2 mg/rat/day) plus tamoxifen (either 50 or 200 μg/rat/day). In the second experiment, adult male rats have been castrated and submitted to the same 6-day treatments, beginning 4 weeks following orchidectomy. In both experiments, the animals were killed 24 h after the last injection, and serum levels of FSH and LH have been measured by radioimmunoassays. The results have clearly shown that, in both experiments, the administration of testosterone results in a significant decrease of serum FSH and in a total suppression of LH release. The administration of tamoxifen, in either dose, does not modify the elevated serum FSH and LH levels present in the orchidetomized animals, and does not antagonize the inhibitory effect on FSH and LH secretion exerted by the concomitant treatment with testosterone propionate. It is concluded that testosterone inhibits FSH secretion in orchidectomized rats acting as such, and not following aromatization to oestrogens.


1976 ◽  
Vol 68 (2) ◽  
pp. 283-287 ◽  
Author(s):  
BRIDGET I. BAKER

SUMMARY Various agents were tested for their ability to oppose the stimulatory effect of dibutyryl cyclic AMP on the release of the melanocyte-stimulating hormone from the rat neuro-intermediate lobe in vitro. Only dopamine exhibited an inhibitory effect; serotonin, γ-aminobutyric acid, tocinoic acid, tocinamide, the tripeptide Pro-Leu-Gly-NH2 and dibutyryl cyclic GMP were all ineffective.


1980 ◽  
Vol 93 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Flavio Piva ◽  
José Borrell ◽  
Patrizia Limonta ◽  
Gilberto Gavazzi ◽  
Luciano Martini

Abstract. Adult female rats castrated 4 weeks before were implanted bilaterally into the basomedial area of the amygdala with drugs known to mimic or to counteract the actions of acetylcholine. The animals were sacrificed at different time intervals after the implantation of the different compounds, and serum levels of LH and FSH were measured by radioimmunoasay. The data obtained indicate that the intra-amygdalar implantation of the muscarinic blocker atropine induces a significant increase of the release of LH without altering FSH secretion. The implantation of two cholinomimetic drugs, pilocarpine, an almost pure muscarinic agonist, and carbachol, which possesses both muscarinic and nicotinic properties, exerted an inhibitory effect only on LH release. On the contrary, the intra-amygdalar placement of the nicotinic blocker mecamylamine was followed by an increase of FSH with no changes in LH. These observations may suggest that cholinergic signals reaching the amygdala may be of some relevance in the mechanisms controlling gonadotrophin secretion. Muscarinic receptors seem to play an inhibitory role in the regulation of LH secretion, while nicotinic receptors seem to modulate in an inhibitory way FSH release.


1990 ◽  
Vol 124 (1) ◽  
pp. 127-132 ◽  
Author(s):  
T. Scimonelli ◽  
M. E. Celis

ABSTRACT We have investigated the effect of administration of α-MSH into the median eminence (ME) of rats on the release of LH and prolactin. Continuous infusion of α-MSH (0·5 μg/h) into the ME from the afternoon of the second day of dioestrus and over the 24 h of pro-oestrus inhibited the preovulatory LH and prolactin surge and the occurrence of ovulation. This inhibitory effect on LH and prolactin release was also observed in chronically ovariectomized rats given a single injection of α-MSH (1 μg/μl per rat) into the ME (blood samples were collected 0,20,60,90,105 and 120 min after injection). The intraperitoneal injection of the dopamine receptor blocker, haloperidol (2 mg/kg), 30 min before the injection of α-MSH into the ME prevented the inhibitory effect of α-MSH on the release of LH and prolactin. These results suggest that hypothalamic α-MSH might be involved in the regulation of LH and prolactin release via the tuberoinfundibular dopaminergic system and that this system also modifies the serum concentrations of α-MSH. Journal of Endocrinology (1990) 124, 127–132


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