Effects of a gonadotropin‐releasing hormone antagonist on gonadotropin levels in masu salmon and sockeye salmon
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Abstract The salmon gonadotropin‐releasing hormone (sGnRH) is considered to be involved in gonadal maturation via gonadotropin (GTH) secretion in salmonid fishes. However, there is no direct evidence for endogenous sGnRH‐stimulated GTH secretion in salmonids. In this study, to clarify whether endogenous sGnRH stimulates GTH secretion, we examined the effects of the mammalian GnRH (mGnRH) antagonist [Ac‐Δ 3 ‐Pro 1 , 4FD‐Phe 2 , D‐Trp 3,6 ]‐mGnRH on luteinizing hormone (LH) levels in 0‐year‐old masu salmon Oncorhynchus masou and sockeye salmon Oncorhynchus nerka . First, the effects of the GnRH antagonist on LH release were examined in 0‐year‐old precocious male masu salmon. GnRH antagonist treatment for 3 hr significantly inhibited an increase in plasma LH levels that was artificially induced by exogenous sGnRH administration, indicating that the GnRH antagonist is effective in inhibiting LH release from the pituitary. Subsequently, we examined the effect of the GnRH antagonist on LH synthesis in 0‐year‐old immature sockeye salmon that were pretreated with exogenous testosterone for 42 days to increase the pituitary LH contents; the testosterone treatment did not affect the plasma LH levels. GnRH antagonist treatment slightly but significantly inhibited an increase in the testosterone‐stimulated pituitary LH content levels. However, no significant differences in the plasma LH levels were observed between the GnRH antagonist‐treated and control groups. These results suggest that endogenous sGnRH is involved in LH secretion in salmonid fishes. J. Exp. Zool. 307A:535–541, 2007 . © 2007 Wiley‐Liss, Inc.Keywords:
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The temporal relationship between cessation of GnRH delivery to the pituitary gland and the loss of responsiveness to the stimulatory action of estradiol (E2) was examined in 4 ovariectomized rhesus monkeys whose endogenous GnRH production had been abolished by hypothalamic lesions. Gonadotropin secretion was re-established by the intermittent administration of GnRH. The GnRH-replacement regimen was then discontinued and estradiol benzoate (EB) injected 24, 48, 72 and 96 hours later. Unambiguous gonadotropin discharges were induced when EB was administered 24 or 48 hours after discontinuation of GnRH replacement. We conclude that E2 can initiate gonadotropin discharges in the absence of circulating GnRH. E2 may, therefore, be viewed as a gonadotropin releasing hormone.
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Abstract Gonadotropin‐releasing hormone (GnRH)‐II stimulates luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) secretion when administered at high doses in mammals, and this effect has been assumed to be mediated through the GnRH‐II receptor expressed on gonadotropes. This study used two selective GnRH‐I receptor antagonists to test the alternative hypothesis that GnRH‐II acts through the GnRH‐I receptor to elicit gonadotropin secretion. The antagonist, antide, was used to characterize the receptor‐relay because it was a pure antagonist in vitro based on inositol phosphate responses in COS‐7 cells transfected with either mammalian GnRH‐I and GnRH‐II receptors and, in vivo , potently antagonized the gonadotropin‐releasing effect of a single injection of 250 ng GnRH‐I in our sexually inactive sheep model. In a series of studies in sheep, antide (i) blocked the acute LH response to a single injection of GnRH‐II (20 µg antide: 10 µg GnRH‐II); (ii) blocked both the acute, pulsatile LH response and the FSH priming response to 2‐hourly injections of GnRH‐II over 36 h (100 µg antide/8 h: 4 µg GnRH‐II/2 h); and (iii) chronically blocked both the pulsatile LH response and the marked FSH priming response to 4‐hourly injections of GnRH‐II over 10 days (75 µg antide/8 h: 4 µg GnRH‐II/4 h). In two final experiments, the GnRH‐I antagonist 135‐18, shown previously to agonize the mammalian GnRH‐II receptor, blocked the gonadotropin‐releasing effects of GnRH‐I (250 ng) but failed to elicit an LH response when given alone, and simultaneous administration of GnRH‐II (250 ng) failed to alter the LH‐releasing effect of GnRH‐I (50–500 ng). These data thus support our hypothesis. Based on additional literature, it is unlikely that the GnRH‐II decapeptide is a native regulator of the gonadotrope in mammals.
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Gonadotropin-releasing hormone receptor
Gonadotropin-releasing hormone antagonist
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