Pituitary gonadotropin-releasing hormone (GnRH) receptor activity in goldfish and catfish: seasonal and gonadal effects

Habibi, Hamid R.; R, De Leeuw; Cs, Nahorniak; Hj, Goos; Re, Peter

doi:10.1007/bf00004696

Cited by 84 publications

(31 citation statements)

References 31 publications

(33 reference statements)

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“…In sheep, there is a correlation between GnRH receptor mRNA and the levels of follicular E 2 (Brooks et al 1993), while GnRH receptor number (Gregg et al 1990) and mRNA (Wu et al 1994) increased following incubation of ovine pituitary cells with estradiol. Also in the goldfish, the number of GnRH receptors in the entire pituitary increased during gonadal recrudescence (Habibi et al 1989). However, in fish, this effect cannot be attributed to any one cell type as GnRH receptors are present on both gonadotrophs and somatotrophs (Cook et al 1991).…”

Section: Discussionmentioning

confidence: 99%

The effects of gonadal development and sex steroids on growth hormone secretion in the male tilapia hybrid (Oreochromis niloticus � O. aureus)

Melamed

Eliahu

Ofir

et al. 1995

Fish Physiol Biochem

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Profiles of plasma growth hormone (GH) in male tilapia hybrid (Oreochromis niloticus x O. aureus) were measured and compared at different times of the year. The profiles did not appear to be repetitive, however, differences in their nature were observed at the different seasons; the most erratic profiles were seen in the height of the reproductive season (July), while the peaks were more subdued in the spring and disappeared in the autumn. Peaks in male fish were more prominent than in the females when measured in July. Perifused pituitary fragments from fish with a high GSI responded to salmon gonadotropin-releasing hormone (sGnRH) analog (10 nM-1 μM), while those from fish with a low GSI barely responded to even the highest dose. Exposure of perifused pituitary fragments from sexually-regressed fish to carp growth hormone-releasing hormone (cGHRH; 0.1 μM) or sGnRH (I μM) stimulated GH release only after injection of the fish with methyl testosterone (MT; 3 injections of 0.4 mg kg (1)). The same MT pretreatment did not alter the response to dopamine (DA; 1 or 10 μM). GH pituitary content in MT-treated fish was lower than in control fish, which may be explained by the higher circulating GH levels in these fish, but does not account for the increased response to the releasing hormones. Castration abolished the response of cultured pituitary cells to sGnRH (I fM-100 nM) without altering either their basal rate of secretion or circulating GH levels. Addition of steroids to the culture medium (MT or estradiol at 10 nM for 2 days) enabled a GH response to sGnRH stimulation in cells from sexually regressed fish. Pituitary cells which had not been exposed to steroids failed to respond to sGnRH, although their response to forskolin or TPA was similar to that of steroid-exposed cells. It would appear, therefore, that at least one of the effects of the sex steroids on the response to GnRH is exerted proximally to the formation of cAMP, or PKC, presumably at the level of the receptor. An increase in the number of receptors to the GH-releasing hormones, following steroid exposure, would explain also the changing nature of the GH secretory profile in different stages of the reproductive season.

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Section: Discussionmentioning

confidence: 99%

The effects of gonadal development and sex steroids on growth hormone secretion in the male tilapia hybrid (Oreochromis niloticus � O. aureus)

Melamed

Eliahu

Ofir

et al. 1995

Fish Physiol Biochem

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“…However, the differ ential involvement of e-Ca2+ in sGnRH-induced, as op posed to cGnRH II-stimulated GtH secretion is both an unexpected and novel hypothesis. Both sGnRH and cGnRH II have been shown to bind to the same class of high affinity, low capacity receptors on goldfish pituitary membrane preparations [11]. The magnitude of the GtH response to the two peptides differs and accordingly one might expect that the signal transduction processes in volved to be similar between the two peptides but of greater magnitude in the case of cGnRH II.…”

Section: Discussionmentioning

confidence: 99%

“…One possible explanation is that the two peptides have different physiological roles. Interestingly, the bind ing capacity of high affinity sites in preparations of gold fish pituitary membranes exhibits two distinct seasonal peaks, the first occurring during early recrudescence (Oc tober/November), the second at the time of ovulation (March/April) [11], Perhaps one GnRH is more involved in gonadal recrudescence and the other with ovulation.…”

Section: Discussionmentioning

confidence: 99%

Differences in Extracellular Calcium Involvement Mediating the Secretion of Gonadotropin and Growth Hormone Stimulated by Two Closely Related Endogenous GnRH Peptides in Goldfish Pituitary Cells

Jobin

Chang²

1992

Neuroendocrinology

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Two endogenous gonadotropin-releasing hormone (GnRH) peptides, salmon GnRH (sGnRH) and chicken GnRH II (cGnRH II), stimulate gonadotropin (GtH) and growth hormone (GH) secretion in the goldfish. The extracellular calcium (e-Ca²⁺) dependence of the GtH and GH response to the two GnRH peptides were compared using static incubations of dispersed goldfish pituitary cells. Incubation with Ca²⁺-depleted medium (without the addition of Ca²⁺ salts and in the presence of EGTA) did not alter basal GtH secretion, but reduced the GtH response to sGnRH, and abolished the cGnRH II-induced GtH release. Blockade of e-Ca²⁺ entry by low concentrations of COCl₂ had no effect on basal GtH secretion but reduced cGnRH II and sGnRH stimulated GtH release when applied at 0.1 and 0.5 mil concentrations, respectively. In general, treatments with voltage-sensitive Ca²⁺ channel (VSCC) antagonists, verapamil, nifedipine and nicardipine, did not alter basal GtH release but attenuated GnRH-stimulated GtH responses. cGnRH II-induced GtH release was decreased by 10 nM verapamil and 1 nM nifedipine, whereas the reduction of GtH responses to sGnRH required 100 times higher concentrations of these VSCC antagonists. cGnRH II but not sGnRH stimulation of GtH secretion was also abolished by 10 µM nicardipine. In contrast to GtH release, exposure to Ca²⁺-depleted medium reduced basal GH release and abolished the GH responses to both GnRH peptides. sGnRH and cGnRH II-stimulated GH responses were both abolished by 0.1 mM COCl₂, decreased by 1 nM verapamil, and reduced by 10 nM nicardipine. Addition of 0.1 and 10 µM nifedipine inhibited the GH responses to sGnRH and cGnRH II, respectively. Basal GH release was not affected by the VSCC antagonists tested. Results from this study indicate that entry of e-Ca²⁺ in part through VSCC, is involved in GnRH stimulation of GtH and GH release from goldfish gonadotropes and somatotropes; however, the e-Ca²⁺ dependence of the GtH and GH responses to the two endogenous GnRHs differ. The stimulatory effects of cGnRH II on GtH secretion is more dependent on and sensitive to e-Ca²⁺ than sGnRH. Whereas the sensitivity of GH responses to manipulations of e-Ca²⁺ availability is, in most instances, similar for both GnRH peptides. These results further suggest that basal secretion of GH is more sensitive to e-Ca²⁺ than basal GtH release; however, VSCC are not involved in the maintenance of basal release of either hormone.

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“…The redundancy of stimulatory GTH regulators may be of physiological impor tance. The number of high-affinity GnRH receptors and the sensitivity of the GTH response to GnRH stimulation varies seasonally [23,26], with the lowest number of receptors and GTH responses occurring in sexually regressed goldfish [26]. This seasonality of the GnRH stimulatory system is in opposite phase compared to the seasonal changes in sensitivity of the gonadotropes to «-adrenergic stimulation.…”

Section: Discussionmentioning

confidence: 99%

Influences of Norepinephrine, and Adrenergic Agonists and Antagonists on Gonadotropin Secretion from Dispersed Pituitary Cells of Goldfish, <i>Carassius auratu</i><i>s</i>

Chang

Goor²,

Acharya³

1991

Neuroendocrinology

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Static incubations of dispersed goldfish pituitary cells with 1–100 nM norepinephrine (NE) stimulated gonadotropin (GTH) release. Additions of the α-agonist phenylephrine, and the αi-agonist 6-fluoronorepinephrine, but not the α₂-agonist clonidine, nor the β-agonist isoproterenol, also enhanced GTH secretion. The GTH responses to 1 nM NE was significantly inhibited by coincubations with 1 µM of the α-antagonist phentolamine, the α₁-antagonists prazosine and benoxathian, but not the α₂-antagonist yohimbine nor the β-antagonist propranolol. The GTH responses to NE and phenylephrine were also additive to salmon GTH-releasing hormone (sGnRH)-induced GTH release. These results suggests that NE directly stimulates GTH secretion independent of sGnRH receptors via α₁-like adrenergic receptors.

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Pituitary gonadotropin-releasing hormone (GnRH) receptor activity in goldfish and catfish: seasonal and gonadal effects

Cited by 84 publications

References 31 publications

The effects of gonadal development and sex steroids on growth hormone secretion in the male tilapia hybrid (Oreochromis niloticus � O. aureus)

The effects of gonadal development and sex steroids on growth hormone secretion in the male tilapia hybrid (Oreochromis niloticus � O. aureus)

Differences in Extracellular Calcium Involvement Mediating the Secretion of Gonadotropin and Growth Hormone Stimulated by Two Closely Related Endogenous GnRH Peptides in Goldfish Pituitary Cells

Influences of Norepinephrine, and Adrenergic Agonists and Antagonists on Gonadotropin Secretion from Dispersed Pituitary Cells of Goldfish, <i>Carassius auratu</i><i>s</i>

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