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Although chronic administration of physiological amounts of oestrogen alone is an effective means of inducing lordosis in female rats (Davidson, Smith, Rodgers & Bloch, 1968), progesterone reliably facilitates lordosis following acute or sub-maximal treatment with oestrogen (Boling & Blandau, 1939; Beach, 1942). In males, spontaneous lordosis occurs only rarely, and there are few reports on the successful induction of this behaviour by ovarian steroids (see Young, 1961). Recently, however, it has been shown that chronic administration of oestradiol benzoate to castrated male rats will result in lordosis response rates approaching in frequency those found in females (Davidson, 1969).
Male rats castrated during the first few days of life, but not later, show behavioural responses closely resembling those of normal females after treatment with ovarian steroids in adulthood. This suggests that testicular secretion in the neonatal period is responsible for the determination of future behavioural patterns (Grady, Phoenix & Young, 1965;
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ABSTRACT
The presence of two endogenous forms of gonadotrophin-releasing hormone (GnRH) in the chicken hypothalamus (chicken GnRH-I ([Gln8]GnRH) and chicken GnRH-II ([His5,Trp7,Tyr8]GnRH)), and the stimulation of gonadotrophins by both forms, suggests the possible existence of GnRH receptor subtypes and gonadotroph subtypes in the chicken pituitary. This question was investigated by assessing the effects of various combinations of the two known forms of chicken hypothalamic GnRH and antagonist analogues of GnRH on LH release from dispersed chicken anterior pituitary cells in both static and perifused systems. The relative inhibition of chicken GnRH-I-stimulated and chicken GnRH-II-stimulated LH release by 12 GnRH antagonists did not differ significantly, suggesting a single GnRH receptor type. Chicken GnRH-II was approximately sixfold more potent than chicken GnRH-I in releasing LH. Release of LH in response to maximal doses of chicken GnRH-I and chicken GnRH-II and to a mixture of both was similar and the two peptides were not additive in their effects, consistent with the presence of a single type of LH gonadotroph and a GnRH receptor which binds both forms of GnRH. Each form of GnRH desensitized cells to subsequent stimulation with the other form, providing additional evidence for a single type of LH gonadotroph. These findings suggest that chicken GnRH-I and -II stimulate gonadotrophin release through a single GnRH receptor type on a single class of LH gonadotroph in the chicken pituitary.
J. Endocr. (1988) 117,43–49
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ABSTRACT
Barium is known to elicit secretion in a number of cell systems. The mechanism of Ba2+ stimulation of LH release in cultured chicken pituitary cells was investigated in the present study. Barium-stimulated LH release was inhibited by extracellular Ca2+, indicating that Ba2+ does not act by stimulating Ca2+ entry. Simultaneous stimulation of the cells with Ba2+ and phorbol ester produced a synergistic response, similar to the synergism obtained with phorbol ester and treatments which increase cytosolic Ca2+. Both Ba2+-stimulated LH release and the synergism of Ba2+ with phorbol ester were inhibited by calcium channel blockers (Co2+, methoxyverapamil and nifedipine) and by calmodulin antagonists (trifluoperazine and chlorpromazine). These results indicate that the actions of Ba2+ are dependent on its entry through Ca2+ channels, and suggest that calmodulin activation is necessary for the synergism between Ba2+ and phorbol ester. Thus, synergism does not result from a direct effect of divalent cations on C-kinase.
J. Endocr. (1987) 114, 11–16
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ABSTRACT
The mechanism of arachidonic acid (AA)-induced LH release was characterized using sheep pituitary cells in primary culture permeabilized with Staphylococcal α-toxin. In intact cells, exogenous AA evoked release of LH in a manner which was partially dependent on extracellular Ca2+. At similar concentrations, AA also caused cell permeabilization as monitored by efflux of [3H]2-deoxyglucose metabolites. In α-toxin-permeabilized cells where cytosolic Ca2+ was clamped at resting levels, AA retained its ability to cause LH release. Unlike the stimulation of exocytosis produced by Ca2+, phorbol ester or cyclic AMP, AA-evoked release was independent of ATP and was not inhibited by pretreatment with N-ethyl maleimide. These findings indicated that exogenous AA does not cause LH release by Ca2+ influx or mobilization or by activating protein kinase C. The results suggest that LH release induced by exogenous AA is probably due to its detergent-like properties, and does not represent true exocytosis.
Journal of Endocrinology (1992) 132, 77–82
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Abstract
In order to investigate the ontogeny of gonadal inhibin production in the male fetal sheep, testes were collected from male fetuses at days 70, 100, 130 and 140 of gestation (term=145 days). The expression and localization of inhibin α- and inhibin βA-subunit mRNA and protein were evaluated using in situ hybridization and immunocytochemistry. The expression of inhibin α-subunit mRNA was localized within the seminiferous cords of the developing fetal testis and progressively increased with gestational age. Immunostaining corresponding to immunoreactive inhibin α-subunit was detected in Sertoli cells within the seminiferous cords at days 100, 130 and 140 of gestation. In addition, immunostaining was detectable in a small proportion of Leydig cells. No expression of inhibin βA-subunit mRNA or immunoreactivity was detected in any testicular tissue at any stage of gestation. These data show that the Sertoli cells of the developing fetal sheep testis have the capacity to produce inhibin α-subunit by day 100 of gestation and that production increases during late gestation.
Journal of Endocrinology (1995) 145, 35–42
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Abstract
In pituitary gonadotrophs GnRH causes biphasic (spike and plateau) increases in cytosolic Ca2+ ([Ca2+]i) and gonadotrophin release. The spike phases reflect mobilization of stored Ca2+ and the plateau responses are attributed, in part, to Ca2+ influx via voltage-sensitive Ca2+ channels. In recent years, store-dependent Ca2+ influx (SDCI), in which depletion of the intracellular inositol 1,4,5-trisphosphate-mobilizable pool stimulates Ca2+ influx, has emerged as a major form of Ca2+ entry activated by phosphoinositidase C-coupled receptors in non-excitable cells. More recent evidence also indicates a role for SDCI in excitable cells. We have used dynamic video imaging of [Ca2+]i, in αT3–1 cells (a gonadotroph-derived cell line) and manipulation of the filling state of the GnRH-mobilizable Ca2+ pool to test the possible role of SDCI in GnRH action.
In Ca2+-containing medium, GnRH caused a biphasic increase in [Ca2+]i whereas in Ca2+-free medium only a transient increase occurred. The response to a second stimulation with GnRH in Ca2+-free medium was reduced by >95% (demonstrating that Ca2+ pool depletion had occurred) and was recovered after brief exposure to Ca2+-containing medium (which enables refilling of the pool). Ionomycin (a Ca2+ ionophore) and thapsigargin (which inhibits the Ca2+-sequestering ATPase of the endoplasmic reticulum) also transiently increased [Ca2+]i, in Ca2+-free medium and depleted the GnRH-mobilizable pool as indicated by greatly reduced subsequent responses to GnRH. Pool depletion also occurs on stimulation with GnRH in Ca2+-containing medium because addition of ionomycin and Ca2+-free medium during the plateau phase of the GnRH response caused only a reduction in [Ca2+]i rather than the transient increase seen without GnRH. To deplete intracellular Ca2+ pools, cells were pretreated in Ca2+-free medium with thapsigargin or GnRH and then, after extensive washing, returned to Ca2+-containing medium. Pretreatment with thapsigargin augmented the increase in [Ca2+]i seen on return to Ca2+-containing medium (to two- to threefold higher than that seen in control cells) indicating the activation of SDCI, whereas pool depletion by GnRH pretreatment had no such effect. To ensure maintained pool depletion after Ca2+ re-addition, similar studies were performed in which the thapsigargin and GnRH treatments were not washed off, but were retained through the period of return to Ca2+-containing medium. Return of GnRH-treated cells to Ca2+-containing medium caused an increase in [Ca2+]i which was inhibited by nicardipine, whereas the increase seen on return of thapsigargin-treated cells to Ca2+-containing medium was not reduced by nicardipine. The quench of fura-2 fluorescence by MnCl2 (used as a reporter of Ca2+ influx) was increased by GnRH and thapsigargin, indicating that both stimulate Ca2+ influx via Mn2+ permeant channels. The GnRH effect was abolished by nicardipine whereas that of thapsigargin was not. Finally, depletion of intracellular Ca2+ pools by pretreatment of superfused rat pituitary cells with GnRH or thapsigargin in Ca2+-free medium did not enhance LH release on return to Ca2+-containing medium. The results indicate that (a) thapsigargin stimulates SDCI in αT3–1 cells via nicardipine-insensitive Ca2+ channels, (b) in spite of the fact that GnRH depletes the hormone-mobilizable Ca2+ pool, it fails to stimulate SDCI, (c) GnRH stimulates Ca2+ entry predominantly via nicardipine-sensitive channels, a route not activated by SDCI and (d) in rat gonadotrophs, GnRH-stimulated LH release is not mediated by SDCI.
Journai of Endocrinology (1996) 149, 155–169