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首页> 外文期刊>Life sciences >THE CATECHOLAMINERGIC STIMULATION OF GONADOTROPIN-RELEASING HORMONE RELEASE BY GT(1-1) CELLS DOES NOT INVOLVE PHOSPHOINOSITIDE HYDROLYSIS
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THE CATECHOLAMINERGIC STIMULATION OF GONADOTROPIN-RELEASING HORMONE RELEASE BY GT(1-1) CELLS DOES NOT INVOLVE PHOSPHOINOSITIDE HYDROLYSIS

机译：GT（1-1）细胞对促性腺激素释放激素的释放进行的泛化学刺激不参与磷脂酰肌醇的水解

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Gonadotropin-releasing hormone (GnRH) secretion is modulated by a large number of neuromediators, among which catecholamines play a central cole. Previous results have shown that both dopamine (DA) and norepinephrine (NE) stimulate GnRH secretion in GT(1) neuronal cell lines. These stimulatory effects appear to involve D-1-dopaminergic and beta(1)-adrenergic receptors positively coupled to adenylate cyclase. However, in spite of a similar efficacy of these catecholamines to stimulate GnRH secretion, DA is two-fold more efficacious than NE to stimulate the formation of cyclic AMP. This rises the possibility that other signaling pathways and other receptor subtypes could be involved in the catecholaminergic stimulation of GnRH release. Since the signaling pathway triggered by phosphoinositide hydrolysis is a potent stimulator of GnRH secretion and appears to mediate the releasing actions of neuromediators such as histamine and endothelin, we investigated if this signaling pathway was also involved in the catecholaminergic stimulation of GnRH release in GT(1) cells. Both DA and NE stimulated inositol phosphates production in GT(1-1) cells with a very low potency and long latency with respect to GnRH secretion. Inositol phosphates production was stimulated by DA and NE only at a concentration of 100 mu M, i.e. two to three orders of magnitude higher than the effective concentrations to maximally stimulate GnRH secretion. The effects of both catecholamines do not appear to be secondary to the stimulation of cyclic AMP production, since treatment of GT(1-1) cells with forskolin did not affect inositol phosphates production. The effects of DA and NE on inositol phosphates production were blocked by specific antagonists such as SCH 23390, spiroperidol and phentolamine. However, specific dopaminergic agonists such as SKF-38393 and bromocriptine, or adrenergic agonists such as clonidine, methoxamine and isoproterenol were not capable of stimulating inositol phosphates production. Thus, due to the low potency and apparent non-specificity of these effects, we conclude that inositol phosphates production is not involved in the catecholaminergic stimulation of GnRH release. [References: 28]
机译：促性腺激素释放激素（GnRH）的分泌受到大量神经介质的调节，其中儿茶酚胺发挥核心作用。先前的结果表明，多巴胺（DA）和去甲肾上腺素（NE）均会刺激GT（1）神经元细胞系中的GnRH分泌。这些刺激作用似乎涉及积极地耦合到腺苷酸环化酶的D-1-多巴胺能和β（1）-肾上腺素能受体。然而，尽管这些儿茶酚胺刺激GnRH分泌的功效相似，但DA刺激NE形成环AMP的功效比NE高两倍。这就增加了其他信号途径和其他受体亚型可能参与GnRH释放的儿茶酚胺能刺激的可能性。由于磷酸肌醇水解触发的信号通路是GnRH分泌的有效刺激物，并且似乎介导组胺和内皮素等神经介质的释放作用，因此我们研究了该信号通路是否也参与了GT中GnRH释放的儿茶酚胺能刺激（1 ） 细胞。 DA和NE都以极低的效力和相对于GnRH分泌的长潜伏期刺激了GT（1-1）细胞中肌醇磷酸的产生。仅在100μM的浓度下，DA和NE刺激肌醇磷酸盐的产生，即比最大刺激GnRH分泌的有效浓度高2至3个数量级。两种儿茶酚胺的作用似乎都不是刺激环AMP产生的，因为用福司可林处理GT（1-1）细胞不会影响肌醇磷酸盐的产生。 DA和NE对肌醇磷酸酯生产的影响被特定的拮抗剂（例如SCH 23390，螺哌啶醇和酚妥拉明）阻断。但是，特定的多巴胺能激动剂（例如SKF-38393和溴隐亭）或肾上腺素能激动剂（例如可乐定，甲氧胺和异丙肾上腺素）不能刺激肌醇磷酸盐的产生。因此，由于这些作用的低效性和明显的非特异性，我们得出结论，肌醇磷酸酯的生产不参与GnRH释放的儿茶酚胺能刺激。 [参考：28]

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