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首页> 外文期刊>Endocrine. >Stimulation of delta subunit-containing GABAA receptor by DS1 increases GnRH receptor expression but reduces GnRH mRNA expression in GnRH-producing GT1-7 cells
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Stimulation of delta subunit-containing GABAA receptor by DS1 increases GnRH receptor expression but reduces GnRH mRNA expression in GnRH-producing GT1-7 cells

机译：DS1刺激含δ亚单位的GABAA受体的刺激增加了GnRH受体表达，但在GNRH产生的GT1-7细胞中降低了GnRH mRNA表达

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摘要

Acting via ionotropic GABA(A) receptors, the neurotransmitter c-aminobutyric acid (GABA) is an important modulator of gonadotropin-releasing hormone (GnRH) neurons. In the present study, we examined the effect of DS1, a GABA(A) alpha 4 beta 3 delta receptor agonist, on a strain of mouse hypothalamic immortalized GnRH neuronal cells, the GT1-7 cell line. DS1 increased the activities of serum-response element (SRE) and cAMP-response element (CRE) promoters, which reflect the activities of extracellular signal-regulated kinase and cAMP/protein kinase A (PKA) pathways, respectively. In G protein-coupled receptor 54 (GPR54)-overexpressing GT1-7 cells, both DS1 and kisspeptin-10 stimulated SRE promoter activity, and combined treatment with DS1 and kisspeptin further increased SRE promoter activity compared with DS1 or kisspeptin alone. Pituitary adenylate cyclase-activating polypeptide (PACAP) increased CRE promoter activity in PACAP type I receptor-overexpressing GT1-7 cells, with an effect similar to that of DS1 alone, and combined stimulation with PACAP and DS1 potentiated their individual effects. DS1 stimulated the transcriptional activity of GnRH receptor, and DS1 induced GnRH receptor mRNA and protein expression. PACAP-increased GnRH receptor expression was enhanced in the presence of DS1. However, DS1 significantly inhibited the basal expression of GnRH mRNA in GT1-7 cells. Our current observations suggest that DS1 exerts its stimulatory effect on the intracellular signal transduction system via GABA(A) alpha 4 beta 3 delta receptors in GnRH-producing neurons. Stimulation with DS1 increased the expression of GnRH receptor but decreased the basal expression of GnRH mRNA.
机译：通过InonoTropic Gaba（A）受体，神经递质C-氨基丁酸（GABA）是促性腺激素释放激素（GNRH）神经元的重要调节剂。在本研究中，我们研究了DS1，GABA（A）α4β3Delta受体激动剂的效果，在小鼠下丘脑永生化GnRH神经元细胞中，GT1-7细胞系。 DS1增加了血清响应元件（SRE）和营养响应元件（CRE）启动子的活性，其反映了细胞外信号调节激酶和阵营/蛋白激酶A（PKA）途径的活性。在G蛋白偶联受体54（GPR54）中，无曲1-7细胞，DS1和Kisspeptin-10刺激的SRE启动子活性，与单独的DS1或Kisspeptin相比，DS1和Kisspeptin的组合治疗进一步增加了SRE启动子活性。垂体腺苷酸环酶活化多肽（PACAP）增加了PACAP型I受体过表达GT1-7细胞中的CRE启动子活性，其单独的DS1与DS1的效果相似，并与PACAP和DS1的组合刺激强调其个体效果。 DS1刺激了GnRH受体的转录活性，DS1诱导的GNRH受体mRNA和蛋白质表达。在DS1存在下，加强了Pacap增加的GnRH受体表达。然而，DS1显着抑制GNRH mRNA在GT1-7细胞中的基础表达。我们目前的观察表明，DS1对通过GBA（A）α4β3δ3Δα受体施加对细胞内信号转导系统的刺激作用。用DS1刺激增加了GnRH受体的表达，但降低了GnRH mRNA的基础表达。

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