IF 2.5 4区 医学 Q3 NEUROSCIENCES Neuroscience Letters Pub Date : 2024-12-12 DOI:10.1016/j.neulet.2024.138081
Akiko Sakata, Kinuyo Iwata, Kimihiko Nakao, Yuyu Kunimura, Shunji Suzuki, Hitoshi Ozawa, Hirotaka Ishii
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引用次数: 0

摘要

下丘脑弓状核(ARC)中的Kisspeptin和galanin样肽(GALP)神经元参与了促性腺激素释放激素(GnRH)神经元介导的脉动性黄体生成素(LH)分泌。扎克脂肪大鼠(Zucker fatty,ZF)显示瘦素受体基因异常,脉冲式促黄体生成素(LH)分泌受到抑制。据报道,ZF大鼠的下丘脑GALP和kisspeptin表达量较低,给ZF大鼠注射GALP可诱导其释放LH。因此,我们进行了组织化学分析,以确定 GALP 诱导的 LH 释放是否由 ZF 大鼠的吻肽素神经元介导。在中心注射 GALP 或载体之前,所有 ZF 大鼠均切除卵巢并皮下植入雌二醇管。注射 GALP 可增加血浆 LH 浓度。然而,在 Kiss1 细胞数量和 Fos 阳性 Kiss1 细胞比例方面未观察到明显差异。给药 GALP 后,c-Fos 阳性的 GnRH 神经元数量明显增加。我们的研究结果表明,下丘脑GALP神经元通过激活GnRH神经元促进LH释放,而不激活ARC中的kisspeptin神经元。
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Effect of galanin-like peptide on hypothalamic kisspeptin expression in female Zucker fatty rats.

Kisspeptin and galanin-like peptide (GALP) neurons in the hypothalamic arcuate nucleus (ARC) are involved in gonadotropin-releasing hormone (GnRH) neuron-mediated pulsatile luteinizing hormone (LH) secretion. Zucker fatty (ZF) rats display a leptin receptor gene abnormality and suppressed pulsatile LH secretion. ZF rats reportedly exhibit low hypothalamic GALP and kisspeptin expression, and GALP administration induces LH release in ZF rats. Therefore, we performed a histochemical analysis to determine whether GALP-induced LH release is mediated by kisspeptin neurons in ZF rats. All ZF rats were ovariectomized and subcutaneously implanted with an estradiol tube before the central injection of GALP or vehicle. GALP administration increased the plasma LH concentration. However, no significant difference was observed in the number of Kiss1 cells and the proportion of Fos-positive Kiss1 cells. The number of c-Fos-positive GnRH neurons significantly increased after GALP administration. Our results suggest that hypothalamic GALP neurons promote LH release by activating GnRH neurons without the activation of kisspeptin neurons in the ARC.

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来源期刊
Neuroscience Letters
Neuroscience Letters 医学-神经科学
CiteScore
5.20
自引率
0.00%
发文量
408
审稿时长
50 days
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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