Role of pituitary adenylate cyclase-activating polypeptide in modulating hypothalamic-pituitary system.
Role of pituitary adenylate cyclase-activating polypeptide in modulating hypothalamic-pituitary system.
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DOI：
10.1002/rmb2.12094
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发表时间：
2018-07
影响因子：
3.4
通讯作者：
Kyo S
中科院分区：
文献类型：
--
作者：
Oride A;Kanasaki H;Kyo S
垂体腺苷酸环化酶激活多肽（垂体腺苷酸环化酶激活多肽，PACAP）是一种从绵羊下丘脑中分离和鉴定出来的多功能肽，其作用和机制已经在许多研究中得到阐明。PACAP及其受体不仅在下丘脑中广泛表达，而且在周围器官中也广泛表达。本文对PACAP在下丘脑-垂体系统中的作用的研究进行了综述，包括作者的研究。在垂体促性腺激素中，PACAP增加促性腺激素α‐、促黄体生成素β‐和促卵泡激素β‐亚基的表达以及促性腺激素释放激素（GnRH）受体及其自身受体PAC1R的表达。此外，在促性腺激素中，低频GnRH脉冲比高频GnRH脉冲更能增加PACAP和PAC1R的表达。PACAP刺激泌乳素的合成和分泌，增加乳养菌的PAC1R。在下丘脑，PACAP增加GnRH受体的表达，尽管它不能增加GnRH产生神经元中GnRH的表达。PACAP不仅直接作用于每个激素产生细胞，它可能通过自身受体或其他激素受体的表达来调节激素合成。
Pituitary adenylate cyclase‐activating polypeptide (PACAP) is a multifunctional peptide that is isolated and identified from the ovine hypothalamus, whose effects and mechanisms have been elucidated in numerous studies. The PACAP and its receptor are widely expressed, not only in the hypothalamus but also in peripheral organs. The studies on the role of PACAP in the hypothalamic‐pituitary system, including those by the authors, were summarized. In the pituitary gonadotrophs, PACAP increases the gonadotrophin α‐, luteinizing hormoneβ‐, and follicle‐stimulating hormone β‐subunit expression and the expression of gonadotropin‐releasing hormone (GnRH) receptor and its own receptor, PAC1R. Moreover, a low‐frequency GnRH pulse increases the expression of PACAP and PAC1R more than a high‐frequency GnRH pulse in the gonadotrophs. The PACAP stimulates prolactin synthesis and secretion and increases PAC1R in the lactotrophs. In the hypothalamus, PACAP increases the expression of the GnRH receptors, although it is unable to increase the expression of GnRH in the GnRH‐producing neurons. The PACAP not only acts directly in each hormone‐producing cell, it possibly might regulate hormone synthesis via the expression of its own receptors or those of other hormones.
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影响因子：
56.9
作者：
BELCHETZ, PE;PLANT, TM;KNOBIL, E
通讯作者：
KNOBIL, E
影响因子：
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通讯作者：
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3.3
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作者：
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通讯作者：
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