Pancreatic polypeptide and peptide YY3-36 induce Ca2+ signaling in nodose ganglion neurons

Pancreatic polypeptide and peptide YY3-36 induce Ca2+ signaling in nodose ganglion neurons
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DOI:
10.1016/j.npep.2012.07.006
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发表时间:
2013-02-01
期刊:
影响因子:
2.9
通讯作者:
Yada, Toshihiko
Yada, Toshihiko
中科院分区:
医学3区
文献类型:
--
作者:
Iwasaki, Yusaku;Kakei, Masafumi;Yada, Toshihiko

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外周注射胰多肽(PP)和肽YY 3 -36(PYY 3 -36)(响应于进食而释放的激素)减少食物摄入,其中效力的等级顺序为PP > PYY 3 -36。这些厌食作用在腹部迷走神经切断的大鼠中被消除,表明PP和PYY 3 -36通过迷走神经传入神经诱导厌食。然而,PP和PYY 3 -36是否直接作用于迷走神经传入神经元尚不清楚。在这项研究中,我们研究了PP和PYY 3 -36对小鼠迷走神经传入神经的结状神经节神经元的胞浆Ca 2+浓度([Ca 2 +](i))的影响。在10(-11)M时,PP而不是PYY 3 -36募集显著的结状神经节神经元群体进入[Ca 2 +](i)增加。10(-11)至10(-7)M的PP和10(-10)至10(-7)M的PYY 3 -36以浓度依赖性方式增加[Ca 2 +](i)。在10(-10)和10(-8)M的次最大至最大浓度下,PP使结状神经节神经元中的[Ca 2 +](i)增加,其数量约为PYY 3 -36的两倍。此外,大多数PP反应神经元也表现出[Ca 2 +](i)对胆囊收缩素-8的反应,胆囊收缩素-8是一种已知通过激活结状神经节神经元诱导饱腹感的激素。结果表明,PP和PYY 3 -36直接激活结状神经节神经元,并表明PP对胆囊收缩素-8反应的结状神经节神经元的显着影响可能与摄食调节有关。(C)2012爱思唯尔有限公司保留所有权利。
Peripheral injection of pancreatic polypeptide (PP) and peptide YY3-36 (PYY3-36), the hormones released in response to meals, reduce food intake, in which the rank order of the potency is PP > PYY3-36. These anorectic effects are abolished in abdominal vagotomized rats, suggesting that PP and PYY3-36 induce anorexia via vagal afferent nerves. However, it is not clear whether PP and PYY3-36 directly act on vagal afferent neurons. In this study, we examined the effects of PP and PYY3-36 on cytosolic Ca2+ concentration ([Ca2+](i)) in isolated nodose ganglion neurons of the mouse vagal afferent nerves. At 10(-11) M, PP but not PYY3-36 recruited a significant population of nodose ganglion neurons into [Ca2+](i) increases. PP at 10(-11) to 10(-7) and PYY3-36 at 10(-10) to 10(-7) M increased [Ca2+](i) in a concentration-dependent manner. At submaximal to maximal concentrations of 10(-10) and 10(-8) M, PP increased [Ca2+](i) in approximately twice greater population of nodose ganglion neurons than PYY3-36. Furthermore, the majority of PP-responsive neurons also exhibited [Ca2+](i) responses to cholecystokinin-8, a hormone known to induce satiety through activating nodose ganglion neurons. The results demonstrate that PP and PYY3-36 directly activate nodose ganglion neurons and suggest that the marked effect of PP on cholecystokinin-8-responsive nodose ganglion neurons could be linked to the regulation of feeding. (C) 2012 Elsevier Ltd. All rights reserved.