Neuropeptide FF and FMRFamide potentiate acid-evoked currents from sensory neurons and proton-gated DEG/ENaC channels
Neuropeptide FF and FMRFamide potentiate acid-evoked currents from sensory neurons and proton-gated DEG/ENaC channels
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DOI：
10.1016/s0896-6273(00)81144-7
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发表时间：
2000-04-01
期刊：
影响因子：
16.2
通讯作者：
Welsh, MJ
中科院分区：
文献类型：
--
作者：
Askwith, CC;Cheng, C;Welsh, MJ
酸中毒与炎症和缺血有关，并激活感觉神经元中的阳离子通道。炎症还诱导调节疼痛的FMRFamide样神经肽的表达。我们发现神经肽FF（Phe-Leu-Phe-G In-Pro-Gln-Arg-Phe amide）和FMRFamide（Phe-Met-Arg-Phe amide）本身不产生电流，但增强培养的感觉神经元和异源表达的ASIC和DRASIC通道的H+门控电流。在酸化过程中，神经肽减缓了失活并诱导了持续电流。这些效应是特异性的;不同的通道对各种肽表现出不同的反应。这些结果表明，酸敏感离子通道可能整合多种细胞外信号，以修改感官知觉。
Acidosis is associated with inflammation and ischemia and activates cation channels in sensory neurons. Inflammation also induces expression of FMRFamide-like neuropeptides, which modulate pain. We found that neuropeptide FF (Phe-Leu-Phe-G In-Pro-Gln-Arg-Phe amide) and FMRFamide (Phe-Met-Arg-Phe amide) generated no current on their own but potentiated H+-gated currents from cultured sensory neurons and heterologously expressed ASIC and DRASIC channels. The neuropeptides slowed inactivation and induced sustained currents during acidification. The effects were specific; different channels showed distinct responses to the various peptides. These results suggest that acid-sensing ion channels may integrate multiple extracellular signals to modify sensory perception.