期刊
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
卷 16, 期 3, 页码 211-217出版社
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
DOI: 10.4196/kjpp.2012.16.3.211
关键词
Dorsal root ganglion neuron; Nitric oxide; Protein kinase G; Rat; TRPV1
资金
- Korea Research Foundation
- Korean government [KRF-2004-003-E00012]
Recent studies have demonstrated that nitric oxide (NO) activates transient receptor potential vanilloid subtype 1 (TRPV1) via S-nitrosylation of the channel protein. NO also modulates various cellular functions via activation of the soluble guanylyl cyclase (sGC)/protein kinase G (PKG) pathway and the direct modification of proteins. Thus, in the present study, we investigated whether NO could indirectly modulate the activity of TRPV1 via a cGMP/PKG-dependent pathway in cultured rat dorsal root ganglion (DRG) neurons. NO donors, sodium nitroprusside (SNP) and S-nitro-N-acetylpenicillamine (SNAP), decreased capsaicin-evoked currents (I-cap). NO scavengers, hemoglobin and 2-(4-carboxyphenyl)4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO), prevented the inhibitory effect of SNP on 1,. Membrane-permeable cGMP analogs, 8-bromoguanosine 3', 5'-cyclic monophosphate (8bromo-cGMP) and 8-(4chlorophenylthio)-guanosine 3',5'-cyclic monophosphate (8-pCPT-cGMP), and the guanylyl cyclase stimulator YC-1 mimicked the effect of SNP on I-cap. The PKG inhibitor KT5823 prevented the inhibition of I-cap by SNP. These results suggest that NO can downregulate the function of TRPV1 through activation of the cGMP/PKG pathway in peripheral sensory neurons.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据