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Title: Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons
Author: Zhang, Fang-Xiong ; Liu, Xing-Jun ; Gong, Li-Qin ; Yao, Jun-Ru ; Li, Kai-Cheng ; Li, Zi-Yan ; Lin, Li-Bo ; Lu, Ying-Jin ; Xiao, Hua-Sheng ; Bao, Lan ; Zhang, Xiao-Hui ; null(张 旭)
Source: JOURNAL OF NEUROSCIENCE
Issued Date: 2010
Volume: 30, Issue:32, Pages:10927-10938
Keyword: DORSAL-ROOT GANGLION ; DEPENDENT PROTEIN-KINASE ; RAT SPINAL-CORD ; GENE-RELATED PEPTIDE ; PERIPHERAL AXOTOMY ; GLUTAMATE RELEASE ; NEUROPEPTIDE-Y ; SUBSTANCE-P ; PRESYNAPTIC INHIBITION ; SOMATOSTATIN RECEPTORS
Subject: Neurosciences & Neurology
Corresponding Author: Zhang, X (reprint author), Chinese Acad Sci, Inst Neurosci, Shanghai Inst Biol Sci, 320 Yue Yang Rd, Shanghai 200031, Peoples R China,xu.zhang@ion.ac.cn
English Abstract: B-type natriuretic peptide (BNP) has been known to be secreted from cardiac myocytes and activate its receptor, natriuretic peptide receptor-A (NPR-A), to reduce ventricular fibrosis. However, the function of BNP/NPR-Apathway in the somatic sensory system has been unknown. In the present study, we report a novel function of BNP in pain modulation. Using microarray and immunoblot analyses, we found that BNP and NPR-A were expressed in the dorsal root ganglion (DRG) of rats and upregulated after intraplantar injection of complete Freund's adjuvant (CFA). Immunohistochemistry showed that BNP was expressed in calcitonin gene-related peptide (CGRP)containing small neurons and IB4 (isolectin B4)-positive neurons, whereas NPR-A was present in CGRP-containing neurons. Application of BNP reduced the firing frequency of small DRG neurons in the presence of glutamate through opening large-conductance Ca(2+)-activated K(+) channels (BK(Ca) channels). Furthermore, intrathecal injection of BNP yielded inhibitory effects on formalin-induced flinching behavior and CFA-induced thermal hyperalgesia in rats. Blockade of BNP signaling by BNP antibodies or cGMP-dependent protein kinase (PKG) inhibitor KT5823 [(9S, 10R, 12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester] impaired the recovery from CFA-induced thermal hyperalgesia. Thus, BNP negatively regulates nociceptive transmission through presynaptic receptor NPR-A, and activation of the BNP/NPR-A/PKG/BK(Ca) channel pathway in nociceptive afferent neurons could be a potential strategy for inflammatory pain therapy.
Indexed Type: sci
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1582
Appears in Collections:神经所(总)_期刊论文
感觉系统研究组_期刊论文

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Zhang, Fang-Xiong; Liu, Xing-Jun; Gong, Li-Qin; Yao, Jun-Ru; Li, Kai-Cheng; Li, Zi-Yan; Lin, Li-Bo; Lu, Ying-Jin; Xiao, Hua-Sheng; Bao, Lan; Zhang, Xiao-Hui; Zhang, Xu.Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons,JOURNAL OF NEUROSCIENCE,2010,30(32):10927-10938
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