Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons

	Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons
	Zhang, FX; Liu, XJ; Gong, LQ; Yao, JR; Li, KC; Li, ZY; Lin, LB; Lu, YJ; Xiao, HS; Bao, L
刊名	JOURNAL OF NEUROSCIENCE
	2010
卷号	30 期号:32 页码:10927-10938
通讯作者	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
英文摘要	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.
学科主题	Neurosciences & Neurology
类目[WOS]	Neurosciences
关键词[WOS]	DORSAL-ROOT GANGLION ; DEPENDENT PROTEIN-KINASE ; RAT SPINAL-CORD ; GENE-RELATED PEPTIDE ; PERIPHERAL AXOTOMY ; GLUTAMATE RELEASE ; NEUROPEPTIDE-Y ; SUBSTANCE-P ; PRESYNAPTIC INHIBITION ; SOMATOSTATIN RECEPTORS
收录类别	SCI
语种	英语
WOS记录号	WOS:000280795900032
内容类型	期刊论文
版本	出版稿
源URL	[http://202.127.25.143/handle/331003/1095]
专题	上海生化细胞研究所_上海生科院生化细胞研究所
推荐引用方式 GB/T 7714	Zhang, FX,Liu, XJ,Gong, LQ,et al. Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons[J]. JOURNAL OF NEUROSCIENCE,2010,30(32):10927-10938.
APA	Zhang, FX.,Liu, XJ.,Gong, LQ.,Yao, JR.,Li, KC.,...&Zhang, X.(2010).Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons.JOURNAL OF NEUROSCIENCE,30(32),10927-10938.
MLA	Zhang, FX,et al."Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons".JOURNAL OF NEUROSCIENCE 30.32(2010):10927-10938.