The role of nitric oxide in nociception

被引:6
作者
Luo Z.D. [1 ]
Cizkova D. [2 ]
机构
[1] Department of Anesthesiology, University of California, San Diego, 92093-0818, La Jolla, CA
[2] Institute of Neurobiology, Slovak Academy of Sciences, 040 01, Soltesovej 6, Kosice
来源
Current Review of Pain | 2000年 / 4卷 / 6期
基金
美国国家卫生研究院;
关键词
Nitric Oxide; Dorsal Root Ganglion; Neuropathic Pain; Capsaicin; Dorsal Horn;
D O I
10.1007/s11916-000-0070-y
中图分类号
学科分类号
摘要
Pharmacologic, electrophysiologic, and immunohistochemical studies have suggested a role of nitric oxide (NO) in nociception processing. Recent studies have indicated that NO may modulate spinal and sensory neuron excitability through multiple mechanisms that may underlie its distinctive roles in different pain states. Differential regulation of a family of NO-producing enzymes, NO synthases, contributes mainly to the complexity underlying the role of NO in nociception. This review summarizes the latest advances in our understanding of the contribution of NO to pain transduction. Possible cellular mechanisms regarding the connection between NO production and the abnormal sensation derived from different stimuli and pathologic conditions are discussed.
引用
收藏
页码:459 / 466
页数:7
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[1]  
Geller DA, Billiar TR, Molecular biology of nitric oxide synthases, Cancer Metastasis Rev, 17, pp. 7-23, (1998)
[2]  
Wang Y, Marsden PA, Nitric oxide synthases: gene structure and regulation, Adv Pharmacol, 34, pp. 71-90, (1995)
[3]  
Lewin MR, Walters ET, Cyclic GMP pathway is critical for inducing long-term sensitization of nociceptive sensory neurons, Nat Neurosci, 2, pp. 18-23, (1999)
[4]  
Lin Q, Palecek J, Paleckova V, Nitric oxide mediates the central sensitization of primate spinothalamic tract neurons, J Neurophysiol, 81, pp. 1075-85, (1999)
[5]  
Lin Q, Wu J, Peng YB, Nitric oxide-mediated spinal disinhibition contributes to the sensitization of primate spinothalamic tract neurons, J Neurophysiol, 81, pp. 1086-1094, (1999)
[6]  
Ferreira J, Santos AR, Calixto JB, The role of systemic, spinal and supraspinal L-arginine-nitric oxide-cGMP pathway in thermal hyperalgesia caused by intrathecal injection of glutamate in mice, Neuropharmacology, 38, pp. 835-842, (1999)
[7]  
Inoue T, Mashimo T, Shibata M, Rapid development of nitric oxide-induced hyperalgesia depends on an alternate to the cGMP-mediated pathway in the rat neuropathic pain model, Brain Res, 792, pp. 263-270, (1998)
[8]  
Ichinose F, Mi WD, Miyazaki M, Lack of correlation between the reduction of sevoflurane MAC and the cerebellar cyclic GMP concentrations in mice treated with 7-nitroindazole, Anesthesiology, 89, pp. 143-148, (1998)
[9]  
Ashina M, Lassen LH, Bendtsen L, Effect of inhibition of nitric oxide synthase on chronic tension-type headache: a randomised crossover trial, Lancet, 353, pp. 287-289, (1999)
[10]  
Kimura S, Watanabe K, Yajiri Y, Cerebrospinal fluid nitric oxide metabolites in painful diseases, Neuroreport, 10, pp. 275-279, (1999)