Takasaki Ichiro
Division of Molecular Genetics Research, Life Science Research Center, University of Toyama.
Yakugaku Zasshi. 2011 Feb;131(2):299-306. doi: 10.1248/yakushi.131.299.
Herpes zoster characterized by clustered vesicles and severe pain is caused by reactivation of varicella-zoster virus in the sensory ganglion in humans. In some herpes zoster patients, pain persists long after healing of the skin lesions, which is postherpetic neuralgia. Patients with postherpetic neuralgia report various types of pain. In addition, a large proportion describes "allodynia", which is a painful sensation elicited by normally innocuous light mechanical stimulation. Once established, postherpetic neuralgia is particularly difficult to treat, and is often resistant to conventional analgesics. The mechanisms that underlie the induction and maintenance of herpetic pain and postherpetic neuralgia remain unclear. Therefore we attempted to establish animal models of herpetic pain and postherpetic neuralgia. This review summarizes our findings regarding the development of mouse models of herpetic pain and postherpetic neuralgia, pharmacological characterization of mouse models, mechanisms of allodynia and risk factors for postherpetic neuralgia.
带状疱疹由人类感觉神经节中的水痘-带状疱疹病毒重新激活引起，其特征为成簇水疱和严重疼痛。在一些带状疱疹患者中，疼痛在皮肤损伤愈合后仍会持续很长时间，这就是带状疱疹后神经痛。带状疱疹后神经痛患者会报告各种类型的疼痛。此外，很大一部分患者描述有“痛觉过敏”，即由通常无害的轻机械刺激引发的疼痛感觉。一旦形成，带状疱疹后神经痛就特别难以治疗，并且常常对传统镇痛药有抗性。疱疹性疼痛和带状疱疹后神经痛的诱发和维持机制仍不清楚。因此，我们试图建立疱疹性疼痛和带状疱疹后神经痛的动物模型。这篇综述总结了我们在疱疹性疼痛和带状疱疹后神经痛小鼠模型的建立、小鼠模型的药理学特征、痛觉过敏机制以及带状疱疹后神经痛风险因素方面的研究结果。
