• Ichiro Takasaki.
• Division of Molecular Genetics Research, Life Science Research Center, University of Toyama. takasaki@cts.u-toyama.ac.jp
• Yakugaku Zasshi. 2011 Feb 1;131(2):299-306.

AbstractHerpes 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.

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