Pharmacological and immunohistochemical characterization of a mouse model of acute herpetic pain

We have recently found that the infection with herpes simplex virus type-1 (HSV-1) of primary sensory neurons induces nociceptive hypersensitivity to noxious mechanical (hyperalgesia) and tactile stimulation (allodynia) in mi ce. In the present experiments, we determined the distribution of HSV-1 in the dorsal root ganglia and examined the effects of four analgesic agents o n hyperalgesia and allodynia. HSV-1 was inoculated on the unilateral shin. HSV-antigen-positive cells were detected in the L4 and L5 dorsal root gangl ia on days 5 and 7, but not day 3, post-inoculation. About 80% of the posit ive cells were small in size. Allodynia and hyperalgesia appeared on day 5 post-inoculation. Antinociceptive effects of analgesic agents were examined on day 6 post-inoculation. Morphine (1-5 mg/kg, subcutaneous) and gabapent in (10-100 mg/kg, peroral) dose-dependently inhibited both allodynia and hy peralgesia. Diclofenac (10-100 mg/kg, intraperitoneal) also produced antino ciceptive effects, but there was a ceiling for the effect on hyperalgesia. Amitriptyline (3, 10 mg/kg, subcutaneous) did not affect allodynia and hype ralgesia. The results suggest that mechanical allodynia and hyperalgesia ap peared when HSV-1 proliferated in the sensory neurons. This mouse model may be useful for studying the mechanisms of acute herpetic pain and anti-neur opathic pain agents.