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- Atsushi Sasaki, Ichiro Takasaki, Tsugunobu Andoh, Kimiyasu Shiraki, Hiroshi Takeshima, Hiroki Takahata, and Yasushi Kuraishi.
- Department of aApplied Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyamai, Japan.
- Neuroreport. 2008 Jan 8;19(1):83-6.
AbstractUsing nociceptin-receptor-deficient mice, we studied the participation of nociceptin in herpetic and postherpetic allodynia in mice. Although nociceptin-receptor deficiency did not affect the development of skin lesions and herpetic allodynia, it prevented postherpetic allodynia. Messenger ribonucleic acid (mRNA) of pronociceptin increased in the dorsal horn of lumbar enlargement on day 6, but not on day 40, after inoculation. No changes were observed in the mRNA of the nociceptin receptor. Inhibition of herpetic allodynia by repeated oral administration of gabapentin (100 mg/kg) alleviated the overexpression of mRNA of pronociceptin, as well as the severity of postherpetic allodynia. These results suggest that the spinal nociceptin system is involved in the transitional process from herpetic allodynia to postherpetic allodynia.
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