We investigated using the mice role of
nitric oxide synthase (NOS) in the spinal dorsal horn in herpetic and postherpetic
pain, especially
allodynia, which was induced by transdermal inoculation of the hind paw with herpes simplex virus type-1 (HSV-1). The virus inoculation induced NOS2 expression in the lumbar dorsal horn of mice with herpetic
allodynia, but not postherpetic
allodynia. There were no substantial alternations in the expression level of NOS1 at the herpetic and postherpetic stages. Herpetic
allodynia was significantly inhibited by i.p. administration of the selective NOS2 inhibitor
S-methylisothiourea, but not the selective NOS1 inhibitor
7-nitroindazole. NOS2 expression was observed around HSV-1
antigen-immunoreactive cells. On the other hand, postherpetic
allodynia was significantly inhibited by i.p. administration of
7-nitroindazole, but not
S-methylisothiourea. The activity of reduced
nicotinamide adenine dinucleotide phosphate diaphorase, an index of NOS1 activity, significantly increased in the laminae I and II of the lumbar dorsal horn of mice with postherpetic
allodynia, but not mice without postherpetic
allodynia. The expression level of NOS1
mRNA in the dorsal root ganglia was similar between mice with and without postherpetic
allodynia. The results suggest that herpetic and postherpetic
allodynia is mediated by
nitric oxide in the dorsal horn and that NOS2 and NOS1 are responsible for herpetic and postherpetic
allodynia, respectively. It may be worth testing the effects of NOS2 and NOS1 inhibitors on herpetic
pain and
postherpetic neuralgia in human subjects, respectively.