Antinociceptive effects of Kami-kihi-to in mice

Abstract

Oral administration of Kami-kihi-to (KMK) dose-dependently inhibited the response to acetic acid-induced writhing in mice. The KMK-induced antinociceptive action was reduced by pretreatment with yohimbine, an α2- adrenergic antagonist, or cyproheptadine, a serotonergic antagonist, but not naloxone, an opiate antagonist. The antinociceptive action of KMK was clearly reduced by pretreatment with α-methyl-DL-p-tyrosine, reserpine or p- chlorophenylalanine or by simultaneous treatment with diethyldithiocarbamate, all of which are monoamine synthetic inhibitors or monoamine depletors. After spinal transection, the antinociceptive effect of KMK was markedly reduced. These findings suggest that the antinociceptive action of KMK may be related to pain inhibitory systems such as the serotonergic and noradrenergic systems at the supraspinal level.