Narita M, Takamori K, Kawashima N, Funada M, Kamei J, Suzuki T, Misawa M, Nagase H
Department of Pharmacology, School of Pharmacy, Hoshi University, Tokyo, Japan.
Psychopharmacology (Berl). 1993;113(1):11-4. doi: 10.1007/BF02244326.
ICV cromakalim, a K+ channel opener, produced antinociception. This effect was completely antagonized by ICV glibenclamide, a selective adenosine triphosphate-sensitive K+ channel (KATP channel) blocker. Furthermore, direct opening of central KATP channels by ICV cromakalim increased the spinal noradrenaline (NA) turnover. On the other hand, the antinociception induced by ICV morphine (mu opioid agonist), but not ICV U-50,488H (kappa opioid agonist) was markedly potentiated by cromakalim. These findings suggest that the opening of central KATP channels may elicit the antinociceptive effect and activate the descending NAergic pathway, and central KATP channels play an important role as a modulator of the antinociception induced by mu agonists but not kappa agonists.
脑室注射（ICV）克罗卡林（一种钾通道开放剂）可产生抗伤害感受作用。该效应被脑室注射格列本脲（一种选择性三磷酸腺苷敏感性钾通道（KATP通道）阻滞剂）完全拮抗。此外，脑室注射克罗卡林直接开放中枢KATP通道可增加脊髓去甲肾上腺素（NA）的周转。另一方面，脑室注射吗啡（μ阿片受体激动剂）诱导的抗伤害感受作用，但不是脑室注射U - 50,488H（κ阿片受体激动剂）诱导的抗伤害感受作用，被克罗卡林显著增强。这些发现表明，中枢KATP通道的开放可能引发抗伤害感受作用并激活下行去甲肾上腺素能通路，并且中枢KATP通道作为μ受体激动剂而非κ受体激动剂诱导的抗伤害感受的调节剂发挥重要作用。
