Quock R M, Walczak C K, Henry R J, Chen D C
Department of Basic Sciences, Marquette University School of Dentistry, Milwaukee, WI 53233.
Pharmacol Res. 1990 May-Jun;22(3):351-7. doi: 10.1016/1043-6618(90)90733-t.
Nitrous oxide antinociception in rats was evaluated by the warm water tail withdrawal test following central pretreatment with blockers of various opioid receptor subtypes. The analgesic dose, 50% (AD50) value for nitrous oxide antinociception was significantly elevated by MR-2266 (which is relatively selective for kappa-opioid receptors) and increased to a lesser degree by ICI-174,864 (which is selective for delta-opioid receptors). However, pretreatment with beta-funaltrexamine (which is selective for mu-opioid receptors), even at extremely high doses, was ineffective in altering the AD50 for nitrous oxide antinociception. According to these findings, nitrous oxide antinociception, as evaluated in this paradigm, appears to be mediated by kappa- and possibly delta- but not mu-opioid receptors.
在大鼠中,通过温水甩尾试验评估一氧化二氮的抗伤害感受,试验前先对大鼠进行各种阿片受体亚型阻断剂的中枢预处理。MR - 2266(对κ-阿片受体具有相对选择性)显著提高了一氧化二氮抗伤害感受的镇痛剂量50%(AD50)值,ICI - 174,864(对δ-阿片受体具有选择性)使其升高程度较小。然而,β-氟纳曲酮(对μ-阿片受体具有选择性)预处理,即使在极高剂量下,也无法改变一氧化二氮抗伤害感受的AD50。根据这些发现,在此范式中评估的一氧化二氮抗伤害感受似乎由κ-阿片受体介导,可能还有δ-阿片受体,但不是由μ-阿片受体介导。