Suh H W, Song D K, Choi S R, Chung K M, Kim Y H
Department of Pharmacology, College of Medicine, Hallym University, Chunchon, Kangwon-Do, South Korea.
Neuropeptides. 1996 Oct;30(5):479-84. doi: 10.1016/s0143-4179(96)90013-x.
The effect of nicotine administered supraspinally on antinociception induced by supraspinally administered opioids was examined in ICR mice. The intracerebroventricular (i.c.v.) injection of nicotine alone at doses from 1 to 12 micrograms produced only a minimal inhibition of the tail-flick response. Morphine (0.2 micrograms), beta-endorphin (0.1 microgram), D-Pen2.5-enkephalin (DPDPE; 0.5 microgram), trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohexyl] benzeocetamide (U50, 488H; 6 micrograms) caused only slight inhibition of the tail-flick response. Nicotine dose dependently enhanced inhibition of the tail-flick response induced by i.c.v. administered morphine (0.2 microgram) or beta-endorphin (0.1 microgram). The degree of enhancing effect of nicotine toward beta-endorphin-induced inhibition of the tail-flick response was greater than toward morphine-induced inhibition of the tail-flick response. However, i.c.v. administered nicotine at the same doses was not effective in enhancing the inhibition of the tail-flick response induced by DPDPE (0.5 microgram) or U50, 488H (6 micrograms) administered i.c.v. Our results suggest that stimulation of supraspinal nicotinic receptors may enhance antinociception induced by morphine (a mu-opioid receptor agonist) and beta-endorphin (an epsilon-opioid receptor agonist) administered supraspinally. However, the activation of nicotinic receptors at supraspinal sites may not be involved in enhancing the antinociception induced by DPDPE (a delta-opioid receptor agonist) or U50, 488H (a kappa-opioid receptor agonist) administered supraspinally.
在ICR小鼠中研究了脊髓以上给予尼古丁对脊髓以上给予阿片类药物诱导的抗伤害感受的影响。脑室内（i.c.v.）注射剂量为1至12微克的尼古丁仅产生对甩尾反应的最小抑制。吗啡（0.2微克）、β-内啡肽（0.1微克）、D- Pen2.5-脑啡肽（DPDPE；0.5微克）、反式-3,4-二氯-N-甲基-N-[2-(1-吡咯烷基)环己基]苯乙酰胺（U50,488H；6微克）仅引起对甩尾反应的轻微抑制。尼古丁剂量依赖性地增强了脑室内给予吗啡（0.2微克）或β-内啡肽（0.1微克）诱导的甩尾反应抑制。尼古丁对β-内啡肽诱导的甩尾反应抑制的增强作用程度大于对吗啡诱导的甩尾反应抑制的增强作用程度。然而，相同剂量的脑室内给予尼古丁对脑室内给予DPDPE（0.5微克）或U50,488H（6微克）诱导的甩尾反应抑制增强无效。我们的结果表明，脊髓以上烟碱受体的刺激可能增强脊髓以上给予吗啡（μ-阿片受体激动剂）和β-内啡肽（ε-阿片受体激动剂）诱导的抗伤害感受。然而，脊髓以上部位烟碱受体的激活可能不参与增强脊髓以上给予DPDPE（δ-阿片受体激动剂）或U50,488H（κ-阿片受体激动剂）诱导的抗伤害感受。
