Fan P
Laboratory of Molecular and Cellular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland 20892.
Mol Pharmacol. 1995 Mar;47(3):491-5.
The effect of morphine on the ion current mediated by 5-hydroxytryptamine (5-HT3) receptors was investigated in rat nodose ganglion neurons and in Xenopus oocytes expressing the cloned 5-HT3 receptor. Morphine reversibly inhibited the 5-HT-induced current and shifted the 5-HT concentration-response curve to the right in a parallel fashion, without reducing the maximal 5-HT response. IC50 values for morphine were 0.3 microM in nodose neurons and 0.32 microM in oocytes. The apparent Kd of morphine in nodose neurons was 0.903 microM. This effect of morphine was immediate not dependent on membrane potential, and not prevented by the opioid receptor antagonists naltrexone and beta-chlornaltrexamine. It is concluded that opioid receptors were not involved in the present study and that morphine acted at the agonist recognition site located on the 5-HT3 receptor.
在大鼠结状神经节神经元和表达克隆的5-羟色胺（5-HT3）受体的非洲爪蟾卵母细胞中，研究了吗啡对由5-羟色胺（5-HT3）受体介导的离子电流的影响。吗啡可逆性抑制5-羟色胺诱导的电流，并使5-羟色胺浓度-反应曲线平行右移，而不降低最大5-羟色胺反应。吗啡在结状神经元中的IC50值为0.3微摩尔，在卵母细胞中为0.32微摩尔。吗啡在结状神经元中的表观解离常数（Kd）为0.903微摩尔。吗啡的这种作用是即时的，不依赖于膜电位，且不受阿片受体拮抗剂纳曲酮和β-氯纳曲酮的阻断。得出的结论是，本研究中未涉及阿片受体，且吗啡作用于位于5-HT3受体上的激动剂识别位点。
