Chen Y, Wang A J, Ma Y L
Research Center of Experimental Medicine, Tongji Medical University, Wuhan, China.
Zhongguo Yao Li Xue Bao. 1993 Sep;14(5):417-20.
Intracellular recordings were performed on 35 neurons from 35 isolated toad spinal ganglia (SG) and the extracellular free calcium ion activities were measured in another 26 isolated toad SG by Ca(2+)-selective microelectrodes. The effects of morphine on the sensitivities of alpha-adrenoceptors were observed. It was found that depolarization of membrane potential induced by norepinephrine (NE 10-100 mumol.L-1) or alpha 1-adrenoceptor agonist phenylephrine (100 mumol.L-1) was depressed by morphine (27 mumol.L-1). Superfusing SG with opioid receptor antagonist naloxone (100 mumol.L-1) blocked the depressing effect of morphine on NE-induced depolarization. The depressing effect of morphine on NE-induced depolarization was not affected by superfusing SG with alpha 2-adrenoceptor antagonist yohimbine (5 mumol.L-1). NE (100 mumol.L-1) reduced the extracellular free calcium ion activity while morphine (27 mumol.L-1) increased the extracellular free calcium ion activity in SG. It is concluded that morphine down-regulates the sensitivity of alpha 1-adrenoceptor in toad SG neuron mediated by opioid receptor and the variation in Ca2+ activity may be involved in this effect.
对35个分离的蟾蜍脊髓神经节（SG）中的35个神经元进行了细胞内记录，并用钙离子选择性微电极在另外26个分离的蟾蜍SG中测量了细胞外游离钙离子活性。观察了吗啡对α-肾上腺素能受体敏感性的影响。发现去甲肾上腺素（NE 10 - 100 μmol·L-1）或α1-肾上腺素能受体激动剂去氧肾上腺素（100 μmol·L-1）诱导的膜电位去极化被吗啡（27 μmol·L-1）抑制。用阿片受体拮抗剂纳洛酮（100 μmol·L-1）灌注SG可阻断吗啡对NE诱导的去极化的抑制作用。用α2-肾上腺素能受体拮抗剂育亨宾（5 μmol·L-1）灌注SG，吗啡对NE诱导的去极化的抑制作用不受影响。NE（100 μmol·L-1）降低了SG中的细胞外游离钙离子活性，而吗啡（27 μmol·L-1）增加了SG中的细胞外游离钙离子活性。结论是，吗啡通过阿片受体下调蟾蜍SG神经元中α1-肾上腺素能受体的敏感性，Ca2+活性的变化可能参与了这一作用。
