Wallenstein M C, Wang S C
Am J Physiol. 1979 May;236(5):R292-6. doi: 10.1152/ajpregu.1979.236.5.R292.
Neurons that increased their firing rate in response to light stimulation were recorded from the pretectal region and the anterior oculomotor nucleus of sedated immobilized cats while morphine (2 mg/kg iv) was administered. The dose produced mydriasis and an increase in spontaneous firing rate of all light-sensitive neurons recorded from the anterior oculomotor nucleus. This suggested that morphine did not produce mydriasis through inhibition of the third nerve. Phenoxybenzamine, iv or topically, antagonized the mydriasis, indicating a peripheral source of sympathetic input as the basis for morphine-induced mydriasis. Morphine (2 mg/kg iv), administered 1 h after adrenalectomy, produced miosis and increased the spontaneous firing rate of light-sensitive neurons recorded from the oculomotor nucleus. These observations suggest that, in the cat, although morphine activates the oculomotor neurons to produce miosis, the effect is masked by the morphine-induced release of catecholamines, mainly from the adrenal glands, which produced mydriasis.
在给镇静制动的猫静脉注射吗啡（2毫克/千克）时，记录了来自顶盖前区和动眼神经前核的对光刺激反应放电频率增加的神经元。该剂量导致瞳孔散大，并使从动眼神经前核记录到的所有光敏感神经元的自发放电频率增加。这表明吗啡并非通过抑制动眼神经来产生瞳孔散大。静脉注射或局部应用酚苄明可拮抗瞳孔散大，表明交感神经输入的外周来源是吗啡诱导瞳孔散大的基础。肾上腺切除术后1小时静脉注射吗啡（2毫克/千克），可产生瞳孔缩小，并增加从动眼神经核记录到的光敏感神经元的自发放电频率。这些观察结果表明，在猫中，尽管吗啡激活动眼神经神经元产生瞳孔缩小，但该效应被吗啡诱导的主要来自肾上腺的儿茶酚胺释放所掩盖，儿茶酚胺释放会产生瞳孔散大。
