Meldrum B S, Menini C, Stutzmann J M, Naquet R
Brain Res. 1979 Jul 13;170(2):333-48. doi: 10.1016/0006-8993(79)90111-2.
The effects of intracerebroventricular (i.c.v.) or systemic injections of Met- or Leu-enkephalin, beta-endorphin, FK 33.824 (D-Ala2, MePhe4, Met(O5)-ol-enkephalin) and of morphine and naloxone have been studied in baboons, Papio papio, which spontaneously show photically induced epileptic responses. Animals were chronically implanted with epidural or deep recording electrodes and a cannula in one lateral ventricle, and tested whilst seated in a primate chair. In some animals the natural syndrome was enhanced by the prior administration of DL-allylglycine, 100--200 mg/kg, i.v. Met- or Leu-enkephalin, 1--10 mg, i.c.v., did not lead to any manifest focal or generalized seizure discharges. Nor did it lead to any consistent enhancement or reduction of photically induced myoclonic responses (as tested 5--10 min after injection). beta-Endorphin, 0.1--0.5 mg, i.c.v., did not enhance or impair photically induced myoclonic responses. FK 33.824, 0.1--0.5 mg, i.c.v., depressed respiration and slowed EEG background rhythms for 9--15 h. This was associated with a loss of myoclonic responses to photic stimulation. These effects were reversed for 20--40 min following the injection of naloxone, 1 mg/kg i.m. A depression of respiration and a slowing of EEG rhythms was seen beginning 5--20 min after FK 33.824, 2 or 4 mg/kg, i.v. The higher dose also abolished photically induced myoclonic responses. Naloxone, 1 mg/kg, definitively reversed these effects. Morphine, 5--10 mg i.c.v., tended to increase the latency to onset of generalized myoclonus during photic stimulation. Myoclonic responses were delayed or diminished after morphine, 5 mg/kg, i.m. Naloxone, 1--2 mg/kg i.m., reversed this effect. Naloxone, 0.2--5.0 mg/kg i.m., alone, did not significantly modify photically induced myoclonus, either in animals of low or high initial responsiveness, or in those pretreated with allylglycine.
在自发出现光诱导癫痫反应的狒狒(豚尾狒狒)中,研究了脑室内(i.c.v.)或全身注射甲硫氨酸脑啡肽或亮氨酸脑啡肽、β-内啡肽、FK 33.824(D-丙氨酸2,甲基苯丙氨酸4,甲硫氨酸(氧5)-脑啡肽)以及吗啡和纳洛酮的作用。动物被长期植入硬膜外或深部记录电极以及一侧脑室的套管,并在坐在灵长类动物椅上时进行测试。在一些动物中,通过静脉注射100 - 200 mg/kg的DL-烯丙基甘氨酸预先增强自然综合征。脑室内注射1 - 10 mg的甲硫氨酸脑啡肽或亮氨酸脑啡肽不会导致任何明显的局灶性或全身性癫痫放电。也不会导致光诱导的肌阵挛反应有任何持续的增强或减弱(在注射后5 - 10分钟测试)。脑室内注射0.1 - 0.5 mg的β-内啡肽不会增强或损害光诱导的肌阵挛反应。脑室内注射0.1 - 0.5 mg的FK 33.824会使呼吸抑制并使脑电图背景节律减慢9 - 15小时。这与对光刺激的肌阵挛反应丧失有关。在肌肉注射1 mg/kg纳洛酮后20 - 40分钟,这些作用被逆转。静脉注射2或4 mg/kg的FK 33.824后5 - 20分钟开始出现呼吸抑制和脑电图节律减慢。较高剂量也消除了光诱导的肌阵挛反应。1 mg/kg的纳洛酮最终逆转了这些作用。脑室内注射5 - 10 mg的吗啡往往会增加光刺激期间全身性肌阵挛发作的潜伏期。肌肉注射5 mg/kg的吗啡后,肌阵挛反应延迟或减弱。肌肉注射1 - 2 mg/kg的纳洛酮可逆转此作用。单独肌肉注射0.2 - 5.0 mg/kg的纳洛酮,无论是在初始反应性低或高的动物中,还是在预先用烯丙基甘氨酸处理的动物中,都不会显著改变光诱导的肌阵挛。