Holaday J W, Tortella F C, Meyerhoff J L, Belenky G L, Hitzemann R J
Ann N Y Acad Sci. 1986;467:249-55. doi: 10.1111/j.1749-6632.1986.tb14633.x.
From the evidence reviewed above, there is little doubt that ECS activates endogenous opioids and modifies their receptors. Thus, this form of SIA is accompanied by many other corollaries of opioid-like actions, including catalepsy, similar EEG patterns, common autonomic effects, and increases in opioid receptor binding sites. Investigations have further indicated that the amnestic effects of ECS can also be attenuated by naloxone, and that pituitary-derived opioids may play an important role as a predominant source of opioids that contribute to these opioid-like effects following ECS. It is hoped that these many attempts to correlate SIA with other behavioral and physiological endpoints following ECS will provide a more global perspective on the role of endogenous opioid systems in ECS. From these results, it is suggested that other forms of SIA may also share many of these properties in common with ECS-induced SIA. Nonetheless, ECS and other forms of SIA, such as cold water exposure and restraint, share with ECS a common history of clinical use in the treatment of human depression. It is possible that the common thread linking these experimental observations to endogenous opioid systems may provide new insights into the cause and treatment of mental disorders as well as the perception of pain.
基于上述回顾的证据,毫无疑问,电惊厥休克激活内源性阿片类物质并改变其受体。因此,这种形式的单次冲击性应激伴随着许多其他类阿片样作用的必然结果,包括僵住症、相似的脑电图模式、常见的自主神经效应以及阿片受体结合位点的增加。研究进一步表明,纳洛酮也可减弱电惊厥休克的遗忘效应,并且垂体衍生的阿片类物质可能作为主要的阿片类物质来源发挥重要作用,这些阿片类物质在电惊厥休克后促成这些类阿片样效应。希望这些众多将单次冲击性应激与电惊厥休克后的其他行为和生理终点相关联的尝试,能为内源性阿片系统在电惊厥休克中的作用提供更全面的视角。从这些结果来看,有人提出其他形式的单次冲击性应激可能也与电惊厥休克诱导的单次冲击性应激有许多共同特性。尽管如此,电惊厥休克和其他形式的单次冲击性应激,如冷水暴露和束缚,在治疗人类抑郁症的临床应用方面与电惊厥休克有着共同的历史。将这些实验观察结果与内源性阿片系统联系起来的共同线索,有可能为精神障碍的病因和治疗以及疼痛感知提供新的见解。