Electroconvulsive shock activates endogenous opioid systems: behavioral and biochemical correlates.
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.
D000698:Analgesia; D000818:Animals; D001522:Behavior, Animal; D002375:Catalepsy / Q000503:physiopathology; D004569:Electroencephalography; D004597:Electroshock; D004723:Endorphins / Q000502:physiology*; D011311:Pressoreceptors / Q000502:physiology; D012119:Respiration; D012640:Seizures / Q000503:physiopathology; D013312:Stress, Physiological / Q000503:physiopathology
D004723:Endorphins