Clinical strategies for evaluating ECT mechanisms--pharmacological, biochemical and psychophysiological approaches.
Although ECT is a highly effective treatment for severe depression and other psychiatric syndromes, its mode of action is not known. Recent studies have suggested that effects of ECT on central neurotransmitter receptors may underlie its therapeutic action. The effects of chronically administered electroconvulsive shock on receptors for dopamine, serotonin, noradrenaline, acetylcholine and endorphins in rodent brain, are reviewed. Strategies for evaluating the relevance of these animal findings to mechanisms of action of ECT in humans are discussed.
D000818:Animals; D001143:Arousal / Q000502:physiology; D001921:Brain / Q000378:metabolism*; D003866:Depressive Disorder / Q000628:therapy*; D004565:Electroconvulsive Therapy; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011941:Receptors, Adrenergic / Q000378:metabolism; D011954:Receptors, Dopamine / Q000378:metabolism; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D011957:Receptors, Opioid / Q000502:physiology; D011985:Receptors, Serotonin / Q000378:metabolism
D018377:Neurotransmitter Agents; D011941:Receptors, Adrenergic; D011954:Receptors, Dopamine; D017981:Receptors, Neurotransmitter; D011957:Receptors, Opioid; D011985:Receptors, Serotonin; D013006:Growth Hormone; D006854:Hydrocortisone