How does convulsive therapy work?
There is no death of hypotheses to explain the antidepressant action of convulsive therapy. Neurohumoral-receptor, kindling-anticonvulsant, and neuroendocrine ideas are prominently discussed. Views based on direct comparisons with antidepressant drugs or based on pharmacologic models are seen as inadequate. The neuroendocrine hypothesis, derived from human studies, appears the most viable. It argues that the affective disorders result from a deficiency of a mood-modifying peptide (antidepressin) derived from the hypothalamus. Convulsive therapy stimulates the production and release of antidepressin. Studies dedicated to the search for this peptide as a replacement for ECT are encouraged.
Fink
M
M
Department of Psychiatry and Behavioral Science, School of Medicine, State University of New York, Stony Brook.
D000324:Adrenocorticotropic Hormone / Q000502:physiology; D000818:Animals; D001921:Brain / Q000503:physiopathology; D003866:Depressive Disorder / Q000628:therapy*; D004565:Electroconvulsive Therapy; D004594:Electrophysiology; D006801:Humans; D007696:Kindling, Neurologic; D008959:Models, Neurological; D018377:Neurotransmitter Agents / Q000502:physiology; D013973:Thyrotropin-Releasing Hormone / Q000502:physiology
D018377:Neurotransmitter Agents; D013973:Thyrotropin-Releasing Hormone; D000324:Adrenocorticotropic Hormone