Abstract
ELECTROCONVULSIVE SHOCK (ECS) is one of the most effective forms of therapy available for patients with depression1. Its mechanism of action, however, is not clear. Like other antidepressants, ECS probably augments the postsynaptic availability of neurotransmitters, for it increases the release and turnover of noradrenaline (NA)2–4, decreases NA uptake5, and raises the activity of tyrosine hydroxylase. Also, synthesis of cyclic AMP stimulated by NA (NA-sensitive adenylate cyclase) is reduced in brain tissues obtained after chronic treatment with ECS6,7. It has been reported that chronic administration of antidepressant drugs reduces β-adrenergic receptor density in the rat brain8. Because ECS is another form of treatment for depressive illness, we examined whether chronic administration of ECS has effects similar to those of other antidepressants on β-adrenergic receptor sensitivity in rat brain. We report here that we observed a significant decrease in β-adrenergic sensitivity following chronic ECS treatment. The relationship between such observed effects and clinical response requires further investigation.
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PANDEY, G., HEINZE, W., BROWN, B. et al. Electroconvulsive shock treatment decreases β-adrenergic receptor sensitivity in rat brain. Nature 280, 234–235 (1979). https://doi.org/10.1038/280234a0
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DOI: https://doi.org/10.1038/280234a0
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