1998
DOI: 10.1016/s0304-3940(98)00650-8
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Paradoxical metabolic response of the human brain to a single electroconvulsive shock

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Cited by 19 publications
(5 citation statements)
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“…17 Hippocampal neurogenesis, recently postulated to be related to the therapeutic effect of ECT, may also occur. 20 The advantages of offering the minimum number of treatments are clear in cost and cumulative risk of adverse effects. 18 Changes in neurotransmitter levels in the frontal cortex after a single ECT in the rat model include increases in extracellular concentrations of dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxyindoleacetic acid.…”
Section: Discussionmentioning
confidence: 99%
“…17 Hippocampal neurogenesis, recently postulated to be related to the therapeutic effect of ECT, may also occur. 20 The advantages of offering the minimum number of treatments are clear in cost and cumulative risk of adverse effects. 18 Changes in neurotransmitter levels in the frontal cortex after a single ECT in the rat model include increases in extracellular concentrations of dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxyindoleacetic acid.…”
Section: Discussionmentioning
confidence: 99%
“…Electroconvulsive therapy is used in humans with severe depressive disorders and has been shown to be effective in 85–90% of cases with mood and memory improvement (42). Interestingly, a single ECS has been shown to lead to a quite large activation in protein synthesis in both humans (43) and rats (44). The activation of this metabolic pathway may be linked to the positive effects of this type of seizure on mood and memory, possibly mediated by the consequences of the electroconvulsive treatment on neurotransmitters, neurotrophic factors, and gene expression (45,46).…”
Section: Discussionmentioning
confidence: 99%
“…Because the available data support this, there may be a possibility of activation of COX an increase in free radical production leading to oxidative stress and apoptosis of GABAergic neurons, thus increasing the glutamate and causing epileptic discharges [3] . So COX‐2 inhibitors might be acting through GABAergic neurons thus increasing the inhibitory neurotransmitter and the expression of GABA receptor protein [3,27–29] …”
Section: Discussionmentioning
confidence: 98%