A glutamatergic model of ECT-induced memory dysfunction.
Electroconvulsive therapy (ECT) is an efficacious treatment for a variety of neuropsychiatric conditions including major depression, mania, catatonia, Parkinson's disease, and neuroleptic malignant syndrome. However, ECT-induced memory dysfunction complicates the treatment and is a major concern for both patients and providers. We briefly review ECT-induced memory dysfunction and propose a glutamatergic model for it. (Articles examined were retrieved by a Medline search on the terms electroconvulsion and glutamate, with language limited to English.) Specifically, we hypothesize that ECT-induced memory dysfunction results from neuronal insults due to excessive release of excitatory amino acids and activation of their receptors, which produce cation and water flux and reversible oxidative stress. This model offers multiple testable hypotheses; exploring them may help to identify the risk factors for this significant side effect of ECT treatment and may thus yield effective agents for its prevention and treatment.
Chamberlin
E
E
Institute of Living, Hartford, Conn., USA.
Tsai
G E
GE
D004565:Electroconvulsive Therapy / Q000009:adverse effects*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D006801:Humans; D008569:Memory Disorders / Q000209:etiology*; D008959:Models, Neurological; D016202:N-Methylaspartate / Q000494:pharmacology; D017470:Receptors, Glutamate / Q000187:drug effects / Q000502:physiology*; D012640:Seizures / Q000503:physiopathology
D018691:Excitatory Amino Acid Antagonists; D017470:Receptors, Glutamate; D016202:N-Methylaspartate