Neurophysiological mechanisms of electroconvulsive therapy for depression
Abstract
The neurobiological foundation of electroconvulsive therapy (ECT) remains fragile. How ECT affects neural activities in the brain of depressives is largely unknown. There has been accumulating knowledge on genes and molecules induced by the animal model of ECT. Exact functions of those molecules in the context of mood disorder remain unknown. Among the dozens of molecules highly expressed by ECT, one that shows an especially prominent induction (>6-fold) is Homer 1a, a member of the intracellular scaffold protein family Homer. We have examined effects of Homer 1a in ECT-subjected cortical pyramidal cells, on the basis of which two neurobiological consequences of ECT are proposed. First, Homer 1a either injected intracellularly or induced by ECT was shown to reduce neuronal excitability. This agrees with diverse lines of mutually consistent clinical investigations, which unanimously point to an enhanced excitability in the cerebral cortex of depressive patients. The GABAergic dysfunction hypothesis of depression was thus revitalized. Second, again by relying on Homer 1a, we have proposed a molecular mechanism by which ECT affects a form of long-term depression (LTD). The possibility is discussed that clinical effects of ECT are exerted at least partly by reducing neural excitability and modifying synaptic plasticity.
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The method of action of ECT on psychosis or sleep remains unclear.
“The method of action of ECT on psychosis or sleep remains unclear (N. Kato, 2009) although it has been proposed that the mechanism of action of ECT is to mimic the EEG characteristics of slow wave/delta sleep (Charlton, 1999).”
From The role of sleep dysfunction in the occurrence of delusions and hallucinations: A systematic review (2015) · cites this paper as N. Kato, 2009
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- Authors
- Kato, N.
- Affiliations
- Kanazawa Medical University (JP)
- Corresponding author
- Kato, Nobuo
- ORCID
- Kato, Nobuo
- Venue
- Neuroscience Research
- Publisher
- Elsevier BV
- Published
- 2009-05
- Volume
- 64
- Issue
- 1
- Pages
- 3-11
- ISSN
- 0168-0102 (ISSN-L)
- OpenAlex
- W2069602531
- Cited by
- 65
- References
- 95
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 3 · 2021: 5 · 2020: 5 · 2019: 5 · 2018: 7 · 2017: 3 · 2016: 3 · 2015: 8 · 2014: 3 · 2013: 1 · 2012: 6
- FWCI
- 0.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Electroconvulsive Therapy Studies
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Neurology › Transcranial Magnetic Stimulation Studies
- Keywords
- electroconvulsive therapy, depression, Homer1a, neuronal excitability, GABAergic dysfunction, long-term depression, synaptic plasticity, cortical pyramidal neurons, mood disorders
- MeSH terms
- Homer Scaffolding Proteins, Animals, Brain, Carrier Proteins, Depressive Disorder, Electroconvulsive Therapy, gamma-Aminobutyric Acid, Humans, Models, Neurological, Neuronal Plasticity, Pyramidal Cells, Long-Term Synaptic Depression
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