Glial cell activation in response to electroconvulsive seizures
Abstract
Electroconvulsive therapy (ECT) is a very efficient treatment for severe depression. However, cognitive side effects have raised concern to whether ECT can cause cellular damage in vulnerable brain regions. A few recent animal studies have reported limited hippocampal cell loss, while a number of other studies have failed to find any signs of cellular damage and some even report that electroconvulsive seizures (ECS; the animal counterpart of ECT) has neuroprotective effects. We previously have described gliogenesis in response to ECS. Loss of glial cells is seen in depression and de novo formation of glial cells may thus have an important therapeutic role. Glial cell proliferation and activation is however also seen in response to neuronal damage. The aim of the present study was to further characterize glial cell activation in response to ECS. Two groups of rats were treated with 10 ECS using different sets of stimulus parameters. ECS-induced changes in the morphology and expression of markers typical for reactive microglia, astrocytes and NG2+ glial cells were analyzed immunohistochemically in prefrontal cortex, hippocampus, amygdala, hypothalamus, piriform cortex and entorhinal cortex. We observed changes in glial cell morphology and an enhanced expression of activation markers 2 h following ECS treatment, regardless of the stimulus parameters used. Four weeks later, few activated glial cells persisted. In conclusion, ECS treatment induced transient glial cell activation in several brain areas. Whether similar processes play a role in the therapeutic effect of clinically administered ECT or contribute to its side effects will require further investigations.
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Therapeutic treatments such as electroconvulsive therapy and transcranial current stimulation in rats are associated with a pro-inflammatory phenotype of microglia, marked by morphological alterations, and increased MHCII expression and proliferation.
“Interestingly, therapeutic treatments such as, electroconvulsive therapy and transcranial current stimulation, in rats were associated with a pro-inflammatory phenotype of microglia, marked by morphological alterations, and increased MHCII expression and proliferation (Jansson et al, 2009;Rueger et al, 2012).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Jansson et al, 2009
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- Authors
- Jansson, L., Wennström, M., Johanson, A., & Tingström, A.
- Affiliations
- Lund University (SE)
- Corresponding author
- Tingström, Anders
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2009-10
- Volume
- 33
- Issue
- 7
- Pages
- 1119-1128
- ISSN
- 0278-5846 (ISSN-L)
- OpenAlex
- W2025582889
- Cited by
- 99
- References
- 66
- Citations by year
- 2026: 6 · 2025: 2 · 2024: 4 · 2023: 10 · 2022: 2 · 2021: 10 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 7 · 2016: 7 · 2015: 10 · 2014: 6 · 2013: 9 · 2012: 4
- FWCI
- 2.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- Royal Society
- Lundbeckfonden
- Vetenskapsrådet
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Electroconvulsive Therapy Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Transcranial Magnetic Stimulation Studies
- Keywords
- electroconvulsive seizures, glial activation, reactive microglia, reactive astrocytes, gliogenesis, ECT side effects, cognitive side effects, depression, neuroprotection, stimulus parameters, prefrontal cortex, hippocampus, amygdala, hypothalamus, piriform cortex, entorhinal cortex
- MeSH terms
- Chondroitin Sulfate Proteoglycan 4, Analysis of Variance, Animals, Antigens, Brain, Calcium-Binding Proteins, Disease Models, Animal, Electroshock, Glial Fibrillary Acidic Protein, Intermediate Filament Proteins, Male, Microfilament Proteins, Nerve Tissue Proteins, Neuroglia, Nuclear Proteins, Proteoglycans, Seizures, Time Factors, Trans-Activators, Rats, Wistar, Rats, Ectodysplasins, Nestin
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