Glial cell activation in response to electroconvulsive seizures.
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.
Jansson
Linda
L
Molecular Psychiatry Unit, Wallenberg Neuroscience Center, S-22184 Lund, Sweden.
Wennström
Malin
M
Johanson
Aki
A
Tingström
Anders
A
D000704:Analysis of Variance; D000818:Animals; D000941:Antigens / Q000378:metabolism; D001921:Brain / Q000473:pathology*; D002135:Calcium-Binding Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D053331:Ectodysplasins / Q000378:metabolism; D004597:Electroshock / Q000009:adverse effects; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007381:Intermediate Filament Proteins / Q000378:metabolism; D008297:Male; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins / Q000378:metabolism; D064231:Nestin; D009457:Neuroglia / Q000145:classification / Q000378:metabolism / Q000502:physiology*; D009687:Nuclear Proteins / Q000378:metabolism; D011509:Proteoglycans / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000209:etiology* / Q000473:pathology*; D013997:Time Factors; D015534:Trans-Activators / Q000378:metabolism; D000099216:Chondroitin Sulfate Proteoglycan 4
D000941:Antigens; D002135:Calcium-Binding Proteins; D053331:Ectodysplasins; D005904:Glial Fibrillary Acidic Protein; D007381:Intermediate Filament Proteins; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins; D064231:Nestin; D009687:Nuclear Proteins; D011509:Proteoglycans; D015534:Trans-Activators; D000099216:Chondroitin Sulfate Proteoglycan 4; C100745:Aif1 protein, rat; C083728:MHC class II transactivator protein; C577486:Nes protein, rat