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Updated: Jul 31, 2025
Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
Serial electroconvulsive Seizure alters dendritic complexity and promotes cellular proliferation in the mouse dentate
K T Meyers1, C C Damphousse2, A B Ozols3
1Interdisciplinary Graduate Program in Neuroscience, Arizona State University, Tempe, AZ, 85281, USA; Basic Medical Sciences, University of Arizona College of Medicine - Phoenix, Phoenix, AZ, 85004, USA.
Background:
Despite being one of the safest, most effective treatments for severe mood disorders, the therapeutic mechanisms of electroconvulsive therapy remain unknown. Electroconvulsive seizure (ECS) induces rapid, high-level expression of immediate early genes (IEGs) and brain-derived neurotrophic factor (BDNF), in addition to stimulation of neurogenesis and dendritic remodeling of dentate gyrus (DG) neurons. We have previously shown that this upregulation of BDNF fails to occur in the hippocampus of mice lacking the IEG Egr3. Since BDNF influences neurogenesis and dendritic remodeling, we hypothesized that Egr3-/- mice will exhibit deficits in neurogenesis and dendritic remodeling in response to ECS.
Objective:
To test this hypothesis, we examined dendritic remodeling and cellular proliferation in the DG of Egr3-/- and wild-type mice following repeated ECS.
Methods:
Mice received 10 daily ECSs. Dendritic morphology was examined in Golgi-Cox-stained tissue and cellular proliferation was analyzed through bromodeoxyuridine (BrdU) immunohistochemistry and confocal imaging.
Results:
Serial ECS in mice results in dendritic remodeling, increased spine density, and cellular proliferation in the DG. Loss of Egr3 alters the dendritic remodeling induced by serial ECS but does not change the number of dendritic spines or cellular proliferation consequences of ECS.
Conclusion:
Egr3 influences the dendritic remodeling induced by ECS but is not required for ECS-induced proliferation of hippocampal DG cells.
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