Abstract
Background: Electroconvulsive therapy (ECT) is a rapid and effective treatment for major depressive disorder. Chronic stress-induced depression causes dendrite atrophy and deficiencies in brain-derived neurotrophic factor (BDNF), which are reversed by anti-depressant drugs. Electroconvulsive seizures (ECS), an animal model of ECT, robustly increase BDNF expression and stimulate dendritic outgrowth. Objective: The present study aims to understand cellular and molecular plasticity mechanisms contributing to the efficacy of ECS following chronic stress-induced depression. Methods: We quantify Bdnf transcript levels and dendritic spine density and morphology on cortical pyramidal neurons in mice exposed to vehicle or corticosterone and receiving either Sham or ECS treatment. Results: ECS rescues corticosterone-induced defects in spine morphology and elevates Bdnf exon 1 and exon 4-containing transcripts in cortex. Conclusions: Dendritic spine remodeling and induction of activity-induced BDNF in the cortex represent important cellular and molecular plasticity mechanisms underlying the efficacy of ECS for treatment of chronic stress-induced depression.
Original language | English (US) |
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Pages (from-to) | 856-859 |
Number of pages | 4 |
Journal | Brain Stimulation |
Volume | 11 |
Issue number | 4 |
DOIs | |
State | Published - Jul 1 2018 |
Keywords
- Brain-derived neurotrophic factor (BDNF)
- Cingulate cortex
- Dendritic spine
- ECT
- Electroconvulsive seizures
- Morphology
ASJC Scopus subject areas
- Biophysics
- Neuroscience(all)
- Clinical Neurology