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Updated: Feb 11, 2026

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons
Published on: July 13, 2011
Electroconvulsive seizures influence dendritic spine morphology and BDNF expression in a neuroendocrine model of
Kristen R Maynard1, John W Hobbs1, Sumita K Rajpurohit1
1Lieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, 21205, United States.
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.
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