Electroconvulsive seizures influence dendritic spine morphology and BDNF expression in a neuroendocrine model of depression

Kristen R. Maynard, John W. Hobbs, Sumita K. Rajpurohit, Keri Martinowich

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


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 languageEnglish (US)
Pages (from-to)856-859
Number of pages4
JournalBrain Stimulation
Issue number4
StatePublished - Jul 1 2018


  • Brain-derived neurotrophic factor (BDNF)
  • Cingulate cortex
  • Dendritic spine
  • ECT
  • Electroconvulsive seizures
  • Morphology

ASJC Scopus subject areas

  • Biophysics
  • General Neuroscience
  • Clinical Neurology


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