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) |
|---|---|
| Journal | Brain Stimulation |
| DOIs | |
| State | Accepted/In press - Jan 1 2018 |
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Keywords
- Brain-derived neurotrophic factor (BDNF)
- Cingulate cortex
- Dendritic spine
- ECT
- Electroconvulsive seizures
- Morphology
ASJC Scopus subject areas
- Neuroscience(all)
- Biophysics
- Clinical Neurology
Cite this
Electroconvulsive seizures influence dendritic spine morphology and BDNF expression in a neuroendocrine model of depression. / Maynard, Kristen R.; Hobbs, John W.; Rajpurohit, Sumita K.; Martinowich, Keri.
In: Brain Stimulation, 01.01.2018.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Electroconvulsive seizures influence dendritic spine morphology and BDNF expression in a neuroendocrine model of depression
AU - Maynard, Kristen R.
AU - Hobbs, John W.
AU - Rajpurohit, Sumita K.
AU - Martinowich, Keri
PY - 2018/1/1
Y1 - 2018/1/1
N2 - 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.
AB - 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.
KW - Brain-derived neurotrophic factor (BDNF)
KW - Cingulate cortex
KW - Dendritic spine
KW - ECT
KW - Electroconvulsive seizures
KW - Morphology
UR - http://www.scopus.com/inward/record.url?scp=85045465364&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85045465364&partnerID=8YFLogxK
U2 - 10.1016/j.brs.2018.04.003
DO - 10.1016/j.brs.2018.04.003
M3 - Article
C2 - 29674117
AN - SCOPUS:85045465364
JO - Brain Stimulation
JF - Brain Stimulation
SN - 1935-861X
ER -