Electroconvulsive seizures influence dendritic spine morphology and BDNF expression in a neuroendocrine model of depression.
Brain Stimul
; 11(4): 856-859, 2018.
Article
em En
| MEDLINE
| ID: mdl-29674117
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.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Convulsões
/
Fator Neurotrófico Derivado do Encéfalo
/
Espinhas Dendríticas
/
Depressão
/
Eletroconvulsoterapia
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Brain Stimul
Ano de publicação:
2018
Tipo de documento:
Article