Effects of esketamine on depression-like behavior and dendritic spine plasticity in the prefrontal cortex neurons of spared nerve injury-induced depressed mice.
Braz J Med Biol Res
; 57: e13736, 2024.
Article
in En
| MEDLINE
| ID: mdl-38985082
ABSTRACT
The present study utilized the spared nerve injury (SNI) to create a mouse model of depression to investigate the impact of esketamine on depressive-like behaviors, on the expression of PSD-95 and CRMP2 proteins, and on changes in neuronal dendritic spine plasticity in the prefrontal cortex (PFC). Depressive-like behavioral tests were performed 1 h after esketamine treatment, and the PFC tissues were obtained on the fourth day after completing the behavioral tests. Then, dendritic spine density and morphology in the PFC were measured using Golgi staining, and CRMP2 and PSD-95 proteins were obtained from PFC tissue by western blotting. The results of this study showed that esketamine significantly increased the immobility time in the forced swimming test and tail suspension test. In the open field test, esketamine increased the time spent in the open arms, the time spent in the central area, and the total distance covered. It also increased the protein expression levels of CRMP2 and PSD-95 in addition to the total and mature dendritic spine density of the PFC in SNI-depressed mice. Esketamine can significantly improve depression-like behaviors in SNI-depressed mice and promote an increase in dendritic spine density and maturation in the PFC. These effects may be associated with changes in CRMP2 and PSD-95 expression.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Prefrontal Cortex
/
Dendritic Spines
/
Depression
/
Disease Models, Animal
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Ketamine
/
Neuronal Plasticity
Limits:
Animals
Language:
En
Journal:
Braz J Med Biol Res
Year:
2024
Document type:
Article
Affiliation country:
China
Country of publication:
Brasil