Effects of esketamine on depression-like behavior and dendritic spine plasticity in the prefrontal cortex neurons of spared nerve injury-induced depressed mice.
Bixin Huang, Xiaoling Li, Yuling Zheng, Ying Mai, Zhongqi Zhang
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas January 1, 2024 DOI: 10.1590/1414-431X2024e13736 via PubMed
Summary
AI-generated from the abstractIn a mouse model of depression created by spared nerve injury, esketamine improved depression-like behaviors, such as increasing time spent in open arms and central area of an open field test and total distance traveled, while also increasing immobility in forced swimming and tail suspension tests. It raised the density of total and mature dendritic spines in the prefrontal cortex and increased expression of CRMP2 and PSD-95 proteins. These findings suggest esketamine promotes brain plasticity in the prefrontal cortex, possibly through changes in these proteins.
Study at a glance
| Characteristics | Animal study Peer reviewed |
|---|---|
| Population | Mice with spared nerve injury |
| Intervention | Esketamine |
| Duration | Behavioral tests performed 1 hour after esketamine treatment; PFC tissues obtained on the fourth day after completing behavioral tests |
| Topics | Neuroplasticity |
| Keywords | Neuroscience Depression treatment Esketamine therapy Chronic pain |
| Citations | 4 |
| Key finding | Esketamine increased dendritic spine density and CRMP2 and PSD-95 expression in the prefrontal cortex of mice with depression-like behaviors. |
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.