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 2024 DOI: 10.1590/1414-431X2024e13736 (opens in new tab)
Study at a glance
AI-extracted from the abstract| 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 Depression Esketamine |
| Keywords | Depression treatment Esketamine therapy Chronic pain |
| Citations | 4 |
| Key points | 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.
Comparable studies
Other preclinical and animal studies on esketamine for depression, most cited first.
Citations in the library
Cited by 3
- Quantitative monitoring of ketamine's impact on synaptic density using 11C-UCB-J PET imaging in the corticosterone mouse model of anxiety/depression. Molecular Psychiatry November 18, 2025
- Multiband ALFF in patients with major depressive disorder treated with esketamine and sertraline: A preliminary study Brain Research Bulletin October 6, 2026
- Ascorbic acid enhances antidepressant-like efficacy of esketamine: Hippocampal TARP-γ8-containing AMPA receptors mediate synaptic modulation. Neurotherapeutics November 11, 2025
Cites 7
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- Synaptic Dysfunction in Depression: Potential Therapeutic Targets Science October 4, 2012
- Mechanisms of Ketamine Action as an Antidepressant Molecular Psychiatry March 13, 2018
- (R)-Ketamine Rapidly Ameliorates the Decreased Spine Density in the Medial Prefrontal Cortex and Hippocampus of Susceptible Mice After Chronic Social Defeat Stress The International Journal of Neuropsychopharmacology August 28, 2019
- Differentially regulated targets in the fast-acting antidepressant effect of (R)-ketamine: A systems biology approach. Pharmacology, Biochemistry, and Behavior February 2023
and 2 more in the library