S-ketamine ameliorates post-stroke depression in mice via attenuation of neuroinflammation, synaptic restoration, and BDNF pathway activation.
Biochemical and biophysical research communications July 8, 2025 Jiaxin Tian, Yanhong Xie, Sen Ye et al. 6 citations
A single acute dose of S-ketamine (10 mg/kg) given to mice with post-stroke depression (PSD) alleviated depressive-like behaviors for at least five days. The treatment reduced pro-inflammatory cytokines in the medial prefrontal cortex, increased dendritic spine density and synaptic proteins (SYP, PSD-95), and upregulated brain-derived neurotrophic factor (BDNF) along with related signaling molecules (TrkB, p-Akt, p-Erk, p-CaMKII, p-CREB). These findings suggest S-ketamine acts through anti-inflammatory, synaptic enhancing, and BDNF pathway modulating effects, offering promise for PSD treatment.