Lithium attenuates ketamine-induced long-term neurotoxicity through DISC1-mediated GSK-3β/β-catenin and ERK/CREB pathways.
Toxicology letters April 1, 2025 Ting-Ting Yang, Zi-Wen Guo, Fang Zhang et al. 2 citations
Repeated ketamine exposure in neonatal rats reduces levels of DISC1 and several signaling proteins (pGSK-3β, β-catenin, pERK, pCREB, PSD95), leading to neuroapoptosis, inhibited neurite growth, and cognitive deficits in adolescence. Lithium treatment upregulates DISC1 and activates the GSK-3β/β-catenin and ERK/CREB pathways, thereby ameliorating these harmful effects. The findings suggest lithium may protect against ketamine-induced long-term neurotoxicity during brain development.