In vivo Protection of Vitamin K in NMDA-Induced Memory Impairment

Background: Stimulation of N-Methyl-D-aspartate (NMDA) receptors with a neurotoxic dose of NMDA is commonly used to model certain characteristics of neurodegenerative disorders. A neurotoxic dose of NMDA injected into the CA1 region of the hippocampus causes excitotoxic damage and likely leads to memory impairment. Objectives: This study aimed to assess the effect of NMDA on passive avoidance learning and open-field tests in male rats, both with and without vitamin K (Vit K), to explore Vit K's potential neuroprotective properties. Methods: Passive avoidance learning and open-field tests were conducted to assess recognition memory. In both tests, a retention session was held 24 hours post-training. N-Methyl-D-aspartate (20 µg/µL) was administered via cannula, and Vit K (10 mg/kg, s.c.) was given daily for 30 days into the CA1 region. Results: N-Methyl-D-aspartate administration reduced step-through latency (STL) and increased time spent in the dark compartment (TDC) during retention sessions. It also decreased locomotor activity and rearing behavior in open-field tests. In contrast, Vit K increased STL and decreased TDC in NMDA-treated rats, with observed improvements in locomotor activity and rearing behavior. Conclusions: N-Methyl-D-aspartate administration in the CA1 region induced memory deficits in passive avoidance and open-field tests. The findings suggest that Vit K may exert neuroprotective effects against NMDA-induced excitotoxic neuronal damage, potentially improving memory impairments.