The Effect of Ascorbic Acid on Glutamate Induced Behavioral Changes

The cellular and molecular factors responsible for neurotoxic effects (e.g.) tardive dyskinesia are incompletely understood. Accumulation of free radical species (ROS) is major contributing factor for such effects. The observation that suppression of glutamate decarboxylase in substantial nigra and increase release of glutamic acid support that neurotoxic effects of glutamic acid mediate through NMDA receptor and could result in excitotoxic effects. Present study reveals locomotion disorder and impaired cognition in animal models. These effects are possibly occurring due to release of glutamate and accumulation of ROS. In present work vitamin C was effective in some of the animal models of exitotoxicity with impaired cognition and movement disorder.