Reversal of motor dysfunction, memory impairment, anxiety-like behaviour and depression after withdrawal from chronic vanadium neurotoxicity in mice

Abstract

Vanadium, a transition metal widely distributed in the environment, has been involved in neurotoxicity through oxidative stress and neuroinflammation. Chronic exposure may impair motor function, cognition, anxiety and depression-like behaviours, but the potential for recovery after withdrawal remains unclear especially in motor function, anxiety and depression-like behaviours. Male BALB/c mice were exposed to sodium metavanadate (3 mg/kg, intraperitoneal) for 3-, 9- or 15-months. Withdrawal groups received vanadium for 3-months followed by 6- or 12-months without exposure. Neurobehavioural assessments included motor coordination (inverted grid, beam walking), cognitive function (Y-maze), anxiety-like behaviour (open field) and depression-like behaviour (tail suspension test). Track and heat maps were used to visualize exploration and activity patterns. Chronic vanadium exposure induced progressive deficits in motor coordination, spatial memory, anxiety-like behaviour and depressive-like states. These impairments were most pronounced at 15-months of exposure. Withdrawal groups demonstrated partial recovery after 6-months and near-complete restoration after 12-months, with neurobehavioural performance approaching control levels across domains. Chronic vanadium exposure impairs motor, cognitive and affective functions in mice, but withdrawal promotes recovery, highlighting the reversibility of vanadium-induced neurotoxicity. These findings draw attention to the risks of chronic vanadium exposure while offering evidence that cessation can mitigate long-term neurobehavioural impairments.