Vanadium is a transition metal, abundant in nature and liberated into the environment mainly through the burning of fossils fuels, forest fires and volcanic emissions. Exposure to vanadium leads to increased reactive oxygen species (ROS) generation, lipid peroxidation and oxidative damage in the brain, with neonates and children being especially vulnerable due to an immature blood-brain barrier. Minocycline is a second-generation tetracycline antibiotic which produces neuroprotective effects in several animal models of neurological diseases, independent of its anti-microbial and anti-inflammatory properties. This study was designed to assess the behavioural and histomorphological changes in the postnatal developing mice brains after vanadium administration and ameliorating effect of minocycline. The animals were divided into 4 groups (n=12 per group): group A (Control), group B (Vanadium, 3 mg/kg body weight), group C (Vanadium 3 mg/kg body weight + Minocycline 30 mg/kg body weight), and group D (Minocycline 25 mg/kg body weight). In all groups, lactating dams were treated from postnatal day (PND) 1-14, and pups treated from PND 15-21. Open field test was conducted on PND 22 for pups before sacrifice and the brains removed for histology. Vanadium led to reduced body weight and movement, morphological changes such as depletion of pyramidal neurones in the hippocampus CA3 and cortex, central chromatolysis of Purkinje cell, gliosis, satelitosis and phagocytic nodules in the cerebral cortex. However, minocycline co-treatment exacerbated body weight loss, attenuated the movement deficits and the neuronal changes induced by vanadium. In conclusion, minocycline reduced the vanadium-induced neurotoxicity in mice pups.