Objective[|]Statins, or 3-hydroxyl-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, which are potent inhibitors of cholesterol synthesis, are widely used in the treatment of hypercholesterolaemia and prevention of coronary artery diseases. Evidence from clinical trials also show other beneficial actions of statins unrelated to their cholesterol lowering effects. In experimental animal studies, it was reported that simvastatin, a statin agent, may alter dopaminergic and glutamatergic functions. Dopaminergic overactivity and dysfunction of glutamatergic transmission is associated with the pathogenesis of schizophrenia. This study aims to examine the chronical effects of simvastatin on experimental psychosis models in mice.[¤]Materials and Methods[|]All the experiments were performed with the decision of the Local Ethics Committee for Animal Experimentation of Eskisehir Osmangazi University (26.04.2011-207). Simvastatin was administered to male Swiss albino mice via oral gavage for 4 weeks at doses of 3, 10, and 30mg/kg. Saline was administered to control group for the same period and route. Apomorphine-induced climbing, MK-801-induced hyperlocomotion, and haloperidol-induced catalepsy were used as experimental psychosis models, and climbing time, the number of total movements, and duration of cataleptic posture were recorded respectively. Results were statistically analyzed with Kruskal–Wallis test.[¤]Results[|]There was no significant difference between the groups in terms of climbing time, the number of total movements, and duration of cataleptic posture (p>0.05).[¤]Conclusion[|]We suggest that chronical administration of simvastatin does not possess antipsychotic effect at all doses when assessed with the above-mentioned psychosis models.[¤]