Parkinson's disease (PD) consists of a degeneration of the striatonigral dopaminergic pathway which modulate GABAergic striatal neurons. In the striatum, dopamine (DA) D2 receptors are co-localized with adenosine A2A receptors on GABAergic neurons of the striopallidal pathway. This co-expression produces an antagonist-like effect from A2A receptor on D2 acting as an inhibitory regulator of dopaminergic signal. The deficit of dopaminergic modulation and the parkinson's symptomatology could be imitate by haloperidol, an antagonist of D₂ receptor, so an A2A receptor antagonist, such as caffeine, could supress extrapyramidal symptoms (catalepsy, akinesia, muscle rigidity) in rodent and primate models of PD. Furthermore, it is believed that main motor symptoms of PD are due to the hiperactivity of the GABAergic striatopallidal pathway. For this reason, the aim of the present study was to find out if haloperidol and caffeine have some effect on striatal acid glutamic decarboxylase (GAD) activity. The present study showed the effects of a unique acute dose of haloperidol (4mg/Kg i.p.) on GAD activity of striatum and general motor behaviour, induction of catalepsy, corporal spasm and tremulous jaw movements in rats. Subsequently, we injected caffeine (30mg/Kg) to some animals with haloperidol-induced parkinsonian effects and we tested the same parameters than before. We realized an assay of GAD activity from GABA concentrations detected by HPLC method. We observed a significant increase in GAD activity in the group with double treatment (haloperidol and caffeine) with respect to control group, but not to haloperidol group. Nevertheless, we did not detect any significant difference between the haloperidol group and the others (control and double-treated group). In the other hand, the behavioural test showed that the haloperidol treatment induces parkinsonian symptoms, such as akinesia, corporal spasm, catalepsy and tremulous jaw movements, which are improved by caffeine.