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Adenosine A2A receptors have been implicated in the pathophysiology of schizophrenia by clinical, anatomical, biochemical and genetic studies. We hypothesized that a genetically determined low number of adenosine A2A receptors could be a vulnerability factor for the development of the disease. The density of adenosine A2A receptors was investigated in human postmortem striatum of patients with schizophrenia (n = 9) and matched controls (n = 9) using [3H)CGS 21680 as a radioligand probe. The maximum number of binding sites (Bmax) was 70% higher in patients with schizophrenia than in matched controls (609.4 ± 259.1 vs 354.0 ± 156.4 fmol/mg protein, p=0.04). No significant difference could be discerned for the affinity of caffeine for adenosine A2A receptors between patients and controls. The increase in receptor density correlated with the dose of antipsychotic medication in chlorpromazine equivalents (r2=0.61, p = 0.014). We failed to provide evidence for a genetically determined reduction of adenosine A2A receptors in schizophrenia. Instead, consistent with findings from animal experiments, our observation supports a role of adenosine A2A receptors in the molecular effects of antipsychotic drugs.