Postmortem studies suggest that schizophrenia is associated with abnormal expression of specific GABA A receptor (GABA AR) α subunits, including α5GABA AR. Positron emission tomography (PET) measures of GABA AR availability in schizophrenia, however, have not revealed consistent alterations in vivo. Animal studies using the GABA AR agonist [ 3H]-muscimol provide evidence that antipsychotic drugs influence GABA AR availability, in a region-specific manner, suggesting a potential confounding effect of these drugs. No such data, however, are available for more recently developed subunit-selective GABA AR radioligands. To address this, we combined a rat model of clinically relevant antipsychotic drug exposure with quantitative receptor autoradiography. Haloperidol (0.5 and 2 mg/kg/day) or drug vehicle were administered continuously to adult male Sprague-Dawley rats via osmotic mini-pumps for 28 days. Quantitative receptor autoradiography was then performed postmortem using the GABA AR subunit-selective radioligand [ 3H]-Ro15-4513 and the non-subunit selective radioligand [ 3H]-flumazenil. Chronic haloperidol exposure increased [ 3H]-Ro15-4513 binding in the CA1 sub-field of the rat dorsal hippocampus (p<0.01; q<0.01; d=+1.3), which was not dose-dependent. [ 3H]-flumazenil binding also increased in most rat brain regions (p<0.05; main effect of treatment), irrespective of the haloperidol dose. These data confirm previous findings that chronic haloperidol exposure influences the specific binding of non-subtype selective GABA AR radioligands and is the first to demonstrate a potential effect of haloperidol on the binding of a α1/5GABA AR-selective radioligand. Although caution should be exerted when extrapolating results from animals to patients, our data support a view that exposure to antipsychotics may be a confounding factor in PET studies of GABA AR in the context of schizophrenia.