Tardive dyskinesia (TD) is a common adverse effect observed in patients with long-term use of typical antipsychotic medications. A vacuous chewing movement (VCM) model induced by haloperidol has been used to study these abnormalities in experimental animals. The cause of TD and its treatment remain unknown, but several lines of evidence suggest that dopamine receptor supersensitivity and gamma-aminobutyric acid (GABA) insufficiency play important roles in the development of TD. This study investigated the effects of treatment with the GABA-mimetic drug gabapentin on the development of haloperidol-induced VCMs. Male mice received vehicle, haloperidol (1.5 mg/kg), or gabapentin (GBP, 100 mg/kg) intraperitoneally during 28 consecutive days. Quantification of VCMs was performed before treatment (baseline) and on day 28, and an open-field test was also conducted on the 28th day of treatment. The administration of gabapentin prevented the manifestation of haloperidol-induced VCMs. Treatment with haloperidol alone reduced the locomotor activity in the open-field test that was prevented by co-treatment with gabapentin. We did not find any differences among the groups nor in the tyrosine hydroxylase (TH) or glutamic acid decarboxylase (GAD) immunoreactivity or monoamine levels in the striatum of mice. These results suggest that treatment with gabapentin, an analog of GABA, can attenuate the VCMs induced by acute haloperidol treatment in mice without alterations in monoamine levels, TH, or GAD67 immunoreactivity in the striatum.