Abstract
The effects of methylazoxymethanol (MAM)-induced brain lesions on vacuous chewing movements (VCM) were examined in rats given chronic haloperidol treatment (0.1 or 1 mg/kg/day) for 18 months. At the end of the experiment striatal, pallidal, and nigral activities of glutamate decarboxylase (GAD) were measured. MAM-lesioned rats had an elevated rate of VCMs compared to unlesioned controls. This effect was stable during the whole 18-month experiment. In unlesioned control rats chronic haloperidol produced a gradual increase in VCM rates, but this effect was not further exacerbated in MAM-lesioned animals. After chronic haloperidol treatment with the higher dose (1 mg/kg/day) GAD activity was reduced in substantia nigra (-20%), globus pallidus (-35%), and striatum (-26%) of unlesioned rats. MAM caused a reduction of GAD activity in substantia nigra (-29%) and globus pallidus (-29%). Chronic haloperidol did not influence these effects of MAM-induced lesion. The present results show that a MAM-induced brain lesion, in contrast to cortical ablations, cannot be used to amplify the haloperidol-induced VCM increase or influence the nigral GAD activity in a rat model for tardive dyskinesia.
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