Acute and chronic haloperidol treatments increase parkin mRNA levels in the rat brain.

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. We examined the effects of acute and chronic treatment with haloperidol on parkin mRNA expression in the rat brain by reverse transcription-polymerase chain reaction. Acute haloperidol treatment (2 mg/kg) increased parkin mRNA levels in the striatum and nucleus accumbens but not in the medial prefrontal cortex and substantia nigra. Four-week-treatment with haloperidol decanoate (25 mg eq/kg) produced a significant increase in parkin mRNA levels in the striatum without affecting to those in the medial prefrontal cortex, nucleus accumbens and substantia nigra. These results suggest that Parkin may be involved in the haloperidol-induced synaptic plasticity, since Parkin regulates the turnover of the synaptic protein, CDCrel-1.