The effects of Madopar (levodopa plus benserazide) on the cataleptic behavioral response to haloperidol and on the locomotor activity in mice were quantitatively compared before and after the administration of 3-O-methyldopa (30MD). The intraperitoneal administration of 30MD (200-400 mg/kg) alone did not modify the haloperidol (1.0 mg/kg s.c.)-induced catalepsy. Madopar, depending on the dose regimen, markedly antagonized the haloperidol-induced catalepsy. Pretreatment with 30MD tended to reverse the antagonistic property of Madopar on the cataleptic behavior in response to haloperidol. The ability of 30MD to significantly inhibit Madopar effects was observed in the locomotor testing paradigm; the locomotor hyperactivity in Madopar-treated animals was significantly inhibited by a prior intraperitoneal injection of 30MD. The results from our animal experiments may provide further evidence that impediment of 30MD formation is meaningful in the treatment of Parkinson’s disease with Madopar or levodopa.

Keywords:
Catalepsy, Locomotor hyperactivity, Mouse, 3-O-methyldopa, Madopar, Haloperidol
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© 1994 S. Karger AG, Basel
1994
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