Himori N, Tanaka Y, Kurasawa M, Mishima K, Akaike N
Department of Pharmacology, Nippon Roche Research Center, Kamakura, Japan.
Pharmacology. 1994 Apr;48(4):226-33. doi: 10.1159/000139184.
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 (3OMD). The intraperitoneal administration of 3OMD (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 3OMD tended to reverse the antagonistic property of Madopar on the cataleptic behavior in response to haloperidol. The ability of 3OMD 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 3OMD. The results from our animal experiments may provide further evidence that impediment of 3OMD formation is meaningful in the treatment of Parkinson's disease with Madopar or levodopa.
在给予3 - O - 甲基多巴（3OMD）之前和之后，定量比较了美多芭（左旋多巴加苄丝肼）对小鼠对氟哌啶醇的僵住行为反应和运动活动的影响。单独腹腔注射3OMD（200 - 400mg/kg）不会改变氟哌啶醇（1.0mg/kg皮下注射）诱导的僵住症。根据给药方案，美多芭可显著拮抗氟哌啶醇诱导的僵住症。用3OMD预处理倾向于逆转美多芭对氟哌啶醇所致僵住行为的拮抗特性。在运动测试范式中观察到3OMD显著抑制美多芭作用的能力；腹腔内预先注射3OMD可显著抑制美多芭治疗动物的运动亢进。我们动物实验的结果可能提供进一步的证据，即3OMD形成的阻碍在使用美多芭或左旋多巴治疗帕金森病中具有重要意义。
