Lorenc-Koci E, Wolfarth S, Ossowska K
Department of Neuropsychopharmacology, Polish Academy of Sciences, Cracow, Poland.
Exp Brain Res. 1996 May;109(2):268-76. doi: 10.1007/BF00231786.
The aim of the present study was to find out whether haloperidol-induced rigidity was similar to that seen in parkinsonism. Simultaneous measurements of the muscle resistance (mechanomyogram, MMG) of the hind foot to passive flexion and extension in the ankle joint, as well as determination of the electromyographic (EMG) activity of the gastrocnemius and tibialis anterior muscles of rats were carried out. Haloperidol was injected in doses of 0.5-10 mg/kg 1 h before the start of measurements. Haloperidol increased, in a dose-dependent manner, the muscle resistance of the rat's hind leg to passive movements. Muscle rigidity was accompanied with an increase resting, as well as in the stretch-induced long-latency EMG activity (in which supraspinal reflexes are most probably involved) in both those muscles, whereas the short-latency EMG activity (first large bursts of EMG activity, beginning ca. 9 ms after the start of a movement, probably of a spinal origin) was significantly decreased. The obtained results suggest that the haloperidol-increased MMG/EMG activity might be a good model of parkinsonian rigidity.
本研究的目的是查明氟哌啶醇诱导的僵硬是否与帕金森病中所见的僵硬相似。同时测量大鼠后足对踝关节被动屈伸的肌肉阻力(机械肌电图,MMG),并测定腓肠肌和胫骨前肌的肌电图(EMG)活性。在测量开始前1小时,以0.5 - 10 mg/kg的剂量注射氟哌啶醇。氟哌啶醇以剂量依赖性方式增加大鼠后腿对被动运动的肌肉阻力。肌肉僵硬伴随着这两块肌肉静息时以及牵张诱导的长潜伏期EMG活性(其中很可能涉及脊髓上反射)增加,而短潜伏期EMG活性(运动开始约9毫秒后开始的第一批大的EMG活性爆发,可能起源于脊髓)显著降低。所得结果表明,氟哌啶醇增加的MMG/EMG活性可能是帕金森病僵硬的一个良好模型。