Kryzhanovskiĭ G N, Shandra A A, Godlevskiĭ L S, Mazarati A M
Biull Eksp Biol Med. 1990 Aug;110(8):129-31.
It was shown in acute experiments on cats that electrical stimulation (ES) (100-300 Hz, 5.0-10.0 V) of cat's cerebellar vermal cortex (lobules V and VI) was followed by head deviation in the direction opposite to that side on which the animal was laying, posture and movement disturbances and also by simultaneously occurred contraction of musculus-antagonists of extremities. The tonic and posture disturbances were observed during 40-60 s after ES cessation. During this time in the zone of ES in cerebellar cortex the high-amplitude synchronized activity was registered which was due to generator of pathologically enhanced excitation (GPEE) formation. Intraperitoneal diazepam (0.5-1.0 mg/kg, 30 min before the observation) pretreatment suppressed GPEE formation that correlated with suppression of syndrome manifestations. The conclusion was made that cerebellar hyperactive cortex, which was due to GPEE induction, might have played the role of pathological hyperactive determinant structure of the described syndrome.
在对猫进行的急性实验中发现,对猫小脑蚓部皮质(V和VI小叶)进行电刺激(ES)(100 - 300 Hz,5.0 - 10.0 V)后,动物头部会向与躺卧侧相反的方向偏斜,出现姿势和运动障碍,同时四肢的拮抗肌会发生收缩。在停止电刺激后的40 - 60秒内可观察到强直性和姿势性障碍。在此期间,在小脑皮质的电刺激区域记录到高振幅同步活动,这是由于病理性增强兴奋发生器(GPEE)的形成所致。腹腔注射地西泮(0.5 - 1.0 mg/kg,观察前30分钟)预处理可抑制GPEE的形成,这与综合征表现的抑制相关。得出的结论是,由GPEE诱导引起的小脑皮质过度活跃可能在所述综合征的病理性过度活跃决定结构中起作用。