Kryzhanovskiĭ G N, Atadzhanov M A, Kucherianu V G
Biull Eksp Biol Med. 1990 Sep;110(9):242-4.
The aim of this study was to investigate the effect of difenin on parkinsonian syndrome and the generator of pathologically enhanced excitation (GPEE) in the caudata nuclei (CN). Repeated i. p. administration of MPTP in 12 month rats induced oligokinesis and rigidity followed by the high amplitude slow and rapid waves in the CN and in sensorimotor cortex (SC). The changes of the electrical activity in the CN were more prominent then in SC. I.p. injection of difenin (20 mg/kg) resulted in an increase of motor activity and decrease of rigidity in rats. The reduction of extrapyramidal symptoms were correlated with at the inhibition of GPEE in the CN. These data suggest that difenin can be a part of the complex pathogenetic therapy of parkinsonian syndrome.
本研究旨在探讨二苯宁对帕金森综合征及尾状核中病理性增强兴奋产生器（GPEE）的影响。对12月龄大鼠反复腹腔注射MPTP可诱发运动减少和僵硬，随后尾状核和感觉运动皮层出现高幅慢波和快波。尾状核电活动的变化比感觉运动皮层更显著。腹腔注射二苯宁（20mg/kg）可使大鼠运动活性增加，僵硬程度降低。锥体外系症状的减轻与尾状核中GPEE的抑制相关。这些数据表明，二苯宁可成为帕金森综合征综合病因治疗的一部分。
