Kryzhanovskiĭ G N, Shandra A A, Godlevskiĭ L S, Mikhaleva I I
Biull Eksp Biol Med. 1990 Feb;109(2):119-21.
Bilateral microinjection of delta-sleep-inducing peptide (DSIP) (10.0 nmol) into the substantia nigra provoked hypokinesia and rigidity in rats observed during 4.0 hours. Injection of DSIP in dose of 5.0 nmol into the substantia nigra or into the nuclei caudati in dose of 10.0 nmol did not induce such symptoms. The enhanced slow-wave activity was recorded in caudate nuclei during hypokinesia and rigidity which demonstrated the formation of the generator of pathologically enhanced excitation (GPEE). The systemically cyclodol administration resulted in abolishment of rigidity and increase in locomotor activity. The conclusion is that bilateral intranigral DSIP injection caused acute parkinson syndrome in rats due to the formation of cholinergic GPEE in caudate nuclei. The hyperactive caudate nuclei act as the pathologic determinant which induces the parkinson syndrome.
向大鼠黑质双侧微量注射δ-睡眠诱导肽(DSIP)(10.0纳摩尔),在4.0小时内观察到大鼠出现运动减少和僵硬。向黑质注射5.0纳摩尔剂量的DSIP或向尾状核注射10.0纳摩尔剂量的DSIP均未诱发此类症状。在运动减少和僵硬期间,尾状核记录到慢波活动增强,这表明形成了病理性增强兴奋发生器(GPEE)。全身给予环苯扎林导致僵硬消失,运动活动增加。结论是,双侧黑质内注射DSIP由于尾状核中胆碱能GPEE的形成,导致大鼠急性帕金森综合征。活跃的尾状核作为诱发帕金森综合征的病理决定因素。