Przedborski S, Wright M, Fahn S, Cadet J L
Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
Brain Res. 1989 Dec 18;504(2):311-4. doi: 10.1016/0006-8993(89)91375-9.
Chronic injection of iminodipropionitrile (IDPN) to rats causes persistent motor abnormalities such as hyperactivity, lateral and vertical dyskinesia of the neck, and random circling. These behavioral changes are very similar to those observed after the acute administration of serotonin (5-HT) agonists in rodents. Moreover, some aspects of this syndrome are reproduced by stimulation of 5-HT1A receptors. The present quantitative autoradiographic study revealed a number of changes in 8-hydroxy-2-[di-n-propylamino-3H]tetralin (8-OH[3H]DPAT)-labeled 5-HT1A receptors in the brains of IDPN-treated rats. There were significant increases of 8-OH[3H]DPAT binding in the frontal cortex and in the caudate-putamen. In contrast, there were significant decreases in the interpeduncular nucleus, the pyramidal layer of the CA3 field of hippocampus, the superior colliculus and the pars reticulata of the substantia nigra. These results provide further evidence for the involvement of the 5-HT system in the development of the IDPN-induced dyskinetic syndrome.
向大鼠慢性注射亚氨基二丙腈(IDPN)会导致持续的运动异常,如多动、颈部的侧向和垂直运动障碍以及随机转圈。这些行为变化与啮齿动物急性给予血清素(5-HT)激动剂后观察到的变化非常相似。此外,刺激5-HT1A受体可重现该综合征的某些方面。目前的定量放射自显影研究揭示了IDPN处理大鼠大脑中8-羟基-2-[二正丙基氨基-3H]四氢萘(8-OH[3H]DPAT)标记的5-HT1A受体的一些变化。额叶皮质和尾状核-壳核中的8-OH[3H]DPAT结合显著增加。相反,脚间核、海马CA3区锥体细胞层、上丘和黑质网状部中的结合显著减少。这些结果为5-HT系统参与IDPN诱导的运动障碍综合征的发展提供了进一步的证据。