Continued administration of GM1 ganglioside is required to maintain recovery from neuroleptic-induced sensorimotor deficits in MPTP-treated mice.
Continued administration of GM1 ganglioside is required to maintain recovery from neuroleptic-induced sensorimotor deficits in MPTP-treated mice.
复制标题
需要持续施用 GM1 神经节苷脂才能维持 MPTP 治疗小鼠从抗精神病药引起的感觉运动缺陷中恢复。
DOI：
10.1016/0024-3205(89)90017-9
复制
发表时间：
1989
期刊：
影响因子：
6.1
通讯作者：
Neff,NH
中科院分区：
文献类型：
--
作者：
Weihmuller,FB;Hadjiconstantinou,M;Bruno,JP;Neff,NH
Injection of a dose of haloperidol that has no obvious behavioral effects in normal mice, produces akinesia, catalepsy, and sensory neglect in MPTP- treated mice. Chronic GM1 ganglioside administration improves the behavioral impairments, partially restores striatal dopamine (DA) content and prevents DA D-2 receptor up-regulation. Discontinuation of GM1 ganglioside treatment results in a time-dependent decline of striatal DA content to pretreatment pathological levels, return of haloperidol-induced sensorimotor deficits and a rise of DA D-2 receptor density in the striatum. Apparently, continuous administration of GM1 ganglioside is necessary to maintain the biochemical and behavioral recovery in the MPTP-treated mouse. These observations may provide useful cues for understanding the mechanism of action of GM1 ganglioside.
