Weihmuller F B, Hadjiconstantinou M, Bruno J P
Department of Psychology, College of Social and Behavioral Sciences, Ohio State University, Columbus 43210.
Pharmacol Biochem Behav. 1989 Sep;34(1):113-7. doi: 10.1016/0091-3057(89)90362-6.
Injection of a low dose of haloperidol, that has no obvious behavioral effects in normal mice, produces akinesia, catalepsy, and somatosensory neglect in MPTP-treated mice. These neuroleptic-induced sensorimotor impairments are exhibited soon after MPTP treatments and coincide with a decrease in both striatal DA and DOPAC levels. DA and DOPAC content gradually return to near-control levels over a 3-5 month period. Interestingly, while the haloperidol-induced somatosensory deficits declined in parallel with the rise in DA and DOPAC levels, the motor deficits persisted for up to 5 months after MPTP administration. These data suggest subtle differences in the neurochemical mediation of these behaviors and that the persistence of neuronal impairments may not necessarily be revealed by near-normal transmitter levels.
注射低剂量的氟哌啶醇，在正常小鼠中不会产生明显的行为影响，但在经MPTP处理的小鼠中会导致运动不能、僵住症和躯体感觉忽视。这些抗精神病药物诱导的感觉运动障碍在MPTP处理后很快出现，并且与纹状体中多巴胺（DA）和3,4-二羟基苯乙酸（DOPAC）水平的降低同时发生。DA和DOPAC含量在3至5个月的时间内逐渐恢复到接近对照水平。有趣的是，虽然氟哌啶醇诱导的躯体感觉缺陷与DA和DOPAC水平的升高平行下降，但运动缺陷在MPTP给药后持续长达5个月。这些数据表明这些行为的神经化学介导存在细微差异，并且神经元损伤的持续存在不一定通过接近正常的递质水平来揭示。
