Worms P, Willigens M T, Continsouza-Blanc D, Lloyd K G
Eur J Pharmacol. 1985 Jul 11;113(1):53-9. doi: 10.1016/0014-2999(85)90342-5.
The effect of bilateral lesions of various cortical areas on neuroleptic- and non-neuroleptic-induced catalepsy was studied in the rat. Ablation of the frontal or parietal cortex led to a marked decrease in haloperidol catalepsy, whereas lesions of the occipital cortex, or of the olfactory bulbs did not affect catalepsy, when measured 3 weeks post lesion in all cases. The frontal cortex lesions also diminished the cataleptic state induced by cis-flupenthixol, (+)-butaclamol and chlorpromazine, but failed to affect that induced by reserpine, tetrabenazine or morphine. Four months after the frontal lesions, haloperidol catalepsy was at control values, and a rebound phenomenon was observed at 10 months post lesion. The homeostatic mechanisms seem to have stabilized at 18 months post lesion when haloperidol catalepsy had returned to control levels.
研究了大鼠双侧不同皮质区域损伤对神经阻滞剂和非神经阻滞剂诱发的僵住症的影响。额叶或顶叶皮质切除导致氟哌啶醇诱发的僵住症显著降低,而枕叶皮质或嗅球损伤在所有病例损伤后3周测量时均不影响僵住症。额叶皮质损伤也减弱了顺式氟奋乃静、(+)-布他拉莫和氯丙嗪诱发的僵住状态,但对利血平、丁苯那嗪或吗啡诱发的僵住状态没有影响。额叶损伤4个月后,氟哌啶醇诱发的僵住症恢复到对照值,损伤后10个月观察到反弹现象。当氟哌啶醇诱发的僵住症恢复到对照水平时,稳态机制似乎在损伤后18个月已稳定。