Hackenberg P
Psychopharmacology (Berl). 1980;70(1):105-8. doi: 10.1007/BF00432378.
Following previous histological studies on the problem of so-called psychopharmacotoxic encephalopathy, we have mesured the incorporation of 3-H-4.5 leucine into the limbic systm (Ncl. amygdaloideus lateralis, Gyrus dentatus) of ICR mice following haloperidol treatments (0.16 and 1.6 mg/kg/d) lasting 4 weeks and 4 months respectively. The results were compared with those obtained by treatment for 10 days. Protein-incorporated activity was significantly elevated throughout treatment, but there were no significant differences between the treated and control animals 4 weeks after treatment had ended. Although the mechanism causing the differences during treatment is unknown, the results show clearly that, although some tolerance is developed, even long-term haloperidol treatment is accompanied by alteration of the protein and or amino acid metabolism which can contribute to neuronal decompensation.
在先前关于所谓精神药物中毒性脑病问题的组织学研究之后，我们测量了在分别持续4周和4个月的氟哌啶醇治疗（0.16和1.6毫克/千克/天）后，3-H-4.5亮氨酸掺入ICR小鼠边缘系统（外侧杏仁核、齿状回）的情况。将结果与治疗10天所获得的结果进行比较。在整个治疗过程中，蛋白质掺入活性显著升高，但在治疗结束4周后，治疗组和对照组动物之间没有显著差异。虽然治疗期间导致差异的机制尚不清楚，但结果清楚地表明，尽管产生了一些耐受性，但即使是长期氟哌啶醇治疗也伴随着蛋白质和/或氨基酸代谢的改变，这可能导致神经元失代偿。
