Johansson P
Psychiatric Research Center, University of Uppsala, Sweden.
Psychopharmacology (Berl). 1990;100(1):72-6. doi: 10.1007/BF02245793.
The effects of methylazoxymethanol (MAM)-induced brain lesions on vacuous chewing movements (VCM) were examined in rats given chronic haloperidol treatment (0.1 or 1 mg/kg/day) for 18 months. At the end of the experiment striatal, pallidal, and nigral activities of glutamate decarboxylase (GAD) were measured. MAM-lesioned rats had an elevated rate of VCMs compared to unlesioned controls. This effect was stable during the whole 18-month experiment. In unlesioned control rats chronic haloperidol produced a gradual increase in VCM rates, but this effect was not further exacerbated in MAM-lesioned animals. After chronic haloperidol treatment with the higher dose (1 mg/kg/day) GAD activity was reduced in substantia nigra (-20%), globus pallidus (-35%), and striatum (-26%) of unlesioned rats. MAM caused a reduction of GAD activity in substantia nigra (-29%) and globus pallidus (-29%). Chronic haloperidol did not influence these effects of MAM-induced lesion. The present results show that a MAM-induced brain lesion, in contrast to cortical ablations, cannot be used to amplify the haloperidol-induced VCM increase or influence the nigral GAD activity in a rat model for tardive dyskinesia.
在接受为期18个月的慢性氟哌啶醇治疗（0.1或1毫克/千克/天）的大鼠中，研究了甲基偶氮甲醇（MAM）诱导的脑损伤对空嚼运动（VCM）的影响。实验结束时，测量了纹状体、苍白球和黑质中谷氨酸脱羧酶（GAD）的活性。与未损伤的对照组相比，MAM损伤的大鼠VCM发生率升高。在整个18个月的实验过程中，这种效应是稳定的。在未损伤的对照大鼠中，慢性氟哌啶醇使VCM发生率逐渐增加，但在MAM损伤的动物中，这种效应并未进一步加剧。在用较高剂量（1毫克/千克/天）的慢性氟哌啶醇治疗后，未损伤大鼠的黑质（-20%）、苍白球（-35%）和纹状体（-26%）中GAD活性降低。MAM导致黑质（-29%）和苍白球（-29%）中GAD活性降低。慢性氟哌啶醇不影响MAM诱导损伤的这些效应。目前的结果表明，与皮质切除不同，MAM诱导的脑损伤不能用于放大氟哌啶醇诱导的VCM增加或影响迟发性运动障碍大鼠模型中的黑质GAD活性。
