Sanberg P R, Pevsner J, Autuono P G, Coyle J T
Neuropharmacology. 1985 Nov;24(11):1057-62. doi: 10.1016/0028-3908(85)90191-1.
Telencephalic hypoplasia induced by methylazoxymethanol acetate (MAM) resulted in increased activity of tyrosine hydroxylase in the striatum, indicative of a relative increase in the density of dopaminergic terminals in the remaining tissue. Administration of the dopamine receptor stimulant, apomorphine, or the receptor blocker, haloperidol, produced less stereotypy and catalepsy, respectively, in rats lesioned with methylazoxymethanol, compared to controls. These behavioral changes probably resulted from the loss of striatal perikarya and consequent decrease in nigrostriatal dopaminergic target sites caused by methylazoxymethanol.
由乙酸甲基氧化偶氮甲醇（MAM）诱导的端脑发育不全导致纹状体中酪氨酸羟化酶活性增加，这表明剩余组织中多巴胺能终末密度相对增加。与对照组相比，给予多巴胺受体兴奋剂阿扑吗啡或受体阻滞剂氟哌啶醇后，用甲基氧化偶氮甲醇损伤的大鼠分别表现出较少的刻板行为和僵住症。这些行为变化可能是由于甲基氧化偶氮甲醇导致纹状体神经元胞体丢失以及黑质纹状体多巴胺能靶位点随之减少所致。
