Melamed E, Hefti F, Pettibone D J, Liebman J, Wurtman R J
Neurology. 1981 Jun;31(6):651-5. doi: 10.1212/wnl.31.6.651.
We studied the distribution of aromatic L-amino acid decarboxylase (AAAD) activity in striatal compartments of rats. After near-total destruction of nigrostriatal dopaminergic neurons, 15 to 20% of the initial enzyme activity remained. Striatal enzyme activity remained unchanged after destruction of serotoninergic terminals by electrolytic raphe lesions. Combined raphe-nigrostriatal lesions or nigrostriatal lesions alone produced similar decreases in striatal decarboxylase. Intrastriatal injection of kainic acid (which selectively destroys striatal interneurons and efferent neurons and also induces marked glial proliferation) reduced activity by 20%. Only 7% of initial striatal activity (perhaps localized in capillaries) remained after combined nigrostriatal-kainic acid lesions. These findings indicate that after degeneration of dopaminergic terminals, striatal interneurons and efferent neurons, but not serotonergic terminals of glia, contain an important fraction of the residual AAAD. This compartment may be the site of enzymatic conversion of exogenous L-dopa to dopamine in the parkinsonian striatum.
我们研究了大鼠纹状体各部分中芳香族L-氨基酸脱羧酶（AAAD）活性的分布。黑质纹状体多巴胺能神经元几乎完全被破坏后，仍保留了15%至20%的初始酶活性。通过电解中缝核损伤破坏5-羟色胺能终末后，纹状体酶活性保持不变。联合中缝核-黑质纹状体损伤或单独的黑质纹状体损伤导致纹状体脱羧酶出现类似程度的降低。纹状体内注射 kainic 酸（它选择性地破坏纹状体中间神经元和传出神经元，并诱导明显的胶质细胞增殖）使活性降低了20%。黑质纹状体-kainic 酸联合损伤后，仅保留了7%的初始纹状体活性（可能定位于毛细血管）。这些发现表明，在多巴胺能终末、纹状体中间神经元和传出神经元变性后，但不是胶质细胞的5-羟色胺能终末，含有残余AAAD的重要部分。这个部分可能是帕金森病纹状体中外源性左旋多巴酶促转化为多巴胺的部位。
