Hagg T, Varon S
Department of Biology, University of California, San Diego, La Jolla 92093-0601.
Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6315-9. doi: 10.1073/pnas.90.13.6315.
We have investigated the neuroprotective effects of recombinant human ciliary neurotrophic factor (CNTF) for injured dopaminergic neurons of the adult rat substantia nigra compacta. Fourteen days after a unilateral transection of the nigrostriatal pathway two-thirds of the neurons (identified by retrograde labeling) had degenerated. In sharp contrast, 73% (a few cases, > 90%) of this cell loss was prevented by continuous infusion of CNTF close to the injured neurons. However, CNTF did not prevent the disappearance of the transmitter-synthesizing enzyme tyrosine hydroxylase. Thus, CNTF has potent neurotrophic effects for injured adult rat dopaminergic substantia nigra neurons, whose degeneration plays a major causative role in Parkinson disease.
我们研究了重组人睫状神经营养因子(CNTF)对成年大鼠黑质致密部受损多巴胺能神经元的神经保护作用。在黑质纹状体通路单侧横断14天后,三分之二的神经元(通过逆行标记鉴定)发生了退化。与之形成鲜明对比的是,通过在受损神经元附近持续输注CNTF,可防止73%(少数情况,>90%)的这种细胞损失。然而,CNTF并不能阻止递质合成酶酪氨酸羟化酶的消失。因此,CNTF对成年大鼠受损的多巴胺能黑质神经元具有强大的神经营养作用,这些神经元的退化在帕金森病中起主要致病作用。