Sendtner M, Kreutzberg G W, Thoenen H
Department of Neurochemistry, Max-Planck-Institute for Psychiatry, Planegg-Martinsried, FRG.
Nature. 1990 May 31;345(6274):440-1. doi: 10.1038/345440a0.
The period of natural cell death in the development of rodent motor neurons is followed by a period of sensitivity to axonal injury. In the rat this early postnatal period of vulnerability coincides with that of very low ciliary neurotrophic factor (CNTF) levels in the sciatic nerve before CNTF increases to the high, adult levels. The developmental time course of CNTF expression, its regional tissue distribution and its cytosolic localization (as suggested by its primary structure) favour a role for CNTF as a lesion factor rather than a target-derived neurotrophic molecule like nerve growth factor. Nevertheless CNTF exhibits neurotrophic activity in vitro on different populations of embryonic neurons. To determine whether the vulnerability of motor neurons to axotomy in the early postnatal phase is due to insufficient availability of CNTF, we transected the axons of newborn rat motor neurons and demonstrated that local application of CNTF prevents the degeneration of the corresponding cell bodies.
啮齿动物运动神经元发育过程中的自然细胞死亡期之后是对轴突损伤敏感的时期。在大鼠中，这种出生后早期的脆弱期与坐骨神经中睫状神经营养因子（CNTF）水平极低的时期相吻合，之后CNTF才会升高到成年时的高水平。CNTF表达的发育时间进程、其区域组织分布及其胞质定位（由其一级结构表明）表明，CNTF作为一种损伤因子发挥作用，而不是像神经生长因子那样作为一种靶源性神经营养分子。然而，CNTF在体外对不同群体的胚胎神经元表现出神经营养活性。为了确定出生后早期运动神经元对轴突切断的易损性是否是由于CNTF供应不足所致，我们切断了新生大鼠运动神经元的轴突，并证明局部应用CNTF可防止相应细胞体的退化。
