Csillik B, Schwab M E, Thoenen H
Brain Res. 1985 Apr 1;331(1):11-5. doi: 10.1016/0006-8993(85)90709-7.
Blockade of axonal transport or transection of the rat sciatic nerve results in transganglionic degenerative atrophy (TDA) of nerve terminals containing fluoride-resistant acid phosphatase (FRAP) in the Rolando substance of the spinal cord. Application of vinblastine (9 micrograms) in a cuff around the sciatic nerve of adult rats blocked the retrograde transport of [125I]NGF in sensory fibers; this amount of vinblastine is identical to the threshold amount that induces TDA. Conversely, application of NGF to the proximal stump of the transected sciatic nerve prevented or delayed the occurrence of TDA as reflected by the maintenance of FRAP in the upper dorsal horn, that otherwise would inevitably disappear following the peripheral nerve lesion. These results suggest that endogenous NGF transported retrogradely in peripheral sensory fibers of the adult rat under normal conditions may be responsible for the regulation of the structural and functional integrity of the central terminals of these FRAP-containing primary sensory neurons and that TDA may be the consequence of the failure of NGF to reach the perikarya of these neurons.
阻断轴突运输或切断大鼠坐骨神经会导致脊髓罗氏物质中含有耐氟酸性磷酸酶(FRAP)的神经终末发生跨节段性变性萎缩(TDA)。在成年大鼠坐骨神经周围的袖带中应用长春碱(9微克)可阻断[125I]神经生长因子(NGF)在感觉纤维中的逆行运输;这个长春碱用量与诱导TDA的阈值量相同。相反,将NGF应用于切断的坐骨神经近端残端,可防止或延迟TDA的发生,这表现为上背角中FRAP的维持,否则在周围神经损伤后FRAP会不可避免地消失。这些结果表明,在正常条件下成年大鼠外周感觉纤维中逆行运输的内源性NGF可能负责调节这些含FRAP的初级感觉神经元中央终末的结构和功能完整性,并且TDA可能是NGF无法到达这些神经元胞体的结果。