Thanos S
Max-Planck Institut für Entwicklungsbiologie, Tübingen, Federal Republic of Germany.
Cell Tissue Res. 1988;254(3):599-609. doi: 10.1007/BF00226510.
Transected ganglion cell axons from the adult retina are capable of reinnervating their central targets by growing into transplanted peripheral nerve (PN) segments. Injury of the optic nerve causes various metabolic and morphological changes in the retinal ganglion cell (RGC) perikarya and in the dendrites. The present work examined the dendritic trees of those ganglion cells surviving axotomy and of those whose served axons re-elongated in PN grafts to reach either the superior colliculus (SC), transplanted SC, or transplanted autologous thigh muscle. The elaboration of the dendritic trees was visualized by means of the strongly fluorescent carbocyanine dye DiI, which is taken up by axons and transported to the cell bodies and from there to the dendritic branches. Alternatively, retinofugal axons regrowing through PN grafts were anterogradely filled from the eye cup with rhodamine B-isothiocyanate. The transection of the optic nerve resulted in characteristic changes in the ganglion cell dendrites, particularly in the degeneration of most of the terminal and preterminal dendritic branches. This occurred within the first 1 to 2 weeks following axotomy. The different types of ganglion cells appear to vary in their sensitivity to axotomy, as reflected by a rapid degeneration of certain cell dendrites after severance of the optic nerve. The most vulnerable cells were those with small perikarya and small dendritic fields (type II), whereas larger cells with larger dendritic fields (type I and III) were slower to respond and less dramatically affected. Regrowth of the lesioned axons in peripheral nerve grafts and reconnection of the retina with various tissues did not result in a significant immediate recovery of ganglion cell dendrites, although it did prevent some axotomized cells from further progression toward posttraumatic cell death.
成年视网膜横断的神经节细胞轴突能够通过生长进入移植的外周神经(PN)段来重新支配其中枢靶标。视神经损伤会导致视网膜神经节细胞(RGC)胞体和树突发生各种代谢和形态变化。本研究检查了轴突切断后存活的神经节细胞以及其轴突在PN移植物中重新伸长以到达上丘(SC)、移植的SC或移植的自体大腿肌肉的神经节细胞的树突。通过强荧光碳青霉烯染料DiI观察树突的形成,DiI被轴突摄取并运输到细胞体,再从那里运输到树突分支。另外,通过PN移植物再生的视网膜神经纤维轴突从眼杯向前用异硫氰酸罗丹明B填充。视神经横断导致神经节细胞树突发生特征性变化,特别是大多数终末和终末前树突分支的退化。这发生在轴突切断后的第1至2周内。不同类型的神经节细胞对轴突切断的敏感性似乎不同,这表现为视神经切断后某些细胞树突的快速退化。最易受损的细胞是那些胞体小且树突野小的细胞(II型),而胞体大且树突野大的细胞(I型和III型)反应较慢且受影响较小。外周神经移植物中受损轴突的再生以及视网膜与各种组织的重新连接并没有导致神经节细胞树突立即显著恢复,尽管它确实阻止了一些轴突切断的细胞进一步发展为创伤后细胞死亡。