Berry M, Hall S, Rees L, Carlile J, Wyse J P
Division of Anatomy and Cell Biology, United Medical School, London, UK.
J Neurocytol. 1992 Jun;21(6):426-48. doi: 10.1007/BF01191507.
We have studied the regeneration of axons in the optic nerves of the BW rat in which both oligodendrocytes and CNS myelin are absent from a variable length of the proximal (retinal) end of the nerve. In the optic nerves of some of these animals, Schwann cells are present. Axons failed to regenerate in the exclusively astrocytic environment of the unmyelinated segment of BW optic nerves but readily regrew in the presence of Schwann cells even across the junctional zone and into the myelin debris filled distal segment. In the latter animals, the essential condition for regeneration was that the lesion was sited in a region of the nerve in which Schwann cells were resident. Regenerating fibres appeared to be sequestered within Schwann cell tubes although fibres traversed the neuropil intervening between the ends of discontinuous bundles of Schwann cell tubes, in both the proximal unmyelinated and myelin debris laden distal segments of the BW optic nerve. Regenerating axons never grew beyond the distal point of termination of the tubes. These observations demonstrate that central myelin is not an absolute requirement for regenerative failure, and that important contributing factors might include inhibition of astrocytes and/or absence of trophic factors. Regeneration presumably occurs in the BW optic nerve because trophic molecules are provided by resident Schwann cells, even in the presence of central myelin, oligodendrocytes and astrocytes. All the above experimental BW animals also have Schwann cells in their retinae which myelinate retinal ganglion cell axons in the fibre layer. Control animals comprised normal Long Evans Hooded rats, BW rats in which both retina and optic nerve were normal, and BW rats with Schwann cells in the retina but with normal, i.e. CNS myelinated, optic nerves. Regeneration was not observed in any of the control groups, demonstrating that, although the presence of Schwann cells in the retina may enhance the survival of retinal ganglion cells after crush, concomitant regrowth of axons cut in the optic nerve does not take place.
我们研究了BW大鼠视神经中轴突的再生情况。在这些大鼠中，神经近端（视网膜端）的不同长度区域内，少突胶质细胞和中枢神经系统髓磷脂均缺失。在其中一些动物的视神经中，存在施万细胞。在BW视神经无髓鞘段仅由星形胶质细胞构成的环境中，轴突无法再生，但在有施万细胞存在的情况下，轴突能够轻易再生，甚至能穿过连接区并长入充满髓磷脂碎片的远端段。在后者这些动物中，再生的必要条件是损伤位于神经中存在施万细胞的区域。再生纤维似乎被隔离在施万细胞管内，尽管纤维穿过了BW视神经近端无髓鞘段和充满髓磷脂碎片的远端段中不连续的施万细胞管束两端之间的神经毡。再生轴突从未生长到施万细胞管的远端终止点之外。这些观察结果表明，中枢髓磷脂并非再生失败的绝对必要条件，重要的促成因素可能包括星形胶质细胞的抑制和/或营养因子的缺乏。推测BW视神经中发生再生是因为即使存在中枢髓磷脂、少突胶质细胞和星形胶质细胞，驻留的施万细胞也能提供营养分子。上述所有实验用的BW动物视网膜中也有施万细胞，这些施万细胞在纤维层中为视网膜神经节细胞轴突形成髓鞘。对照动物包括正常的长 Evans 戴帽大鼠、视网膜和视神经均正常的BW大鼠，以及视网膜中有施万细胞但视神经正常（即由中枢神经系统髓鞘化）的BW大鼠。在任何对照组中均未观察到再生现象，这表明尽管视网膜中存在施万细胞可能会提高视网膜神经节细胞在挤压伤后的存活率，但视神经切断后轴突并不会随之再生。
