Dubový P, Aldskogius H
Department of Anatomy, Medical Faculty, Brno, Czech Republic.
Microsc Res Tech. 1996 Jul 1;34(4):362-75. doi: 10.1002/(SICI)1097-0029(19960701)34:4<362::AID-JEMT7>3.0.CO;2-Q.
Auxiliary structures of the cutaneous sensory nerve formations (SNF) are dependent on sensory innervation during their critical period of development. Denervation of mature cutaneous corpuscles results in survival of the terminal Schwann cells and the capsular structures which are probably responsible for successful reinnervation of the cutaneous SNF. In addition, the basal lamina tubes of Schwann cells are connected with the terminal Schwann cells and play an important role in the guidance of regrowing axons to their original targets. Long-lasting denervation causes atrophic changes of the terminal Schwann cells and alterations of their molecular equipment. These atrophic changes in the terminal Schwann cells may be responsible for erroneous reinnervation of cutaneous SNF. A population of the cutaneous Merkel cells surviving denervation may also serve as targets for regrowing sensory axons. The basal laminae of terminal Schwann cells are produced under control of the sensory terminals during maturation of cutaneous SNF. In adult animals, the basal laminae are capable of stimulating differentiation of migrated Schwann cells to the terminal Schwann cells without the presence of the sensory terminals. Nonspecific cholinesterase (nChE) is secreted by the terminal Schwann cells and is attached to their extracellular matrix. The synthesis of these molecules in adult animals is not influenced by the sensory terminals. However, the presence of nChE molecules is associated with living terminal Schwann cells. Fetal orthotopically grafted dorsal root ganglion (DRG) neurons have the ability to reinnervate cutaneous SNF of adult hosts. When cutaneous areas are denervated, axons from adjacent sensory nerves may extend collateral branches into this area. The capacity for such extension is dependent on: (1) type of sensory nerve ending, C and A delta fibers having significantly greater capacity than sensory axons of larger caliber; (2) age of the animal, immature animals generally showing a greater capacity for collateral sprouting; (3) the state of the adjacent axons, those already in a growth mode being more capable than "resting" ones; and (4) the regional and mechanical conditions at the site of denervation, hindpaw skin being much less extensively reinnervated by collateral fibers than that of the trunk.
皮肤感觉神经结构(SNF)的辅助结构在其发育关键期依赖于感觉神经支配。成熟皮肤小体去神经支配会导致终末施万细胞和被膜结构存活,这些结构可能是皮肤SNF成功重新神经支配的原因。此外,施万细胞的基膜管与终末施万细胞相连,在引导再生轴突回到其原始靶点方面发挥重要作用。长期去神经支配会导致终末施万细胞发生萎缩性变化及其分子装备改变。终末施万细胞的这些萎缩性变化可能是皮肤SNF错误重新神经支配的原因。一群在去神经支配后存活的皮肤默克尔细胞也可能成为感觉轴突再生的靶点。终末施万细胞的基膜在皮肤SNF成熟过程中受感觉终末控制产生。在成年动物中,基膜能够在没有感觉终末的情况下刺激迁移的施万细胞分化为终末施万细胞。非特异性胆碱酯酶(nChE)由终末施万细胞分泌并附着于其细胞外基质。成年动物中这些分子的合成不受感觉终末影响。然而,nChE分子的存在与存活的终末施万细胞相关。胎儿原位移植的背根神经节(DRG)神经元有能力重新神经支配成年宿主的皮肤SNF。当皮肤区域去神经支配时,来自相邻感觉神经的轴突可能会延伸侧支进入该区域。这种延伸能力取决于:(1)感觉神经末梢类型,C纤维和Aδ纤维的能力明显大于较大口径的感觉轴突;(2)动物年龄,未成熟动物通常侧支发芽能力更强;(3)相邻轴突的状态,已处于生长模式的轴突比“静止”轴突更有能力;(4)去神经支配部位的局部和机械条件,后爪皮肤通过侧支纤维重新神经支配的范围比躯干皮肤小得多。