Mervart M, Kiernan J A
Acta Neuropathol. 1978 Mar 15;41(3):197-200. doi: 10.1007/BF00690435.
It has recently been suggested that severed axons fail to regenerate in the mammalian central nervous system as a result of an autoimmune reaction to myelin basic protein released into the circulation at the time of injury. Since the autoantigenic components of peripheral myelin are rapidly phagocytosed after axonal transection, it is claimed that a comparable immune response does not occur following injury to peripheral nerves, so the regenerative process is not hindered. If this contention is correct, it should be possible to inhibit the regeneration of peripheral axons by inoculating animals with suitable neuritogenic homogenates of peripheral nervous tissue. It has been shown that axonal regneration proceeds at the same rate in rats with experimental allergic neuritis as in healthy controls inoculated only with Freund's adjuvant. It is unlikely, therefore, that myelin basic proteins can stimulate the production of antibodies capable of inhibiting regenerative axonal growth.
最近有人提出,在哺乳动物中枢神经系统中,切断的轴突无法再生是由于对损伤时释放到循环系统中的髓鞘碱性蛋白产生自身免疫反应所致。由于轴突横断后外周髓鞘的自身抗原成分会迅速被吞噬,因此有人声称,外周神经损伤后不会发生类似的免疫反应,所以再生过程不会受到阻碍。如果这一论点正确,那么通过给动物接种合适的外周神经组织神经原性匀浆,应该能够抑制外周轴突的再生。研究表明,患有实验性过敏性神经炎的大鼠的轴突再生速度与仅接种弗氏佐剂的健康对照组相同。因此,髓鞘碱性蛋白不太可能刺激产生能够抑制轴突再生生长的抗体。