Axonal regeneration in experimental allergic peripheral neuritis.
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.
D000818:Animals; D001327:Autoimmune Diseases / Q000473:pathology*; D001369:Axons; D004195:Disease Models, Animal; D008297:Male; D009185:Myelin Proteins; D009416:Nerve Regeneration; D009443:Neuritis / Q000473:pathology*; D010587:Phagocytosis; D051381:Rats
D009185:Myelin Proteins