Nerve transplantation shows that motor end-plate disease is not a primary Schwann cell defect.
Motor end-plate diseased (MED) mice have altered nerve impulse conduction velocities and refractory periods. To test whether these pathological properties are caused by a primary Schwann cell defect, nerves were transplanted from MED and wildtype (WT) animals onto WT recipients. The donor origin of cells in the regenerated nerve was assessed by prelabeling with [3H]thymidine and by electrophoretic analysis of glucose phosphate isomerase allotypes. Nerve fiber regeneration through MED and WT implants was equally efficient. No difference was found in nerve conductivities of MED and WT grafts. Therefore a primary defect in the Schwann cells of the MED mouse is unlikely.
D000200:Action Potentials; D000818:Animals; D051379:Mice; D008818:Mice, Neurologic Mutants; D009045:Motor Endplate / Q000503:physiopathology; D009046:Motor Neurons / Q000502:physiology* / Q000637:transplantation; D009416:Nerve Regeneration; D009431:Neural Conduction; D009468:Neuromuscular Diseases / Q000503:physiopathology*; D010525:Peripheral Nerves / Q000503:physiopathology* / Q000637:transplantation; D012032:Refractory Period, Electrophysiological; D012583:Schwann Cells / Q000502:physiology* / Q000637:transplantation; D012584:Sciatic Nerve / Q000503:physiopathology