IMPAIRED PERIPHERAL NERVE REGENERATION IN A MUTANT STRAIN OF MICE (ENR) WITH A SCHWANN CELL DEFECT

摘要: Schwann cell-axon interactions in the development, maintenance, and regeneration of normal peripheral nervous system are complex. A previously described transgene-induced insertional mutation (BPFD#36), now referred to as Enervated (Enr), results disrupted cell- axon interactions. In this report, after a crush or transection injury Enr nerves, we demonstrate impaired nerve regeneration. There fewer myelinated fibers per mm2 thinner myelin sheaths surrounding regenerating axons nerves homozygous mutant mice compared wild type at 28 d sciatic nerve. Abnormal remain Enr/Enr animals evidenced by relatively frequent ultrastructural finding unmyelinated large diameter nerves. Additionally, graft experiments indicate that impairment is due cell defect. Morphologic morphometric findings conjunction with molecular analysis suggest defect causes disruption ability “early ” cells differentiate more mature phenotype. 7 there similar levels mRNA for low-affinity growth factor receptor, but 11-fold less glial fibrillary acidic protein, phenotypic marker cells. This differentiation likely accounts both neuropathy observed mice.