| First Author | Chen S | Year | 1993 |
| Journal | J Comp Neurol | Volume | 335 |
| Issue | 4 | Pages | 576-85 |
| PubMed ID | 8227536 | Mgi Jnum | J:14468 |
| Mgi Id | MGI:62636 | Doi | 10.1002/cne.903350409 |
| Citation | Chen S, et al. (1993) Long-term consequences of impaired regeneration on facial motoneurons in the C57BL/Ola mouse. J Comp Neurol 335(4):576-85 |
| abstractText | Peripheral nerves of the C57BL/Ola mouse mutant undergo markedly slowed Wallerian degeneration following injury. This is associated with impaired regeneration of both sensory and motor axons. Following a crush lesion of the facial nerve, there was no cell loss in facial nuclei of normal (C57BL/6J) adult mice, but 40% cell loss occurred in Ola mice and the survivors increased in size during the period when functional reinnervation was established. These results are interpreted as a result, first, of prolonged deprivation of target-derived trophic factor in the slowly regenerating Ola motoneurons and second, increased peripheral field size of the survivors. Within the regenerated facial nerve, there was marked heterogeneity of myelinated fibre size in Ola mice. Some Ola axons, both proximal and distal to the lesion site, had areas over twice as great as the largest 6J axons when measured 1 year following injury. A population of small diameter fibres, not observed in 6J nerves, persisted distal to the crush site in Ola nerves, and this was associated with an increase in the total number of myelinated axons in the distal nerve: on average, each parent Ola axon retained three persistent daughter axons. The delayed Wallerian degeneration in Ola mice not only impairs immediate axon regrowth, but also results in a breakdown of the normal mechanisms which regulate axon number and size in regenerating nerve. |
