Wallerian degeneration of spinal cord dorsal columns was produced in three dogs by unilateral extradural dorsal rhizotomy at the lower thoracic level. The spinal cord was studied 1 month, 2 months, and 3 months after surgery. Transverse cryostat sections at the site of rhizotomy and at the mid-thora
Sequential loss of myelin proteins during Wallerian degeneration in the rat spinal cord
โ Scribed by Armin Buss; Martin E. Schwab
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 654 KB
- Volume
- 42
- Category
- Article
- ISSN
- 0894-1491
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โฆ Synopsis
Abstract
Axotomy of nerve fibers leads to the subsequent degeneration of their distal part, a process termed Wallerian degeneration (WD). While WD in the peripheral nervous system is usually followed by regeneration of the lesioned axons, central nervous system (CNS) neurons are generally unable to regrow. In this study, we investigated the process of WD in the dorsal columns of the rat spinal cord rostral to a midโthoracic lesion. We confirm earlier studies describing a very delayed microglial and an early and sustained astroglial reaction finally leading to scar formation. Interestingly, we found a differential time course in the loss of myelin proteins depending on their location. Proteins situated on the periaxonal myelin membrane such as myelin associated glycoprotein disappeared early, within a few days after lesion, concomitantly with cytoskeletal axonal proteins, whereas compact myelin and outer myelin membrane proteins such as MBP and NogoโA remained for long intervals in the degenerating tracts. Two distinct mechanisms are probably responsible for this difference: processes of protein destruction emanating from and initially probably located in the axon act on a time scale of 1โ3 days. In contrast, the bulk of myelin destruction is due to phagocytosis known to be slow, prolonged, and inefficient in the CNS. These results may also have implications for future intervention strategies aiming at enhancing CNS regeneration. GLIA 42:424โ432, 2003. ยฉ 2003 WileyโLiss, Inc.
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