Nerve regeneration in Wlds mice is normalized by actinomycin D
| Autor: | Felipe A. Court, Jaime Alvarez |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Nerve Crush
Ratón Schwann cell Biology Mice Peripheral nerve medicine Animals Axon Molecular Biology Nucleic Acid Synthesis Inhibitors Dactinomycin General Neuroscience Anatomy Sciatic Nerve Axons Mice Mutant Strains Nerve Regeneration Cell biology Mice Inbred C57BL Microscopy Electron medicine.anatomical_structure nervous system Dactinomicina Nerve Degeneration Neuroglia Schwann Cells Neurology (clinical) Developmental Biology Sprouting medicine.drug |
| Zdroj: | Brain Research. 867:1-8 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/s0006-8993(00)02140-5 |
| Popis: | Injured nerves of Wld s mice neither degenerate nor regenerate for several weeks. We have conjectured that Wld s axons have the ability to regenerate but its expression is impaired by the Schwann cells of the undegenerated distal stump. To test this conjecture, transcription was locally arrested with actinomycin D (ActD), nerves were crushed, and regrowth was evaluated. In normal CD1 nerves injected with ActD 3 days before the crush, the rate of elongation was not affected but the delay of regrowth was shortened. In sharp contrast, ActD normalized the elongation of Wld s axons. When Wld s nerves were crushed past the treated segment, axons did not regenerate. After 7, but not 4, days of treatment, intact CD1 and Wld s axons presented a local sprouting response. We conclude that Wld s axons can regenerate in a normal way but do not do so because the undegenerated Schwann cells of the distal stump repress the regrowth program. We present a model axon that includes a destruction program and a post-transcriptional trophic regulation of its phenotype. |
| Databáze: | OpenAIRE |
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