Peripheral Demyelination and Neuropathic Pain Behavior in Periaxin-Deficient Mice
| Autor: | Ian R. Griffiths, Steven Tait, Diane L. Sherman, Emer M. Garry, C.Stewart Gillespie, Austin Smith, D. F. Cottrell, Peter J. Brophy, Jan Ure, Victoria C. J. Wallace, Susan M. Fleetwood-Walker |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Neuroscience(all)
PDZ domain Neural Conduction Pain Mice Myelin Demyelinating disease medicine Animals Humans Peripheral Nerves Mice Knockout Behavior Animal business.industry Mental Disorders General Neuroscience Membrane Proteins Peripheral Nervous System Diseases medicine.disease Axons Electrophysiology medicine.anatomical_structure nervous system Hyperalgesia Peripheral nervous system Neuropathic pain Somatosensory Disorders Reflex NMDA receptor Schwann Cells medicine.symptom business Excitatory Amino Acid Antagonists Neuroscience Demyelinating Diseases |
| Zdroj: | Neuron. 26:523-531 |
| ISSN: | 0896-6273 |
| DOI: | 10.1016/s0896-6273(00)81184-8 |
| Popis: | The Prx gene in Schwann cells encodes L- and S-periaxin, two abundant PDZ domain proteins thought to have a role in the stabilization of myelin in the peripheral nervous system (PNS). Mice lacking a functional Prx gene assemble compact PNS myelin. However, the sheath is unstable, leading to demyelination and reflex behaviors that are associated with the painful conditions caused by peripheral nerve damage. Older Prx −/− animals display extensive peripheral demyelination and a severe clinical phenotype with mechanical allodynia and thermal hyperalgesia, which can be reversed by intrathecal administration of a selective NMDA receptor antagonist. We conclude that the periaxins play an essential role in stabilizing the Schwann cell–axon unit and that the periaxin-deficient mouse will be an important model for studying neuropathic pain in late onset demyelinating disease. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|