期刊
JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM
卷 16, 期 4, 页码 277-286出版社
WILEY
DOI: 10.1111/j.1529-8027.2011.00362.x
关键词
axonal transport; glia; nerve; neuropathy; pain; Schwann cell; spinal cord; TNF-a
资金
- NIDCR NIH HHS [R01 DE022757] Funding Source: Medline
- BLRD VA [I01 BX000638] Funding Source: Medline
This 2011 Peripheral Nerve Society plenary lecture reviews the role of axonal transport in neuroimmune communication following peripheral nerve injury, linking focal changes in Schwann cell activation and release of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-a) with subsequent activation and sensitization of ascending sensory neurons and glia which culminate in the neuropathic pain state. New data demonstrate that axonally transported (biotinylated) TNF-a activates and localizes with dorsal horn astrocytes within 96 h after injection into sciatic nerve, and that glial fibrillary acidic protein (GFAP) activation in these glial cells is diminished in TNF receptor 1 knockout mice. The pathophysiology, neuropathology and molecular biology of Wallerian degeneration are also reviewed from a perspective that links it to upregulation of proinflammatory cytokines and the development of neuropathic pain states. Finally, insights into neuroimmune communication provide rationale for new therapy based on interference with the processes of Wallerian degeneration, cytokine signaling and TNF-a protein sequestration.
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