Journal
NEUROREPORT
Volume 11, Issue 3, Pages 599-602Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200002280-00033
Keywords
glial fibrillary acidic protein (GFAP); neuropathic pain; proinflammatory cytokines; von Frey filaments
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Funding
- NIDA NIH HHS [DA11276] Funding Source: Medline
- NIMH NIH HHS [MH50426] Funding Source: Medline
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It has been hypothesized that increased expression of proinflammatory cytokines mediate a variety of central nervous system disorders such as multiple sclerosis, Alzheimer's disease, cerebral ischemia, spinal cord injury, HIV encephalopathy and chronic pain. In order to further examine the central role of TNF in neuropathic pain, transgenic mice were used in which expression of murine TNF was targeted to astrocytes using a glial fibrillary acidic protein (GFAP)-TNF fusion gene. Spinal nerve (L5) transection was performed in either the GFAP-TNF transgenic or wild type mice. Mechanical allodynia was significantly enhanced in the GFAP-TNF transgenic mice compared with the wildtype mice. These data support a central role of glial expression of TNF in the generation of neuropathic pain. NeuroReport 11:599-602 (C) 2000 Lippincott Williams & Wilkins.
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