| First Author | DeLeo JA | Year | 2000 |
| Journal | Neuroreport | Volume | 11 |
| Issue | 3 | Pages | 599-602 |
| PubMed ID | 10718321 | Mgi Jnum | J:137903 |
| Mgi Id | MGI:3803385 | Doi | 10.1097/00001756-200002280-00033 |
| Citation | DeLeo JA, et al. (2000) Transgenic expression of TNF by astrocytes increases mechanical allodynia in a mouse neuropathy model. Neuroreport 11(3):599-602 |
| abstractText | 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 wild type mice. These data support a central role of glial expression of TNF in the generation of neuropathic pain. |
