Alterations in fibroblast growth factor receptor expression following brain injury.

Traumatic injuries to the central nervous system result in astrogliosis and the formation of a dense scar at the site of the wound. Basic fibroblast growth factor (bFGF) has mitogenic and morphogenic effects on astrocytes, and an interaction between bFGF and its receptor is likely to play a role in astrogliosis. We examined trauma-induced changes in the spatial and temporal expression of FGF receptor (FGFR) in adult rats over a 28-day period following a stereotaxic lesion through the cortex and hippocampus. Immunohistochemistry and image analysis were used to evaluate the changes. Antibody characterization studies strongly suggested that staining represented FGFR 1, but did not rule out possible cross-reactivity with FGFR 2 or 3. Double immunohistochemistry for FGFR and glial fibrillary acidic protein demonstrated that mature astrocytes expressed FGFR. Expression was increased on astrocytes adjacent to the wound cavity by Day 2 postlesion. Staining increased further through Day 10 and decreased to control values by Day 28, except for a sustained increase in staining of reactive astrocytes immediately adjacent to the wound cavity. Basic FGF was detected in the nuclei of cells staining for FGFR, suggesting that FGFR-expressing astrocytes also contained bFGF. These data demonstrate a time course for astrocyte expression of FGFR that precedes and parallels the time course for astrocyte hypertrophy. Our observations suggest that endogenous bFGF, acting directly on FGFR-expressing astrocytes, may contribute to astrogliosis.