A traumatic injury to the rat brain is known to induce astrocyte proli
feration and hypertrophy leading to astrogliosis. In addition, trauma
also induces microglial proliferation in the brain. Since basic fibrob
last growth factor (bFGF) is believed to play a role in mediating glia
l responses to brain injury, we examined the effects of bFGF administr
ation on astrocyte and microglial proliferation and astrocyte hypertro
phy resulting from a traumatic injury to the rat brain. Intracerebrove
ntricular infusion of bFGF for 2 days prior to and following injury fa
iled to alter glial reactivity. In contrast, a single intralesion inje
ction of bFGF immediately after injury increased total cell. division
2 and 5 days later, with an exclusive effect on glial fibrillary acidi
c protein-negative glia which consisted mostly of cells of macrophage-
microglial phenotype. In addition, bFGF also enhanced injury-induced a
strocyte hypertrophy. These results support a role for bFGF in macroph
age-microglia proliferation and astrocyte hypertrophy following brain
injury. They also suggest that alteration of injury responses of nonne
uronal cells of the brain may be a potential side effect of intracereb
ral administration of bFGF. (C) 1994 Academic Press, Inc.