Intracisternal basic fibroblast growth factor (bFGF) enhances behavioral recovery following focal cerebral infarction in the rat

被引:141
|
作者
Kawamata, T
Alexis, NE
Dietrich, WD
Finklestein, SP
机构
[1] MASSACHUSETTS GEN HOSP EAST, CNS, GROWTH FACTOR RES LAB, DEPT NEUROL, CHARLESTOWN, MA 02129 USA
[2] MASSACHUSETTS GEN HOSP EAST, CNS, GROWTH FACTOR RES LAB, DEPT NEUROSURG, CHARLESTOWN, MA 02129 USA
[3] UNIV MIAMI, SCH MED, DEPT NEUROL, CEREBRAL VASC DIS RES CTR, MIAMI, FL USA
来源
关键词
basic fibroblast growth factor; cerebral infarction; behavior; recovery;
D O I
10.1097/00004647-199607000-00003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Basic fibroblast growth factor (bFGF) is a potent neurotrophic agent that promotes neuronal survival and outgrowth. Previous studies have shown that bFGF, administered intraventricularly or intravenously before or within hours after ischemia, reduces infarct size and neurological deficits in models of focal cerebral ischemia in rats. In the current study, we tested the hypothesis that bFGF, administered at later time points after ischemia, might improve behavioral recovery without affecting infarct size. Mature Sprague-Dawley rats received bFGF(I mu g/injection) or vehicle by biweekly intracisternal injection for 4 weeks, starting at 1 day following permanent proximal middle cerebral artery (MCA) occlusion. Animals were examined every other day using four different behavioral tests to assess sensorimotor and reflex function. At 4 weeks after ischemia, there was no difference in infarct volume between bFGF- and vehicle-treated animals. There was, however, an enhancement in the rate and degree of behavioral recovery among bFGF-treated animals, as measured by all four tests. There were no apparent side effects of bFGF treatment, except that bFGF-treated animals tended to recover body weight more slowly than did vehicle-treated animals following stroke. The mechanisms of enhancement of behavioral recovery by bFGF require further study, but may include protection against retrograde neuronal death and/or stimulation of neuronal sprouting.
引用
收藏
页码:542 / 547
页数:6
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