BASIC FIBROBLAST GROWTH-FACTOR (BFGF) INJECTION ACTIVATES THE GLIAL REACTION IN THE INJURED ADULT-RAT BRAIN

Citation
F. Eclancher et al., BASIC FIBROBLAST GROWTH-FACTOR (BFGF) INJECTION ACTIVATES THE GLIAL REACTION IN THE INJURED ADULT-RAT BRAIN, Brain research, 737(1-2), 1996, pp. 201-214
Citations number
72
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
737
Issue
1-2
Year of publication
1996
Pages
201 - 214
Database
ISI
SICI code
0006-8993(1996)737:1-2<201:BFG(IA>2.0.ZU;2-5
Abstract
Reactive gliosis is a reaction of glial cells to trauma which is chara cterized by a phenotypic modification of astrocytes, as well as by a p roliferation and a migration of some of these cells to form a glial sc ar. This scar is currently considered as a physical impediment to neur onal regrowth but it may also be involved in wound healing since the a strocytes beside microglia play a phagocytic role in the clearance of post-traumatic debris. Growth factors are released in the area of the injury and at least some of them could be involved in gliosis. In orde r to test directly this possibility, we have injected one of them, the basic fibroblast growth factor (bFGF), into several brain areas (cort ex, striatum, hippocampus or corpus calIosum) of adult 2-month-old rat s in the absence of lesion. A glial reaction was observed after 3 days and was maximum after 7 days. It was characterized by an increase in astrocyte proliferation and in glial fibrillary acidic protein (GFAP) expression, resulting in a higher number of GFAP-positive cells per su rface unit, and by an increase in the size and branching of the astrog lial processes. The GFAP mRNA levels were also strongly increased foll owing the bFGF injection. These effects resemble the reactive gliosis observed after lesion and suggest that bFGF is actually involved in th e triggering of glial reactions which follow brain injury. In further experiments, bFGF was injected in the site of electrolytic lesions mad e in the same various parts of the brain. These injections did not inc rease significantly the normal reactive gliosis induced by the lesion alone, but it accelerated some of the effects. It also resulted in a h igher labeling index and GFAP mRNA levels were strongly enhanced after a 3-day-post-operative delay. This last observation strengthens the i dea that one of the main factors driving the astrogliosis is the bFGF normally released in and around the site of the lesion.