title: Basic fibroblast growth factor (bFGF) injection activates the glial reaction in the injured adult rat brain.
abstract: Reactive gliosis is a reaction of glial cells to trauma which is characterized by a phenotypic modification of astrocytes, as well as by a proliferation and a migration of some of these cells to form a glial scar. This scar is currently considered as a physical impediment to neuronal regrowth but it may also be involved in wound healing since the astrocytes 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 order to test directly this possibility, we have injected one of them, the basic fibroblast growth factor (bFGF), into several brain areas (cortex, striatum, hippocampus or corpus callosum) of adult 2-month-old rats 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 surface unit, and by an increase in the size and branching of the astroglial processes. The GFAP mRNA levels were also strongly increased following the bFGF injection. These effects resemble the reactive gliosis observed after lesion and suggest that bFGF is actually involved in the triggering of glial reactions which follow brain injury. In further experiments, bFGF was injected in the site of electrolytic lesions made in the same various parts of the brain. These injections did not increase significantly the normal reactive gliosis induced by the lesion alone, but it accelerated some of the effects. It also resulted in a higher labeling index and GFAP mRNA levels were strongly enhanced after a 3-day-post-operative delay. This last observation strengthens the idea that one of the main factors driving the astrogliosis is the bFGF normally released in and around the site of the lesion.
authors.affiliation: Laboratoire de Neurobiologie Ontogénique, Centre de Neurochimie du CNRS, Strasbourg, France.
authors.forename: F
authors.initials: F
authors.lastname: Eclancher
authors.forename: P
authors.initials: P
authors.lastname: Kehrli
authors.forename: G
authors.initials: G
authors.lastname: Labourdette
authors.forename: M
authors.initials: M
authors.lastname: Sensenbrenner
mesh_terms: D000818:Animals; D000918:Antibody Specificity; D001253:Astrocytes / Q000737:chemistry / Q000187:drug effects*; D015152:Blotting, Northern; D001921:Brain / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D001930:Brain Injuries / Q000473:pathology*; D004558:Electric Stimulation; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis / Q000235:genetics / Q000276:immunology; D005911:Gliosis / Q000139:chemically induced*; D008297:Male; D008845:Microinjections; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar
chemical_list: D005904:Glial Fibrillary Acidic Protein; D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2