EXPRESSION OF THE BASIC FIBROBLAST-GROWTH-FACTOR GENE IN MILD AND MORE SEVERE HEAD-INJURY IN THE RAT

Object. The goal of this study was to investigate the relationship bet ween basic fibroblast growth factor (bFGF) gene expression and neuropa thological changes in the hippocampus after varying degrees of brain i njury. Methods. Mild and severe brain injury in rats was produced by u sing Marmarou's method. There were 25 animals in each brain injury gro up and 25 additional animals served as controls. Basic fibroblast grow th factor gene expression was investigated by means of RNA hybridizati on, in situ hybridization, immunohistochemical analysis, and histologi cal analysis using hematoxylin and eosin staining. A 3.7-kb bFGF messe nger (m)RNA was detected in the rat hippocampus in both control and in jured rats. In the mild injury group its expression was increased at 1 2 hours after injury and peaked on the 3rd day. Neuronal degeneration in the hippocampal CA2 and CA3 sectors was maximum on that day. In the severe injury group, the expression of the bFGF gene was the same as that in the mild injury group at corresponding times, but the number o f surviving neurons in the CA2 and CA3 sectors was much lower than in the mild injury group. In situ hybridization showed that the main cell s that expressed bFGF mRNA were pyramidal and granulocytic neurons in all three experimental groups. The number of neurons expressing bFGF m RNA in the severe injury group was less than that in the mild injury g roup, but the intensity of expression was greater. Immunohistochemical staining showed that the number of neurons expressing the bFGF protei n was less in the severe injury group than in the mild injury group. C onclusions. It is concluded that after mild injury then is a close rel ationship between the expression of the bFGF gene and the degree of hi stological change in the hippocampus; this indicates that as one of th e growth factors, bFGF may participate in the protection and repair pr ocesses of neurons following brain injury. In severe injury there is a reduced expression of bFGF. The reason for this appears to be that mo re of the cells that have the potential to express bFGF have died, red ucing the ability of express the bFGF gene. Conversely, it is possible that there may be an intrinsic insufficiency of expression of the gen e, compatible with the known vulnerability of the hippocampus to many pathological conditions. Consideration should be given to supplying ex ogenous bFGF to protect the brain, particularly the hippocampus, after injury.