Time-dependent increase in basic fibroblast growth factor protein in limbic regions following electroshock seizures.
Brief experimentally induced seizures have been shown to increase the expression of mRNA encoding basic fibroblast growth factor (FGF-2) in specific brain regions. However, the extent to which this change in mRNA affects the expression of FGF-2 protein in these brain regions has not been examined. In the present study, we exposed rats to brief non-injurious seizures to determine whether this treatment would lead to an increase in FGF-2 protein expression in selected brain regions. Because initial results indicated that the elevation of FGF-2 protein was not significant following acute seizure exposure, we examined both acute and chronic seizure treatment to determine whether FGF-2 protein expression could be increased under conditions of repeated seizures. Brief limbic seizures were induced by minimal electroconvulsive shock (ECS) given as daily treatments for 1 (acute) or 7 (chronic) days. FGF-2 protein was measured in hippocampus, rhinal cortex, frontal cortex, and olfactory bulb at 20, 48, and 72 h following the last seizure. No significant increases in FGF-2 protein were observed in any region following acute ECS. In the chronic ECS-treated groups, significantly elevated FGF-2-like immunoreactivity was found in the frontal and rhinal cortex as compared with the same regions from both control and acute ECS animals. Increases after chronic ECS were maximal at 20 h, and remained significantly elevated as long as 72 h. These increases were predominantly observed for the 24-kDa and 22/22.5-kDa FGF-2 isoforms. Because chronic ECS, which has been shown to be protective against neuronal cell death, induced significantly more FGF-2 immunoreactivity than did acute ECS, we suggest that FGF-2 expression may be an important substrate for the neuroprotective action of non-injurious seizures. A prolonged induction of the high molecular weight isoforms of FGF-2, as occurs after chronic ECS, may selectively reduce the vulnerability of certain brain regions to a variety of neurodegenerative insults.
Gwinn
R P
RP
Department of Neurosurgery, Georgetown University, Washington, DC 20007, USA.
Kondratyev
A
A
Gale
K
K
D000818:Animals; D016923:Cell Death / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology; D004195:Disease Models, Animal; D004565:Electroconvulsive Therapy; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism*; D005625:Frontal Lobe / Q000378:metabolism / Q000503:physiopathology; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D015151:Immunoblotting; D008032:Limbic System / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009474:Neurons / Q000378:metabolism*; D009830:Olfactory Bulb / Q000378:metabolism / Q000503:physiopathology; D009833:Olfactory Pathways / Q000378:metabolism / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000378:metabolism* / Q000503:physiopathology; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology*
D016222:Fibroblast Growth Factor 2