The effect of basic fibroblast growth factor on glutamate-injured neuroarchitecture and arachidonic acid release in adult hippocampal neurons.

Abstract

During development in culture, basic fibroblast growth factor (bFGF) protected immature primary hippocampal neurons against glutamate-induced neurotoxicity. We investigated the effects of bFGF on mature, differentiated rat hippocampal neurons cultured for 10-12 days after an 8-min exposure to 500 microM glutamate. Seven days post-injury, hippocampal cells demonstrated severe reductions in cellular viability and axonal and dendritic outgrowth, which were accompanied by a marked increase in [3H]arachidonic acid (ARA) release from prelabelled neurons. bFGF applied post-injury attenuated cell death and cytoarchitectural destruction at all concentrations used (500 pg/ml, 1, 10, 20 ng/ml). However, neurite elongation and branching processes were only significantly protected by 10 ng/ml bFGF. [3H]ARA release decreased in a dose-related fashion within a concentration range of 1-10 ng/ml bFGF. 20 ng/ml bFGF was not superior to 10 ng/ml bFGF. Therefore, bFGF's neurotropic actions appear to be concentration-dependent. Our data suggest that bFGF applied post-injury may have a neuroprotective potential for mature, differentiated, completely polarized hippocampal neurons.

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@article{Himmelseher1996TheEO, title={The effect of basic fibroblast growth factor on glutamate-injured neuroarchitecture and arachidonic acid release in adult hippocampal neurons.}, author={Sabine Himmelseher and Ernst G. Pfenninger and Michael K Georgieff}, journal={Brain research}, year={1996}, volume={707 1}, pages={54-63} }