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Survival‐promoting and Protein Kinase C‐regulating Roles of Basic FGF for Hippocampal Neurons Exposed to Phorbol Ester, Glutamate and Ischaemia‐like Conditions
Author(s) -
Louis JeanClaude,
Magal Ella,
Gerdes Wilhelm,
Seifert Wilfried
Publication year - 1993
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1993.tb00230.x
Subject(s) - protein kinase c , glutamate receptor , basic fibroblast growth factor , hippocampal formation , neurotrophic factors , neurotrophin , ischemia , medicine , neuron , fibroblast growth factor , endocrinology , microbiology and biotechnology , biology , neuroscience , chemistry , kinase , biochemistry , growth factor , receptor
Recent evidence suggests that protein kinase C (PKC) is involved in the pathophysiology of neurodegenerative diseases. We examined the effect of basic fibroblast growth factor (bFGF) on the survival of cultured rat hippocampal neurons exposed to conditions in which PKC is likely to play a role. bFGF reduced neuron damage caused by the PKC‐activating phorbol ester 12‐ O ‐tetradecanoylphorbol 13‐acetate (TPA), glutamate and ischaemia‐like culture conditions. bFGF was able to counteract the excessive activation of PKC caused by these treatments. Moreover, bFGF prevented the loss of PKC occurring after prolonged exposure to TPA or ischaemia‐like conditions. These results indicate that both the overactivation and the abnormal degradation of PKC can lead to neuron degeneration, and that the neurotrophic competence of bFGF may reside in its ability to regulate and normalize the PKC phosphorylating system.