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Toward the Development of Strategies to Prevent Ischemic Neuronal Injury
Author(s) -
MARINI ANN M.,
SPIGA GIULIO,
MOCCHETTI ITALO
Publication year - 1997
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1997.tb48431.x
Subject(s) - neuroprotection , nmda receptor , neurotoxicity , glutamate receptor , neurotrophic factors , basic fibroblast growth factor , neuroscience , programmed cell death , neurotrophin , chemistry , excitotoxicity , pharmacology , microbiology and biotechnology , biology , growth factor , biochemistry , toxicity , apoptosis , receptor , organic chemistry
Cerebellar granule cells in culture, which are extremely vulnerable to excitotoxin glutamate or N-methyl-D-aspartate (NMDA), were used to study mechanisms of neuronal cell death and protection. Paradoxically, pretreatment of these cells with subtoxic concentrations of NMDA markedly blocked the neurotoxicity resulting from subsequent exposure to glutamate or NMDA. The NMDA-mediated neuroprotection can be antagonized by pretreatment of these cells with protein synthesis inhibitors, suggesting an involvement of protein(s) with neuroprotectant properties, most likely neurotrophic factors. Because basic fibroblast growth factor (BFGF) is well known to prevent neuronal cell death following mechanical or chemical injury, we have tested whether NMDA increases the synthesis of bFGF in cerebellar granule cells. NMDA elicited a rapid and time-dependent increase in bFGF mRNA, suggesting that availability of this trophic factor may play a role in the NMDA-mediated neuroprotection.