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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Quinolinic acid protects rat cerebellar granule cells from glutamate-induced apoptosis.

The effects of quinolinic acid (QUIN) on glutamate-induced excitotoxicity were examined in primary cultures of rat cerebellar granule neurons. Exposing these neurons to QUIN (< or =2.5 mM) in the presence of glucose and Mg2+ had no effect on their viability. Although pretreating neurons with QUIN (10 microM) for 6 h did not reduce necrotic death induced by glutamate exposure in the absence of glucose and Mg2+, QUIN pretreatment significantly suppressed glutamate-induced apoptosis by 68% (as indicated by DNA fragmentation) in cultures containing glucose and Mg2+. Furthermore, the N-methyl-D-aspartate (NMDA) receptor antagonist AP-5 reversed QUIN-induced neuroprotection, while the non-NMDA antagonist CNQX had no effect. This study demonstrates that pathophysiologically relevant concentrations of QUIN can protect neurons from apoptosis mediated via the NMDA receptor.[1]


  1. Quinolinic acid protects rat cerebellar granule cells from glutamate-induced apoptosis. Sei, Y., Fossom, L., Goping, G., Skolnick, P., Basile, A.S. Neurosci. Lett. (1998) [Pubmed]
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