Abstract:
: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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Sei Y,Fossom L,Goping G,Skolnick P,Basile ASdoi
10.1016/s0304-3940(97)00980-4subject
Has Abstractpub_date
1998-01-30 00:00:00pages
180-4issue
2-3eissn
0304-3940issn
1872-7972pii
S0304-3940(97)00980-4journal_volume
241pub_type
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