Introduction: We tested the hypothesis that NMDA or non-NMDA receptor mediated mechanisms may predominate to induce neuronal injury following glucose deprivation in human neuronal cells (NT2-N). The mechanisms of glucose deprivation induced neuronal cell death have been studied in numerous in vitro systems, most of which use fetal rat or mouse neurons not human neurons. Methods: NT2-N cells were cultured. Cells were washed with DMEM with 0 mM glucose, 25 mM HEPES, 4 mM glutamine, 100 IU/ml penicillin, 100 μg/ml streptomycin. Wells were divided into 4 groups: 1) Control-6 hours of glucose deprivation at 37°C and 0.21 FiO2 followed by normoglycemic recovery; 2) MK801 (NMDA receptor antagonist)-same as control except MK801 for 6 hours; 3) CNQX-(AMPA receptor antagonist)-same as control except CNQX for 6 hours; 4) MK801 + CNQX-same as control except MK801 and CNQX for 6 hours. Release of the cytoplasmic enzyme lactate dehydrogenase (LDH) was used as a measure of cell viability at 24 hours (LDH supernatant/LDH total × 100). Data were analyzed by ANOVA. Results: %LDH is less in the glucose-deprived neuronal cells exposed to MK801 (p<0.05), CNQX (p<0.05), and combined MK801 and CNQX (p<0.05) compared to control. (Figure Presented) Conclusions: Glucose deprivation causes a large release of LDH in NT2-N cells. NMDA receptor blockade as well as non-NMDA receptor blockade with CNQX decreases the release. Both NMDA and non-NMDA receptors play a mechanistic role in cell damage in hypoglycemia.
|Original language||English (US)|
|Journal||Critical Care Medicine|
|Issue number||1 SUPPL.|
|State||Published - 1999|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine