Figure 2.
Effects of blockers of Cl− channels or transporters on varicosity formation and necrotic cell death induced by NMDA exposure in cultured mouse cortical neurons. A–C, Varicosity formation (A), LDH release (B), and PI uptake (C) were assessed 20 min, 3 h, and 3 h, respectively, after application of 30 μm NMDA in the absence and presence of VSOR Cl− channel blockers (NPPB 40 μm, phloretin 100 μm, IAA-94 1 mm), GABAA receptor blockers (bicuculline 10 μm, picrotoxin 100 μm), and Cl− cotransporter blockers (bumetanide 10 μm, furosemide 1 mm). On the varicosity formation (A), there was no statistically significant difference between the effect of NPPB or phloretin and that of bicuculline or picrotoxin, whereas the inhibiting effect of IAA-94 was significantly stronger than that of bicuculline or picrotoxin. On the NMDA-induced neuronal cell death (B, C), the effect of each of three Cl− channel blockers was significantly different from that of either GABAA receptor blocker. *p < 0.05 versus NMDA exposure in the absence of drugs. †p < 0.05 between NMDA exposure in the presence of 40 μm NPPB and that in the combined presence of 40 μm NPPB and 100 μm picrotoxin. Each symbol represents the mean ± SEM (error bars).