n | LDH (% of Control) | Glu (% of Control) | Asp (% of Control) | |
---|---|---|---|---|
Oxygen/glucose deprivation | 7 | 100.0 ± 6.1 | 100.0 ± 8.4 | 100.0 ± 10.0 |
CGS 19755 (10 μM) | 6 | 78.0 ± 10.0a | 81.2 ± 9.9 | 78.1 ± 11.4 |
NBQX (30 μM) | 6 | 84.8 ± 6.0 | 60.5 ± 7.5b | 66.3 ± 12.0c |
Nifedipine (10 μM) | 7 | 91.7 ± 8.7 | 82.4 ± 6.2 | 71.9 ± 4.4a |
+ ω-conotoxin GVIA (3 μM) | ||||
+ ω-Aga-TK (1 μM) | ||||
TTX (1 μM) | 6 | 96.2 ± 5.2 | 73.3 ± 5.6a | 58.2 ± 8.0c |
Cultured hippocampal neurons were incubated in the absence of oxygen in KR buffer solution without glucose for 80 min. The concentrations of glutamate and aspartate accumulated in the KR buffer solution sampled at 80 min and the activity of LDH in the medium at 20 hr were measured. Each value represents the ischemic injury as a percentage of the control value (mean ± S.E.M., n= 6–7). a P < 0.05, b P < .001,c P < 0.01 vs. ischemic injury control. Data were analyzed by means of analysis of variance and Fisher’s PLSD.