n | LDH (% of Control) | Glu (% of Control) | Asp (% of Control) | |
---|---|---|---|---|
Oxygen/glucose deprivation | 15 | 100.0 ± 6.1 | 100.0 ± 9.6 | 100.0 ± 13.2 |
NMDA antagonists | ||||
MK-801 | ||||
0.1 μM | 10 | 40.7 ± 8.0a | 65.4 ± 14.3b | 57.7 ± 15.7b |
1 μM | 6 | −5.2 ± 3.6a | 41.7 ± 5.7c | 42.3 ± 8.8b |
10 μM | 6 | −18.9 ± 4.8a | 26.2 ± 4.6a | 18.7 ± 4.5a |
CGS 19755 | ||||
1 μM | 6 | 82.4 ± 13.0 | 96.8 ± 14.0 | 95.7 ± 16.6 |
10 μM | 6 | 15.1 ± 6.1a | 50.3 ± 8.6c | 41.9 ± 9.2b |
50 μM | 6 | −9.2 ± 7.1a | 23.8 ± 5.4a | 24.8 ± 7.2c |
CPP | ||||
1 μM | 6 | 101.1 ± 10.7 | 87.1 ± 15.2 | 88.2 ± 20.3 |
10 μM | 6 | 29.0 ± 12.8a | 53.1 ± 11.8c | 43.9 ± 11.0b |
50 μM | 6 | −8.3 ± 5.7a | 28.6 ± 6.5a | 24.6 ± 5.3c |
Non-NMDA antagonists | ||||
CNQX | ||||
10 μM | 10 | 93.9 ± 15.2 | 95.4 ± 16.0 | 88.7 ± 14.9 |
30 μM | 10 | 76.7 ± 9.4b | 68.2 ± 7.8b | 61.7 ± 9.5b |
100 μM | 8 | 50.4 ± 8.3a | 62.6 ± 9.0b | 41.4 ± 8.1c |
NBQX | ||||
3 μM | 8 | 100.3 ± 14.8 | 82.7 ± 16.1 | 77.7 ± 18.7 |
10 μM | 12 | 91.7 ± 10.8 | 69.9 ± 11.8b | 57.4 ± 10.8b |
30 μM | 12 | 82.0 ± 11.6 | 65.5 ± 11.1b | 54.5 ± 10.6b |
100 μM | 6 | 46.4 ± 8.0a | 40.0 ± 8.1c | 50.3 ± 11.0b |
GYKI52466 | ||||
10 μM | 10 | 101.7 ± 13.0 | 77.7 ± 15.6 | 65.0 ± 15.7 |
30 μM | 10 | 74.7 ± 12.3b | 52.4 ± 9.7c | 43.2 ± 8.6c |
100 μM | 6 | 40.5 ± 10.9a | 26.0 ± 3.9a | 21.9 ± 1.7c |
MK-801 + NBQX | ||||
0.1 + 30 μM | 8 | 14.9 ± 5.2a | 35.2 ± 5.4a | 28.9 ± 7.1c |
Cultured hippocampal neurons were incubated in the absence of oxygen in KR buffer solution without glucose for 50 min. The concentrations of glutamate and aspartate accumulated in the KR buffer solution sampled at 50 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= 6–15). a P < .001, b P < .05,c P < .01 vs. ischemic injury control value. Data were analyzed by means of analysis of variance and Fisher’s Protected Least Significant Difference (PLSD).