Fig. 3.
Injury transiently increased the contribution of NMDARs and CP-AMPARs to neuronal [Ca2+]i oscillations. A: percent inhibition of [Ca2+]i oscillation amplitude by the NMDAR antagonist APV (20 μM) was significantly greater immediately post-injury [44 ± 2.0% for control (n = 79 cells from 9 wells) vs. 52.4 ± 2.0% for injured neurons (n = 87 cells from 8 wells, P < 0.05)] and 4 h post-injury [42.3 ± 1.7% for control (n = 110 cells from 9 wells) vs. 53.8 ± 1.2% for injured neurons (n = 109 cells from 9 wells, P < 0.001)] and did not differ at 2 days post-injury [33.6 ± 4.0% for control (n = 83 cells from 8 wells) vs. 32.6 ± 4.6% for injured neurons (n = 66 cells from 8 wells, P > 0.05)]. B: percent inhibition of [Ca2+]i oscillation amplitude by the selective CP-AMPAR antagonist Naspm (50 μM) was significantly greater 4 h post-injury [15.5 ± 3.4% for control (n = 95 cells from 8 wells) vs. 33.8 ± 1.7% for injured neurons (n = 92 cells from 8 wells, P < 0.001)] yet did not differ from controls immediately post-injury [12.9 ± 1.9% for control (n = 58 cells from 5 wells) vs. 6.3 ± 3.6% for injured neurons (n = 33 cells from 3 wells, P > 0.05)] or at 2 days post-injury [18.3 ± 2.8% for control (n = 44 cells from 4 wells) vs. 20.5 ± 3.5% for injured neurons (n = 33 cells from 4 wells, P > 0.05)]. All measurements were made in the presence of 30 μM BMI. C: calcium oscillation amplitude did not differ at 4 h when measured in the presence 30 μM BMI only yet was significantly decreased when measured in the presence of 30 μM BMI + 20 μM APV [0.22 ± 0.01 for control (n = 111 cells from 9 wells) vs. 0.19 ± 0.01 for injured (n = 109 cells from 9 wells; P < 0.01)]. Oscillation amplitude was also significantly reduced when recorded in the presence of BMI + APV + 50 μM Naspm [0.18 ± 0.01 for control (n = 96) vs. 0.14 ± 0.01 for injured (n = 92), P < 0.001].