Fig. 2.
Injury decreased neuronal [Ca2+]i oscillation frequency and amplitude A: percentage of neurons displaying spontaneous [Ca2+]i oscillations before disinhibition with BMI was significantly decreased immediately post-injury (n = 105 cells, 9 wells) vs. control (n = 96 cells from 9 culture wells, P < 0.001 by Fisher's exact test) and 2 days post-injury (n = 87 cells, 9 wells) vs. control (n = 92 cells, 8 wells, P < 0.01), yet was not statistically different at 4 h post-injury (n = 112 cells, 9 wells) vs. control (n = 109 cells, 9 wells, P > 0.05) B: frequency of [Ca2+]i oscillations recorded in the presence of 30 μM BMI did not differ immediately post-injury [0.042 ± 0.001 Hz for control (n = 91) vs. 0.042 ± 0.001 Hz for injured neurons (n = 105, P > 0.05)] but was significantly decreased 4 h post-injury [0.043 ± 0.002 Hz for control (n = 112) vs. 0.034 ± 0.001 Hz for injured neurons (n = 109, P < 0.01)] and at 2 days post-injury [0.033 ± 0.002 Hz for control (n = 83) vs. 0.022 ± 0.001 Hz for injured neurons (n = 78, P < 0.001)]. C: injury decreased the amplitude of [Ca2+]i oscillations recorded in the presence of 30 μM BMI immediately post-injury [0.31 ± 0.01 for control (n = 91) vs. 0.18 ± 0.01 for injured neurons (n = 105, P < 0.001)] and 2 days post-injury [0.32 ± 0.02 for control (n = 83) vs. 0.24 ± 0.02 for injured neurons (n = 78, P < 0.01)] but was not significantly different at 4 h post-injury [0.40 ± 0.02 for control (n = 112) vs. 0.41 ± 0.02 for injured neurons (n = 109, P > 0.05)]. Measurements are baseline subtracted (F340/F380) relative units.