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. 2011 Feb 23;105(5):2350–2363. doi: 10.1152/jn.00467.2010

Fig. 9.

Fig. 9.

Injury increases postsynaptic CP-AMPAR function. A–D: cumulative probability distributions of mEPSC amplitude recorded in the presence (dashed gray line) and absence (solid black line) of 50 μM Naspm (+BMI and APV). Insets: average mEPSC in the presence (black) and absence (gray) of Naspm from individual neurons. Naspm significantly decreased mEPSC amplitude (noted as a leftward shift of the cumulative distribution) for control neurons, 4 h post-injury, and 2 days post-injury (***P < 0.001). E: Naspm decreased mean mEPSC amplitude in control neurons (n = 21, P < 0.05), 4 h post-injury (n = 12, P < 0.01), and 2 days post-injury (n = 19, P < 0.05) but not immediately post-injury (n = 10, P > 0.05). F: percent inhibition of mEPSC amplitude by Naspm was significantly increased at 4 h post-injury when compared with control (22.1 ± 3.7% vs. 8.9 ± 4.1%; P < 0.05) but not immediately (0.01 ± 4.5%, P > 0.05) or 2 days post-injury (6.0 ± 3.5%, P > 0.05).