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. 2012 Oct 31;109(2):485–496. doi: 10.1152/jn.00076.2011

Fig. 3.

Fig. 3.

Nerve growth factor (NGF) potentiated EPSC amplitude via p75 activation. A: the neurotrophin NGF potentiated EPSC amplitude as seen in the shift of the cumulative percent histogram plot for NGF compared with control (n = 6 cells; 294 and 330 EPSCs for control and NGF, respectively, P < 0.001). Mean amplitudes were also significantly different as seen in a bar plot (inset; −61.5 ± 6.3 pA vs. −72.4 ± 8.2 pA for control and after application of 50 ng/ml NGF, respectively; n = 6; **P = 0.005). B: NGF/αNGF30, which blocks NGF activation of p75, did not alter the EPSC amplitude as seen in the cumulative percent histogram plot (n = 8 cells, 440 and 408 EPSCs for control and after NGF/αNGF, respectively) and the bar plot of mean EPSC amplitude (inset; −52 ± 4 pA vs. −49.6 ± 3.9 pA for control and NGF/αNGF, respectively, n = 8). C: coapplication of NGF with the anti-NGF antibody αNGF30 blocks NGF activation of p75, resulting in only TrkA activation. We have previously shown that TrkA increases sympathetic tonic firing and spike output. A plot of spike output vs. stimulus amplitude (normalized to threshold) shows that NGF/αNGF30 (molar ratio 1:2 NGF/αNGF30, 50 ng/ml NGF) caused an increase in spike output over the amplitude range tested (n = 24 and n = 10 for saline control and NGF/αNGF30, respectively; P < 0.001, 2-way ANOVA). NGF/αNGF30 promoted tonic firing as seen by a plot of % of spikes that occurred in the second half of the stimulus, a measurement that we previously have shown represents firing pattern (inset; n = 24 and n = 10 for saline control and NGF/αNGF30, respectively; ***P < 0.001, t-test).