Figure 3.

Knockout of Rac1 in astrocytes prevented the development of hyperreflexia after SCI. Representative control (black line) and test (orange line) traces of evoked H-reflex and M-wave responses in A baseline-Rac1^wt, baseline-Rac1KO, SCI-Rac1^wt, and SCI-Rac1KO. The control and test pulses were separated with a range of interpulse latencies between 50 and 2,000 ms. B–D, Comparison of %H-reflex, %M-wave, and H/M ratio between Rac1^wt and Rac1KO at baseline, prior to receiving spinal cord injury. B, As expected at baseline in Rac1^wt animals, at shorter interpulse intervals (e.g., 50 ms), the amplitude of the test pulse H-reflex was reduced. B, At baseline, Rac1KO animals displayed a slight increase in the %H-reflex at the 50 ms interval compared to Rac1^wt animals (*p < 0.05). C, There was no difference in %M-wave between Rac1^wt and Rac1KO groups at baseline. D, In addition, there was no difference in the H/M ratio between Rac1^wt and Rac1KO. Rac1^wt and Rac1KO animals had similar H/M ratios across all interpulse intervals, demonstrating RDD in both groups. E–G, Comparison of %H-reflex, %M-wave, and H/M ratio between Rac1^wt and Rac1KO 3-weeks post-SCI. E, After SCI, Rac1^wt animals have an exaggerated %H-reflex at 50 and 100 ms interpulse intervals, indicative of hyperreflexia. Rac1KO in astrocytes restored %H-reflex to levels similar to baseline (*p < 0.05). F, There was no difference in %M-wave amplitude between Rac1^wt, Rac1KO, and baseline. G, SCI increased the H/M ratio as demonstrated as a flat linear trend line compared to a closer-to-normal H/M ratio, with a steeper linear trend line in Rac1KO and baseline groups. Note that in Figure 3G,K, the interpulse interval is graphed as a linear scale, to reflect the linear regression analysis (*p < 0.05). Scale bars in A–D = 2 ms (x-axis) and 0.1 spike volts (y-axis), n = 19–20 per group, and graphs are mean ± SEM.