Fig. 5

Effects of modulation of ROS and TRPA1 on cortical susceptibility to CSD and their interaction during CSD in the mouse brain slice. Submaximal CSD was induced by KCl at 50 mM. There were six groups: Kreb’s (i, n = 6) as control, 3 mM of the ROS inhibitor, tempol (ii, n = 7), 50 μM of ROS activator, H₂O₂ (iii, n = 6), 3 mM of tempol with 50 μM of H₂O₂ (vi, n = 8) or with 15 μM of the TRPA1 agonist, UMB (v, n = 7), 50 μM of H₂O₂ with 1 μM of the TRPA1 antagonist, A967079 (vi, n = 6). In order to minimize the animal use, data in Kreb’s control group were adopted and transformed from that in Fig. 4 in our previous paper [5]. Representative trace of the 2nd CSD episode in each group were shown in the panel a. The data showed that cortical susceptibility to CSD is suppressed by tempol, facilitated by H₂O₂, and there is a bidirectional interaction between ROS and TRPA1 in modulating latency (b) and magnitude (c) of CSD. CSD latency (second) was given as median (rang). CSD magnitude were plotted as percentage of their initial levels (1st CSD episode) and indicated as median (range). Mann-Whitney U test (one-tailed) was for significant analysis between two independent groups. * p < 0.05, ** p < 0.01, ***p < 0.001 indicate significance