Fig. 6

Both ROS and the TRPA1 activation reversed the inhibitory effects of the anti-CGRP antibody on CSD in the mouse brain slice. CSD was induced by 260 mM KCl. There were four groups: anti-IgG antibody at 0.025 μM (i, n = 6) as the control, anti-CGRP antibody at 0.4 μM in the absence (ii, n = 6) or presence of 50 μM of the TRPA1 agonist, AITC (iii, n = 6) or the ROS activator, H₂O₂ (vi, n = 6). In order to minimize the animal use, data in anti-IgG antibody control group and the anti-CGRP antibody were adopted and transformed from that in Fig. 5 in our recent paper [5]. Representative trace of the 2nd CSD episode in each group are shown in the panel a. The data showed that both ROS and the TRPA1 activation reversed the prolonged CSD latency (b), but not magnitude (c) under the perfusion of the anti-CGRP antibody. Data were plotted as percentage of their initial levels (1st CSD episode) and indicated as median (range). Mann-Whitney U test, one-tailed, was used for significant analysis between two independent groups. *p < 0.05, **p < 0.01. Abbreviation: Ab indicates antibody