Fig. 3

Effects of the anti-TRPA1 antibody, perfused into the contralateral ventricle, on cortical susceptibility to CSD in rats. a CSD was induced by topical application of 2 M KCl for 30 min onto cerebral cortex with dura intact via the posterior burr hole on the right parietal bone. The ipsilateral anterior hole was used for CSD recording. The anti-TRPA1 antibody (i, n = 10) or anti-IgG antibody (ii, n = 8) was perfused through a cannula implanted in the contralateral ventricle (i.c.v) at 4 days prior to CSD induction. In the sham group (iii), the anti-IgG antibody was i.c.v perfused in the absence of KCl application as the control (n = 7). The whole ipsilateral cerebral cortical tissue was subsequently used for detecting MDA level immediately after the in vivo experiment. b A representative trace showing CSD propagation wave after i.c.v perfusion of the anti-IgG antibody. CSD number, latency (minute) and magnitude (area under the curve of each CSD wave, mV × minute) were used for quantifying the excitation phase of CSD. The effects of the anti-TRPA1 antibody at 0.8 μg on CSD number are shown in panel (c), latency in panel (d) and magnitude in panel (e). All the values shown are median (range). *p < 0.05, Mann-Whitney U test with one-tailed calculation was used for comparison of the anti-IgG antibody and the anti-TRPA1 antibody group