asc 023  (Alomone Labs)

Journal: The Journal of Headache and Pain

Article Title: ROS/TRPA1/CGRP signaling mediates cortical spreading depression

doi: 10.1186/s10194-019-0978-z

Figure Lengend Snippet: 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, H 2 O 2 (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. in our recent paper . 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

Article Snippet: Three groups were designed: (i) pretreatment of the anti-TRPA1 antibody with a total 0.8 μg (Alomone Labs, n = 10) 4 days before CSD induction. (ii, iii) Unconjugated rabbit IgG (H + L) (Sangon, D110502, n = 8) with a total 0.8 μg being applied for both the CSD group and the sham group as controls ( n = 7 in each group).

Techniques: Activation Assay, Slice Preparation, Transformation Assay, MANN-WHITNEY, One-tailed Test

Journal: The Journal of Headache and Pain

Article Title: ROS/TRPA1/CGRP signaling mediates cortical spreading depression

doi: 10.1186/s10194-019-0978-z

Figure Lengend Snippet: Effects of the anti-TRPA1 antibody on MDA level (μmol/mg protein) induced by CSD in the ipsilateral cerebral cortex of rat and correlation analysis of each CSD characteristic with levels of cortical ipsilateral MDA between the anti-TRPA1 antibody or anti-IgG antibody groups. a CSD promoted ipsilateral cortical MDA level, which was inhibited by the pretreatment of anti-TRPA1 antibody perfused into the contralateral i.c.v in rats. Mann-Whitney U test, one-tailed, for significance between each group (* p < 0.05, *** p < 0.001). The reduced CSD magnitude ( d ), but not CSD number ( b ) and latency ( c ) positively correlated with a lower MDA level after the anti-TRPA1 antibody perfusion. Red dotted lines indicated positive correlation between CSD magnitude and MDA level

Article Snippet: Three groups were designed: (i) pretreatment of the anti-TRPA1 antibody with a total 0.8 μg (Alomone Labs, n = 10) 4 days before CSD induction. (ii, iii) Unconjugated rabbit IgG (H + L) (Sangon, D110502, n = 8) with a total 0.8 μg being applied for both the CSD group and the sham group as controls ( n = 7 in each group).

Techniques: MANN-WHITNEY, One-tailed Test

Journal: The Journal of Headache and Pain

Article Title: ROS/TRPA1/CGRP signaling mediates cortical spreading depression

doi: 10.1186/s10194-019-0978-z

Figure Lengend Snippet: 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

Article Snippet: Three groups were designed: (i) pretreatment of the anti-TRPA1 antibody with a total 0.8 μg (Alomone Labs, n = 10) 4 days before CSD induction. (ii, iii) Unconjugated rabbit IgG (H + L) (Sangon, D110502, n = 8) with a total 0.8 μg being applied for both the CSD group and the sham group as controls ( n = 7 in each group).

Techniques: In Vivo, MANN-WHITNEY, One-tailed Test