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. 2019 Jun 5;127(6):067003. doi: 10.1289/EHP4583

Figure 9.

Figure 9A are representative images of WT and R yR1 super T4826I virgule T4826I mutation neurons that were exposed to V e h and deltamethrin. Figure 9B shows two bar graphs plotting length of axon at 100, 150, 200, 250, and 300 micrometers (y-axis) for WT and R yR1 super T4826I virgule T4826I across exposures V e h and deltamethrin 30 and 100 nanomolars (x-axis), representing data as standard error of mean.

Impacts of RyR1T4826I/T4826I mutation on DM-induced axonal outgrowth. (A) Representative images of WT and RyR1T4826I/T4826I mutation neurons exposed to Veh (0.1% DMSO) and DM (30  nM and 100  nM) commencing 3 h after plating and immunostained with MAP-2B antibody at 2 DIV. (B) Quantification of the axon length after DM exposure in WT and RyR1T4826I/T4826I mutation neurons. The total number of neurons tested was inserted in the bar graph, and axonal length of each neuron was used as analysis unit. Each data point represents the mean±standard error of the mean  (SEM) from two independent sister cultures, each with three wells. Statistical significance between WT and RyR1T4826I/T4826I neurons was performed using two-way analysis of variance (ANOVA) followed by post hoc Bonferroni comparison. Note: DM, deltamethrin; DMSO, dimethylsulfoxide; RyRs, ryanodine receptors; Veh, vehicle; WT, wild type. *p<0.05; **p<0.01, DM vs. Veh; #p<0.05; ##p<0.01, RyR1T4826I/T4826I vs. WT at same treatment condition. Bar=50μm.