Fig. 8.
RvD1 treatment prevents neuronal and motor deficits in 4-month-old Syn rats. a DA neuron firing in treated rats (scale: 2 s, 0.2 mV) and firing frequency plots (14 WT/saline, 14 WT/RvD1 cells from 3 rats; 27 Syn/saline and 27 Syn/RvD1 cells from 4 rats; ANOVA for genotype × treatment, F1,78 = 16.34, P = 1.00 × 10−4; genotype, F1,78 = 10.04, P = 0.002; treatment, F1,78 = 7.43, P = 0.008; WT/saline-Syn/saline ***P < 1.00 × 10−4, WT/RvD1-Syn/saline ***P = 5.00 × 10−4, Syn/saline−Syn/RvD1 ***P < 1.00 × 10−4, with Bonferroni’s) and CV-ISI (14 WT/saline, 14 WT/RvD1 cells from 3 rats; 29 Syn/saline and 27 Syn/RvD1 cells from 4 rats; ANOVA for genotype × treatment, F1,80 = 12.58, P = 7.00 × 10−4; genotype, F1,80 = 10.10, P = 0.002; treatment, F1,80 = 8.40, P = 0.005; WT/saline-Syn/saline *** P < 1.00 × 10−4, WT/RvD1-Syn/saline ***P = 3.00 × 10−4, Syn/saline-Syn/RvD1 ***P < 1.00 × 10−4, with Bonferroni’s). b DA neuron firing (scale: 1 s, 0.2 mV) from treated rats before (CTRL) and during DA (30 µM, 2 min) and plot showing % inhibition by DA (14 WT/saline, 14 WT/RvD1 cells from 3 rats; 22 Syn/saline and 26 Syn/RvD1 cells from 4 rats; ANOVA for genotype × treatment, F1,72 = 5.06, P = 0.028; genotype, F1,72 = 4.38, P = 0.040; treatment, F1,72 = 3.93, P = 0.051; WT/saline-Syn/saline *P = 0.021, WT/RvD1-Syn/saline *P = 0.035, Syn/saline-Syn/RvD1 **P = 0.005, with Bonferroni’s). c Cytoplasmic [Ca2+] in DA neurons at −60 mV (11 WT/saline, 6 WT/RvD1 cells from 3 rats; 10 Syn/saline, 7 Syn/RvD1 cells from 4 rats; ANOVA: genotype×treatment, F1,30 = 21.5, P < 1.00 × 10−4; genotype, F1,30 = 12.82, P = 0.001; treatment, F1,30 = 19.08, P = 1.00 × 10−4; WT/saline-Syn/saline ***P < 1.00 × 10−4, WT/RvD1-Syn/saline ***P < 1.00 × 10−4, Syn/saline-Syn/RvD1 ***P < 1.00 × 10−4, with Bonferroni’s). d Amperometric traces (scale: 500 ms, 50 pA) and striatal DA release (49 WT/saline, 71 WT/RvD1 slices from 4 rats; 49 Syn/saline, 77 Syn/RvD1 slices from 4 rats; ANOVA: genotype×treatment, F1,242 = 36.43, P < 1.00 × 10−4; genotype, F1,242 = 90.56, P < 1.00 × 10−4; treatment, F1,242 = 35.29, P < 1.00 × 10−4; WT/saline-Syn/saline ***P < 1.00 × 10−4, WT/RvD1-Syn/saline ***P < 1.00 × 10−4, Syn/saline-Syn/RvD1 ***P < 1.00 × 10−4, WT/RvD1-Syn/RvD1 *P = 0.038 with Bonferroni’s). e Entries in centre zone during open field test in treated rats (16 WT/saline, 7 WT/RvD1, 15 Syn/saline and 7 Syn/RvD1 rats; two-way ANOVA for genotype×treatment, F1,41 = 4.75, P = 0.035; genotype, F1,41 = 0.85, P = 0.362; treatment, F1,41 = 4.59, P = 0.038; WT/saline-Syn/saline *P = 0.048, Syn/saline-Syn/RvD1 *P = 0.025, with Bonferroni’s). f Time performance in the accelerating rotarod (11 WT/saline, 9 WT/RvD1, 12 Syn/saline, 9 Syn/RvD1 rats; ANOVA: genotype × treatment, F1,37 = 4.34, P = 0.044; genotype, F1,37 = 43.04, P < 1.00 × 10−4; treatment, F1,37 = 3.64, P = 0.064; WT/saline-Syn/saline ***P < 1.00 × 10−4, WT/saline-Syn/RvD1 *P = 0.014, WT/RvD1-Syn/saline ***P < 1.00 × 10−4, WT/RvD1-Syn/RvD1 *P = 0.030, Syn/saline-Syn/RvD1 *P = 0.043). Source data are provided as a Source Data file