Fig. 6: RIM tyramine influences reorientations through multiple parallel pathways.
From: Neural sequences underlying directed turning in Caenorhabditis elegans

a, RIM GCaMP trace from a single animal. b, RIM activity aligned to reversal starts (dashed line, reversal is shaded red), split by reversal length. Two-sided Wilcoxon rank-sum test with Bonferroni correction, comparing activity before (P < 0.0001) and after (P < 0.0001) reversal start. n = 738 reversals (n values on the plot show the number of recordings with data for RIM). Data show mean ± 95% CI. c, RIM activity as in b, with reversals split by reversal speed. Two-sided Wilcoxon rank-sum test with Bonferroni correction, comparing before (P = 0.65) and after (P < 0.0001) reversal start. n = 738 reversals. Data show mean ± 95% CI. d, RIM activity as in b, split by direction of the postreversal turn, either dorsal or ventral. Reversals are subsampled to match length and speed. Two-sided Wilcoxon rank-sum test with Bonferroni correction, separately comparing activity before (P = 0.0015) and after (P = 0.15) reversal start. n = 148 dorsal turn and 163 ventral turn reversals. Data show mean ± 95% CI. e, RIM activity as in b, split by postreversal turn angle. Reversals are subsampled to match length and speed. Two-sided Wilcoxon rank-sum test with Bonferroni correction. n = 74 reversals. Data show mean ± 95% CI. f, Fraction of animals reversing, with the shading showing optogenetic activation of RIM. Animals are tdc-1::cre + glr-1::inv(CoChR). n = 12–15 recording plates, 10 optogenetic stimulations per recording (only the first stimulation is shown here). Two-sided Wilcoxon rank-sum test (P < 0.0001). Data are mean ± 95% CI. g, Fraction of animals reversing across time, with the blue bar showing optogenetic inhibition of RIM. Animals are tdc-1::cre + glr-1::inv(GtACR2). n = 11–14 recording plates, 3 optogenetic stimulations per recording (only the first stimulation is shown here). Two-sided Wilcoxon rank-sum test (P < 0.0001). Data are mean ± 95% CI. h, Reversal speed for WT animals and animals lacking each of the five known tyramine receptors. Animals were off food without odor. n = 10 recording plates per genotype. Two-sided Wilcoxon rank-sum test with Bonferroni correction, comparing each mutant to WT (from left to right, P = 0.001, 0.00018, 0.0006, 0.0003, 0.0017). Data are mean ± 95% CI. i, Reversal length for WT animals and animals lacking each of the five known tyramine receptors. n = 10 recording plates per genotype. Two-sided Wilcoxon rank-sum test with Bonferroni correction, comparing each mutant to WT (P = 0.00018 and 0.0002). Data are mean ± 95% CI. j, Chemotaxis of WT animals and animals lacking each of the five known tyramine receptors. None of the comparisons is significant with a Mann–Whitney U test with Bonferroni correction. For butanone, n = 14 plates per genotype. For nonanone, from left to right, n = 19, 17, 15, 14, 19, 20, 14, 14, 14, 14 plates. Data show mean ± s.e.m. k, Chemotaxis of WT animals and quintuple mutant animals lacking all of the five known tyramine receptors. From left to right, n = 20, 21, 18, 18, 15, 14, 19, 20 plates. Mann–Whitney U test with Bonferroni correction (from left to right, P = 0.006, 0.0006, 0.05, 0.83). Data show mean ± s.e.m. l, Reversal speed for WT animals and quintuple mutant animals lacking all of the five known tyramine receptors. Animals were off food without odor. From left to right, n = 16, 16, 16 and 18 plates. Two-sided Wilcoxon rank-sum test with Bonferroni correction (P = 0.011 and 0.01). Data are mean ± 95% CI. m, Postreversal turn angle as in l. Two-sided Wilcoxon rank-sum test with Bonferroni correction (P = 0.005 and 0.0127). Data are mean ± 95% CI. For all panels, significance is noted as: NS (not significant), *P < 0.05, **P < 0.01, ***P < 0.001 and **P < 0.0001. For panels with multiple comparisons, symbols denote Bonferroni-adjusted P values.