Fig. 3: Optogenetic manipulation of the rACC→Pn pathway affects PAC-induced analgesia and pain behaviours.
a, The strategy and experimental timeline to optogenetically manipulate the activity of the rACC→Pn pathway. Scale bar, 2 mm. b, The latency preceding first paw licking (left; P = 0.005), rearing (middle; P = 0.04) and jumping (right; P = 0.009) during the post-test. n = 10 mice per group. c, The strategy to measure thermal pain using a hot plate while optogenetically activating or inhibiting the rACC→Pn pathway. d, The latency preceding paw withdrawal on a 48 °C plate (left; F2,26 = 10.66, P < 0.001) or 52 °C plate (right; F2,26 = 7.38, P = 0.003). n = 10 (eYFP control), 10 (NpHR) and 9 (ChR2) mice. e, The strategy to measure the mechanical pain threshold with von Frey filaments while optogenetically activating or inhibiting the rACC→Pn pathway. f, Quantification of changes in paw withdrawal frequency in response to six different von Frey filaments induced by optogenetic manipulation of the rACC→Pn pathway (F2,156 = 62.965, P = 2 × 10−16). n = 10 (eYFP control), 10 (NpHR) and 9 (ChR2) mice. g, The pain threshold of mice with or without light stimulation (F2,26 = 25.98, P = 1.3 × 10−9). n = 10 (eYFP control), 10 (NpHR) and 9 (ChR2) mice. Statistical analysis was performed using two-sided Wilcoxon rank-sum tests (b), one-way ANOVA with Tukey post hoc test (d) and two-way ANOVA with Tukey post hoc test (f and g). For the box plots, the centre lines show the median values, the box limits show the quartiles, and the whiskers show the most extreme datapoints ≤interquartile range from the box edges. For f, data are mean ± s.e.m. *P < 0.05, **P < 0.01 and ***P < 0.001.
