Extended Data Fig. 6: Activation of the left CeAGA neurons modulated pain-related behaviors in naïve mice and acute pain models.
From: General anesthetics activate a potent central pain-suppression circuit in the amygdala
a, Quantification of effects of optogenetic activation of the left CeAGA neurons on the paw withdrawal frequency to six graded von Frey filaments ranging from 0.4 to 4.0 grams applied to the ipsilateral (Off: 0 ± 0 (0.40g), 2.50 ± 0.56 (0.60g), 5.00 ± 0.63 (1.0g), 6.33 ± 0.95 (1.40g), 8.33 ± 1.09 (2.0g), 10 ± 0 (4.0g); On: 0 ± 0 (0.40g), 0.33 ± 0.21 (0.60g), 2.50 ± 0.50 (1.0g), 3.67 ± 0.80 (1.40g), 5.33 ± 1.38 (2.0g), 9.33 ± 0.49 (4.0g)) or contralateral paw (Off: 0 ± 0 (0.40g), 2.00 ± 0.82 (0.60g), 6.83 ± 1.11 (1.0g), 7.83 ± 0.17 (1.40g), 8.83 ± 0.65 (2.0g), 9.83 ± 0.17 (4.0g); On: 0 ± 0 (0.40g), 0.67 ± 0.33 (0.60g), 3.00 ± 0.45 (1.0g),5.0 ± 0.37 (1.40g), 6.0 ± 1.15 (2.0g), 9.67 ± 0.21 (4.0g)) to the left CeA. (Ipsilateral and contralateral, ChR2, n = 6 animals; two-way ANOVA; *P = 0.0500 (2.0g), *P = 0.0217 (1.4g), ****P < 0.0001, **P = .0023 (1.4g), **P = .0029 (2.0g); F1,60 = 20.51 (ipsi), F1,60 = 28.81 (contra)). b, Quantification of optogenetic activation of the left CeAGA neurons showed that this manipulation did not induce any change in the head withdrawal frequency to eight von Frey filaments ranging from 0.008 to 1.0 gram applied to either the ipsilateral (Off: 0 ± 0 (0.008g), 0 ± 0 (0.02g), 0 ± 0 (0.04g), 1.0 ± 0.52 (0.07g), 4.33 ± 0.61 (0.16g), 6.50 ± 0.85 (0.40g), 9.67 ± 0.21 (0.60g), 10.0 ± 0 (1.0g); On: 0 ± 0 (0.008g), 0 ± 0 (0.02g), 0 ± 0 (0.04g), 0.67 ± 0.49 (0.07g), 4.17 ± 0.54 (016g), 7.00 ± 0.89 (0.40g), 9.83 ± 0.17 (0.60g), 10.0 ± 0 (1.0g)) or the contralateral whisker pad (Off: 0 ± 0 (0.008g), 0 ± 0 (0.02g), 0.50 ± 0.34 (0.04g), 2.50 ± 0.50 (0.07g), 4.67 ± 0.49 (0.16g), 8.0 ± 0.68 (0.40g), 10.0 ± 0 (0.60g), 10.0 ± 0 (1.0g); On: 0 ± 0 (0.008g), 0 ± 0 (0.02g), 0.17 ± 0.17 (0.04g), 2.33 ± 0.80 (0.07g), 5.17 ± 0.17 (016g), 8.17 ± 0.79 (0.40g), 9.83 ± 0.17 (0.60g), 10.0 ± 0 (1.0g)) to the left CeA. (Ipsilateral and contralateral, ChR2, n = 6 animals; two-way ANOVA; not significant P > 0.05; F1,80 = 0.9205 (ipsi), F1,40 = 0.000 (contra)). c, Quantification of the optogenetics induced changes in withdrawal latency (sec) to dry ice (2.29 ± 0.33 s (off-left), 6.86 ± 3.70 s (on-left), 2.33 ± 0.25 s (off-right), 5.81 ± 2.75 s (on-right)) (ChR2, n = 7 animals; one-way ANOVA; **P = 0.0045, *P = 0.0311; F3,24 = 6.241) and heat (6.61 ± 0.93 s (off-left), 12.94 ± 1.89 s (on-left), 6.09 ± 0.65 s (off-right), 15.04 ± 1.80 s (on-right)) (ChR2, n = 7 animals; one-way ANOVA; ****P < 0.0001; F3,24 = 59.93). d, Quantification of total licking and face wiping latency (sec) from left CeAGA neurons optogenetic activation after formalin injection during the second phase of inflammatory pain (134.33 ± 22.88 s (paw licking-off), 10.33 ± 8.24 s (paw licking-on), 151.67 ± 35.99 s (face wiping-off), 12.00 ± 8.74 s (face wiping-on)). (ChR2, n = 6 animals; one-way ANOVA; ****P < 0.0001; F3,20 = 59.54).
