Extended Data Fig. 7. 3.0 mA ES of ST36 produced anti-inflammatory effects independent of PROKR2^ADV neurons.

a, Compared with control littermates, no difference of 3.0 mA ST36 ES-evoked Fos (green) induction in ChAT⁺ (red) sympathetic preganglionic neurons in the spinal intermediolateral nuclei (“IML”) in PROKR2^ADV-Abl mice (two-way ANOVA, n = 5 mice per group, F_{1, 16} = 0.236, P = 0.633; post-hoc Tukey’s test: ***P < 0.001). b, No changes in 3.0 mA ST36 ES-evoked reduction of LPS-induced TNF-a and IL-6 production in PROKR2^ADV-Abl mice (two-way ANOVA, n = 5 mice per group; for TNF-a: F_{1, 16} = 1.392, P = 0.255; post-hoc Tukey test: ***P < 0.001; for IL-6: F_{1, 16} = 1.382, P = 0.257; post-hoc Tukey test: ***P < 0.001). Thus, although PROKR2^ADV neurons are necessary for low-intensity ES to drive the vagal-adrenal anti-inflammatory axis, they are dispensable for high-intensity ES to drive spinal-sympathetic anti-inflammatory axis from either ST25 or ST36. Data are shown as mean ± SEM. Scale bars: 100 μm.