Figure 3
Neurodegeneration of catecholaminergic axons involved the local energy deficit and depended on Sarm1. (A–C) The degeneration of catecholaminergic axons in the colon was caused by TNFα. (A) The wild-type mice were subjected to the DSS-induced colitis. TNFα mRNA levels in the colon tissues were determined by the qPCR analysis. n = 5, mean ± SEM, *P < 0.01 (ANOVA test). (B and C) The wild-type mice were administered with the anti-TNFα neutralizing antibody or control IgG and then subjected to the DSS-induced colitis. The unsectioned colon tissues were processed for the whole-tissue TH-immunolabeling. (B) Representative 3D-projection images (longitudinal view) of the 500-μm thickness of the tissues at 12.6× magnification of the lightsheet imaging. (C) TH-positive catecholaminergic axons within the mucosa were quantified. n = 5, mean ± SEM, *P < 0.01 (ANOVA test). (D–G) TNFα directly triggered the axonal degeneration of catecholaminergic neurons of the celiac ganglia. Catecholaminergic neurons of the celiac ganglia of wild-type mice were in vitro cultured. The neurons were then treated with 50 ng/mL recombinant TNFα, in combination with 10 mmol/L methylpyruvate or 50 mmol/L nicotinamide. (D) Representative images of TH-positive axons of the cultured catecholaminergic neurons. (E) The integrity of TH-positive catecholaminergic axons was quantified. n = 4, mean ± SEM, *P < 0.01 (ANOVA test). (F and G) ATP (F) or NAD+ (G) levels of the catecholaminergic neurons were measured. n = 4, mean ± SEM, *P < 0.01 (ANOVA test). (H to K) TNFα-triggered axonal degeneration of catecholaminergic neurons of the celiac ganglia depended on Sarm1. Catecholaminergic neurons of the celiac ganglia of Sarm1+/+ or Sarm1-/- mice were in vitro cultured and then treated with 50 ng/mL recombinant TNFα. (H) Representative images of TH-positive axons of the cultured catecholaminergic neurons. (I) The integrity of TH-positive catecholaminergic axons was quantified. n = 4, mean ± SEM, *P < 0.01 (ANOVA test). (J and K) ATP (J) or NAD+ (K) levels of the catecholaminergic neurons were measured. n = 4, mean ± SEM, *P < 0.01 (ANOVA test)

Neurodegeneration of catecholaminergic axons involved the local energy deficit and depended on Sarm1. (A–C) The degeneration of catecholaminergic axons in the colon was caused by TNFα. (A) The wild-type mice were subjected to the DSS-induced colitis. TNFα mRNA levels in the colon tissues were determined by the qPCR analysis. n = 5, mean ± SEM, *P < 0.01 (ANOVA test). (B and C) The wild-type mice were administered with the anti-TNFα neutralizing antibody or control IgG and then subjected to the DSS-induced colitis. The unsectioned colon tissues were processed for the whole-tissue TH-immunolabeling. (B) Representative 3D-projection images (longitudinal view) of the 500-μm thickness of the tissues at 12.6× magnification of the lightsheet imaging. (C) TH-positive catecholaminergic axons within the mucosa were quantified. n = 5, mean ± SEM, *P < 0.01 (ANOVA test). (D–G) TNFα directly triggered the axonal degeneration of catecholaminergic neurons of the celiac ganglia. Catecholaminergic neurons of the celiac ganglia of wild-type mice were in vitro cultured. The neurons were then treated with 50 ng/mL recombinant TNFα, in combination with 10 mmol/L methylpyruvate or 50 mmol/L nicotinamide. (D) Representative images of TH-positive axons of the cultured catecholaminergic neurons. (E) The integrity of TH-positive catecholaminergic axons was quantified. n = 4, mean ± SEM, *P < 0.01 (ANOVA test). (F and G) ATP (F) or NAD+ (G) levels of the catecholaminergic neurons were measured. n = 4, mean ± SEM, *P < 0.01 (ANOVA test). (H to K) TNFα-triggered axonal degeneration of catecholaminergic neurons of the celiac ganglia depended on Sarm1. Catecholaminergic neurons of the celiac ganglia of Sarm1+/+ or Sarm1-/- mice were in vitro cultured and then treated with 50 ng/mL recombinant TNFα. (H) Representative images of TH-positive axons of the cultured catecholaminergic neurons. (I) The integrity of TH-positive catecholaminergic axons was quantified. n = 4, mean ± SEM, *P < 0.01 (ANOVA test). (J and K) ATP (J) or NAD+ (K) levels of the catecholaminergic neurons were measured. n = 4, mean ± SEM, *P < 0.01 (ANOVA test)

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