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. 2018 May 29;6(3):321–344. doi: 10.1016/j.jcmgh.2018.05.009

Figure 8.

Figure 8

The NK2R antagonist GR 159897 limits neuropathy and reactive gliosis in the myenteric plexus during inflammation. (A) Representative confocal microscopy images of dual-label immunohistochemistry for GFAP (green) and the pan-neuronal marker Hu (magenta) in healthy (saline) and inflamed (DNBS) mice treated with vehicle or GR 159897 at 48 hours or 3 weeks after induction of colitis. Scale bar: 30 μm (applies to all images). Labeling is representative of experiments performed on a minimum of 4 mice. (B) Quantification of myenteric neuron packing density in healthy and inflamed mice treated with vehicle or GR 159897 at 48 hours or 3 weeks after induction of colitis (n = 3–8 mice; 2-way analysis of variance with multiple comparisons; *P = .02239; **P = .0097). (C and D) Quantification of (C) GFAP protein expression (integrated density, n = 4–6 mice; 2-way analysis of variance with multiple comparisons, normalized to group vehicle saline) and (D) GFAP mRNA levels (n = 4–7 mice; 2-way analysis of variance with multiple comparisons, normalized to glyceraldehyde-3-phosphate dehydrogenase [GAPDH]; *P = .0114) in samples of myenteric plexus from the distal colons of healthy and inflamed mice treated with vehicle or GR 159897 at 48 hours or 3 weeks after induction of colitis. (E and H) Quantification of glial morphology including (E) total process length, (F) process thickness, and Scholl analysis for process branching at (G) 48 hours or (H) 3 weeks after induction of colitis (n = 16 glia; 2-way analysis of variance with multiple comparisons; *P = .0185; ***P = .0003; ****P < .0001).