Fig. 4: Inflammatory state increases the number of active nodose ganglia neurons but decreases their response levels.
From: Neural representation of cytokines by vagal sensory neurons
a Example ROI maps from a Control and DSS-colitis experiment, with sample traces from individual neurons during 50 s recording period. ROI map scale bar, 50 µm. b There were a higher number of spontaneously active nodose ganglia neurons in DSS-colitis mice at baseline (per mouse n = 11, whiskers indicate min/max value, bounds of box indicate 25% and 75% quartile, and line within box indicates median, ** P = 0.0033, two-tailed Mann–Whitney test). c Example spontaneous activity traces from individual neurons from Control and DSS‐colitis mouse groups. d Comparison of baseline activity reveals a significant reduction in the amplitude of calcium transients during DSS‐colitis (Control, n = 14 mice; DSS-colitis, n = 10 mice, * P = 0.026, two-tailed Mann–Whitney test). e Daily measurements of disease activity index reveal increased disease severity in DSS mice (Control = 7 mice, DSS-colitis n = 9 mice, *** P < 0.0001, Mixed-effects analysis with Šidák correction). f Measurement of post‐mortem colon length displays significant shortening on days 7 and 14 in the DSS group compared to controls (per mouse, n = 12, day 7 ** P = 0.0078, day 14 * P = 0.0274, Mixed-effects analysis with Šidák correction). g Analysis of baseline activity at several time points during disease progression reveals a significant reduction in the amplitude of spontaneous calcium transients in the DSS-colitis group at days 7 and 14 (per mouse, n = 9, day 7 * P = 0.0162, day 14 * P = 0.0354, Mixed-effects analysis with Šidák correction). All error bars represent ± SEM.
