Fig. 3: C26 cancer causes increased IL-6 and neuron hyperactivity in the AP.

a A schematic of the experimental procedure. b IL-6 levels in the area postrema (AP) during cancer progression. IL-6 levels were normalized to total protein levels (n = 8-10 mice in each group; left, IL-6, F = 5.883, P = 0.0024, *P = 0.011, *P = 0.0483, **P = 0.001; right, total protein, F = 0.61, P = 0.61 (n.s., nonsignificant); one-way ANOVA followed by Tukey’s post-hoc test). c Confocal immunohistochemical images showing Fos expression in different brain areas in tumor-bearing (top) or control (bottom) mice. d Quantification of Fos⁺ cells in different brain areas (n = 4 mice in each group; AP, t = 2.91, *P = 0.027, NTS, T = 9.77, ****P = 6.62×10⁻⁵, PBN, t = 11.65, ****P = 2.41 × 10⁻⁵, CeA, t = 4.37, **P = 0.0047, PVN, t = 3.65, *P = 0.011, BNST, t = 5.86, **P = 0.0011; unpaired t test). e A diagram showing the AP in a coronal brain section for electrophysiological recording. f Representative miniature EPSC traces from AP neurons in control (top) and cachectic (bottom) mice. g Quantification of miniature EPSC frequency (left) and amplitude (right) (control, n = 30 cells / 6 mice, cachexia, n = 32 cells / 7 mice; frequency, n.s. (nonsignificant), P = 0.2513, amplitude, **P = 0.0017, Mann-Whitney test). h Representative spontaneous IPSC traces from AP neurons in control (top) and cachectic (bottom) mice. i Quantification of spontaneous IPSC frequency (left) and amplitude (right) (control, n = 36 cells / 7 mice, cachexia, n = 34 cells / 6 mice; frequency, n.s., P = 0.1637, amplitude, n.s., P = 0.4580, Mann-Whitney test). AP, area postrema; NTS, nucleus tractus solitarii; PBN, parabrachial nucleus; CeA, central amygdala; PVN, paraventricular nucleus of hypothalamus; BNST, bed nucleus of the stria terminalis. Data in b, d, g, i are presented as mean ± s.e.m. Source data are provided as a Source Data file.