Fig. 10: Inhibition of Gfral+ AP neurons attenuates AP network hyperactivity in the Lewis lung cancer (LLC) model. | Nature Communications

Fig. 10: Inhibition of Gfral+ AP neurons attenuates AP network hyperactivity in the Lewis lung cancer (LLC) model.

From: Area postrema neurons mediate interleukin-6 function in cancer cachexia

Fig. 10

a Confocal immunohistochemical images showing Fos expression in different brain areas in the mice where Gfral+ AP neurons were infected with the AAV expressing TeLC (top) or GFP (bottom). b Quantification of Fos+ cells in different brain areas (TeLC group, n = 9 mice, GFP group, n = 8 mice; AP, t = 2.33, *P = 0.0343; NTS, t = 3.3, **P = 0.0049; PBN, t = 4.04, **P = 0.0011; PVN, t = 3.09, **P = 0.0094; CeA, t = 2.62, *P = 0.0193; BNST, t = 2.56, *P = 0.022; t test with false discovery rate adjusted). c Tumor (left) and spleen (right) mass of the mice at 23 days after tumor inoculation (TeLC tumor group, n = 9, GFP tumor group, n = 8, GFP sham group, n = 6; tumor, F = 13.57, P = 0.0002; spleen, F = 19.12, P = 0.00002, ***P = 0.00012, ****P = 0.000035; one-way ANOVA followed by Tukey’s multiple comparisons 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, c are presented as mean ± s.e.m. Source data are provided as a Source Data file.

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