Fig. 6: ACC expression of CCKBRs is increased in NCI mice. | Nature Communications

Fig. 6: ACC expression of CCKBRs is increased in NCI mice.

From: Paraventricular hypothalamic input to anterior cingulate cortex controls food preferences in chronic visceral pain mice

Fig. 6

a Representative western blot of CCKAR and CCKBR expression in the ACC. b CCKB receptor expression was significantly greater in the ACC of NCI mice than in that of CON mice (n = 6 mice/group, p = 0.0002). c The mRNA level of CCKBRs was markedly greater in the ACC of NCI mice than in that of CON mice (n = 6 mice/group, p < 0.0001). d Schematic of proglumide sodium or tetragastrin injection (left), and the red boxes show the site of microinjection into the ACC (right). e Bar plot showing the colorectal distension (CRD) threshold in NCI mice treated with proglumide sodium compared with those in the NCI and NS groups (n = 8 mice/group, p < 0.0001). f Bar plot showing the CRD threshold in CON mice treated with tetragastrin compared with those in the CON and NS groups (n = 8 mice/group, p < 0.0001). g Representative images showing the colocalization of CCKBR (green) and glutamatergic neurons (red) in the ACC of NCI mice. Scale bar:20 µm. h Percentage of colocalization in the ACC region (n = 3 mice). All the data are presented as the means ± SEMs. Two-way ANOVA with Sidak’s multiple comparisons test (b, c). Ordinary one-way ANOVA with Dunnett’s multiple comparisons test (e, f). **p < 0.01.

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