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. 2018 Aug 28;596(20):4923–4944. doi: 10.1113/JP276431

Figure 6. Psychosocial stress induces increased responsiveness to acute stress, which was ameliorated by SCFAs.

Figure 6

Stress responsiveness and HPA‐axis reactivity were assessed using the stress‐induced hyperthermia test 3 weeks after psychosocial stress (A), and by assessing the corticosterone levels in response to acute stress 6 weeks after psychosocial stress (B and C). The stressor used for the latter was the forced swim test. Hypothalamic genes involved in HPA‐axis signalling of which expression was investigated were corticotrophin‐releasing factor (CRF), mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) (D). For the hippocampus, these were corticotrophin‐releasing factor receptor 1 (CRFR1), MR and GR (E). All data were non‐parametrically distributed and analysed using the Kruskal‐Wallis test, followed by the Mann‐Whitney test. Significant differences are depicted as: * P < 0.05, ** P < 0.01 and *** P < 0.001; Control/Control compared to SCFA/Control or Control/Stress, $ P < 0.05, $$ P < 0.01; SCFA/Control compared to SCFA/Stress, # P < 0.05 and ## P < 0.01; Control/Stress compared to SCFA/Stress. All data are expressed as means ± SEM (n = 8–10). [Color figure can be viewed at http://wileyonlinelibrary.com]