Fig. 5
ME/CFS-like pathophysiology in Htr1a-/- mice and reverse effects of 5-HT synthesis inhibitor. In CRISPR/Cas9-mediated Htr1a-knockdown mice, the protein expression of the 5-HT1A receptor in both the hypothalamus and RN was determined by western blot analysis (A). Plasma corticosterone levels in Htr1a-knockdown mice were assessed by EIA (B). The latency to fall from the drum in the rota-rod test (C), the latency to paw withdrawal in the plantar test (D) and the time spent in the center in the open field test (E) were assessed. Reverse effects of pCPA (5-HT synthesis inhibitor) against ME/CFS-like behaviors was evaluated by rota-rod and nest building test (F and G). The data are expressed as the mean ± SD (n = 4, 5 or 8/group). **p < 0.01 compared to the wild-type group or saline-injected group without pCPA treatment, #p < 0.05 and ##p < 0.01 compared to the scrambled virus-infected group or fluoxetine-injected group without pCPA treatment