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Fig. 6 | Alzheimer's Research & Therapy

Fig. 6

From: Serotonin 5-HT6 receptors affect cognition in a mouse model of Alzheimer’s disease by regulating cilia function

Fig. 6

5-HT6 regulated axonal length in hippocampal neurons. (a) 5-HT6 regulated axonal length of neurons in WT mice. AnkG (purple), mCherry (red), and DAPI (blue) indicated the axons of hippocampal neurons. (b) 5-HT6 influenced axonal length in WT and APP/PS1 mice. Axonal length in APP/PS1 mice was shorter than that of WT mice. Overexpression of 5-HT6 decreased axonal length. Knocking down 5-HT6 increased axonal length. 5-HT6 versus vector in WT, **p < 0.01; 5-HT6 siRNA versus vector in WT, **p < 0.01; 5-HT6 versus vector in APP/PS1, **p < 0.01; 5-HT6 siRNA versus vector in APP/PS1, **p < 0.01; APP/PS1 versus WT in vector, *p < 0.05 (two-way ANOVA: interaction, F 2,115 = 1.05, p = 0.35; treatment, F 2,115 = 20.22, p < 0.001; gene, F 1,115 = 7.94, p < 0.01) (c) AnkG indicated the AIS. NF186 (red) and AnkG (green) were markers of the AIS. MAP2 (purple) marked neurons. (d) 5-HT6 regulated AIS length. NF186 (purple) indicated the AIS. (e) Overexpression of 5-HT6 increased AIS length. Knocking down 5-HT6 decreased AIS length. 5-HT6, **p < 0.01; 5-HT6 siRNA, **p < 0.01 (Kruskal–Wallis test, p < 0.001). (f) 5-HT6 mutations influenced AIS length. Mutations F69L, T70I, D72A, D106A, A230F, and K262A recovered normal AIS length. EGFP, **p < 0.01; F69L, **p < 0.01; T70I, **p < 0.01; D72A, **p < 0.01; D106A, **p < 0.01; A230F, **p < 0.01; K262A, **p < 0.01 (Kruskal–Wallis test, p < 0.001). (g) Overexpression of 5-HT6 reduced the distance between the AIS and cell body. (h) Overexpression of 5-HT6 decreased the distance between the AIS and cell body. 5-HT6, **p < 0.01 (Kruskal–Wallis test, p < 0.001). (i) 5-HT6 mutations influenced the distance between the AIS and cell body. Mutations D72A and K265A significantly recovered the decreased distance between the AIS and cell body. EGFP, *p < 0.05; D72A, *p < 0.05; K265A, *p < 0.05 (Kruskal–Wallis test, p < 0.01). (j) Overexpression of 5-HT6 increased the percentage of neurons with branched AIS. (k) High expression of 5-HT6 significantly increased the percentage of neurons with branched AIS. 5-HT6, **p < 0.01 (Kruskal–Wallis test, p < 0.001). (l) F69L + T70I + D72A mutation restored the percentage of neurons with branched AIS. EGFP, *p < 0.05; F69L + T70I + D72A, *p < 0.05 (Kruskal–Wallis test, p < 0.01). All groups were compared with the vector group or EGFP group. Scale bars, 10 μm. All data presented as mean ± SEM (≥3 independent experiments). 5-HT6, serotonin 6 receptor, AIS axon initial segment, AnkG ankyrin-3, DAPI 4',6-diamidino-2-phenylindole

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