Fig. 2: HFD/STZ induced neuronal morphological changes and a neurotoxic astrocyte phenotype in the hippocampus. | Experimental & Molecular Medicine

Fig. 2: HFD/STZ induced neuronal morphological changes and a neurotoxic astrocyte phenotype in the hippocampus.

From: Cholesterol-driven pathological astrocytic responses in diabetes-associated cognitive impairment through astrocytic SCAP accumulation and NF-κB–C3 signaling modulation

Fig. 2

a, b The representative traces of granule cells in the DG (a) and pyramidal cells in the CA3 region (b) along with a graphic description of Sholl analysis parameters. Scale bars, 50 µm. c The representative photomicrographs of the secondary apical branches of granule neurons in the DG neurons in the CA3 region. d, e The Sholl analysis showed reduced total dendritic length in the DG (d1) and CA3 (d2), as well as reduced dendritic complexity in the DG (e1) and CA3 (e2), in HFD/STZ mice compared with NCD controls. f The number of dendritic spines per 10 µm in the DG (f1) and CA3 (f2) regions was reduced in HFD/STZ-induced mice (n = 20 per group). g The representative immunoblots of the synaptic proteins PSD95 and SYP (n = 3 per group). h, i The representative maximum intensity projections of confocal images of GFAP- and C3-labeled astrocytes from the NCD (h) and HFD/STZ (i) groups. Scale bars, 20 µm. j The confocal orthogonal view of C3 encapsulated by astrocytes in i. C3, indicated by the arrow in the x–y projection, can be visualized within astroglia in the orthogonal x–z and y–z projections (also indicated by the arrow). Scale bars, 10 µm. k The average integrated fluorescence intensity (IntDen) of C3 colocalized with GFAP per astroglia in the DG (k1), CA3 (k2) and CA1 (k3). All of the data are presented as the mean ± s.e.m. Two-tailed unpaired Student’s t-tests were used. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. n.s., not significant. See also Supplementary Fig. 2 for further information.

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