Icariin Attenuates Synaptic and Cognitive Deficits in an Aβ_1–42-Induced Rat Model of Alzheimer’s Disease

Figure 3

Effect of ICA on synaptic ultrastructure in the CA1 region of the hippocampi of -infused rats (×10,000). Typical electron photomicrographs of different groups. (A) Sham group, (B) vehicle group, (C) ICA-L group, (D) ICA-M group, and (E) ICA-H group. Statistical graphs showing the parameters of synaptic structure (a–g) in the CA1 region. (a) Number of synapses. (b) Width of synaptic cleft. (c) Thickness of PSD. (d) Length of synaptic active zone. (e) Percentage of perforated synapses. (f) Percentage of flat synapses. (g) Curvature of synaptic interface. Sham group: normal presynaptic mitochondria, postsynaptic densities, synaptic cleft, and concave synapses. Vehicle group: unclear presynaptic mitochondria, thin postsynaptic density, reduced concave synapses, increased synaptic cleft, and flat synapses. ICA treatment group: compared with the vehicle group, the synaptic cleft is narrowed, the synaptic active zones are longer, the postsynaptic density is thicker, and the synapses have become curved. All data were analysed using one-way ANOVA and are presented as the mean ± SD. and versus the vehicle group. versus the ICA-H group.