Protective Effects of Testosterone on Presynaptic Terminals against Oligomeric -Amyloid Peptide in Primary Culture of Hippocampal Neurons

Figure 5

Oligomeric Aβ-induced impairment of synaptic vesicle unloading was ameliorated by pretreatment of testosterone. Primary hippocampal neurons were treated with testosterone or letrozole (aromatase inhibitor) + testosterone, followed by exposure to 5 μM oligomeric Aβ for 24 h. Neurons were stained with FM4-64 fluorescent probe. (a)–(d) represent synaptic vesicle uptake FM probe capability. (a) Control, (b) testosterone 10 nM for 25 h, (c) Aβ 5 μM for 24 h, and (d) 10 nM testosterone for 1 h, followed by exposure to 5 μM Aβ for 24 h. (e–j) represent synaptic vesicle release FM probe capability. (e) Control, (f) testosterone 10 nM for 25 h, (g) Aβ 5 μM for 24 h, (h) 10 nM testosterone for 1 h, followed by exposure to 5 μM Aβ for 24 h, (i) Let 1 μM for 25 h, (j) treatment of 1 μM Let, and 10 nM testosterone for 1 h, followed by exposure to 5 μM Aβ for 24 h. (k) The statistical analysis of FM probe loading fluorescent intensity and (l) the fluorescent intensity of FM probe unloading were measured by Image J software as described in the above section. ^∗∗∗𝑃<0.001 versus control group, ^∗∗𝑃<0.01 versus Aβ group, and ^##𝑃<0.01 versus Aβ group.