Figure 3: High glucose and oligomeric Aβ induce formation of SNO-Drp1 in cortical cultures and cortico-hippocampal slices and impair respiratory reserve. | Nature Communications

Figure 3: High glucose and oligomeric Aβ induce formation of SNO-Drp1 in cortical cultures and cortico-hippocampal slices and impair respiratory reserve.

From: Elevated glucose and oligomeric β-amyloid disrupt synapses via a common pathway of aberrant protein S-nitrosylation

Figure 3

(a) Mitochondrial O2 consumption by cortical cultures was monitored using the Seahorse platform after exposure to high glucose (20 mM), equimolar mannitol as an osmolarity control or oligomeric Aβ (250 nM) for 72 h. Basal respiratory rate was measured in triplicate. Values are mean+s.e.m., n≥12, *P<0.05 by ANOVA with Tukey’s post hoc test. (b) Cortical cultures (15 DIV) were exposed to high glucose (20 mM) or oligomeric Aβ (250 nM) for 2 h. Equimolar mannitol served as an osmolarity control for high glucose. Lysates were then analysed by biotin switch for SNO-Drp1. Values are mean+s.e.m., n≥3, *P<0.05 by ANOVA with Fisher’s PLSD post hoc test. (c) Acute rat cortico-hippocampal slices were exposed to high glucose, equimolar mannitol osmolarity control or oligomeric Aβ for 2 h. Biotin switch detected SNO-Drp1. Values are mean+s.e.m., n=3, *P<0.05 by ANOVA with Fisher’s PLSD post hoc test.

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