Figure 4: High glucose and oligomeric Aβ decrease dendritic spine density in a Drp1-dependent manner. | Nature Communications

Figure 4: High glucose and oligomeric Aβ decrease dendritic spine density in a Drp1-dependent manner.

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

Figure 4

(a) Dendritic spine density in organotypic cortico-hippocampal slices from YFP-transgenic mice after a 7-day exposure to high (25 mM) glucose or oligomeric Aβ (250 nM). Left: images of YFP-labelled dendritic spines (arrows) under epifluorescence microscopy (Scale bar, 10 μm). Right: quantification of spine density. The NOS inhibitor L-NAME (1 mM) prevented the decrease in spine density engendered by high glucose. Values are mean+s.e.m., n≥4 for each group, ***P<0.001, ****P<0.0001 by ANOVA with Tukey’s post hoc test. (b) Overexpression of WT Drp1 did not substantially attenuate the spine loss due to high glucose of oligomeric Aβ in cortical cultures. Values are mean+s.e.m., n≥6, ****P<0.0001 by ANOVA with Tukey’s post hoc test. (c) Overexpression of non-nitrosylatable Drp1 (C644A) mutant during exposure to high glucose or oligomeric Aβ resulted in spine number that was not statistically different from control. Values are mean+s.e.m., n≥10.

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