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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Pharmacological inhibition of HDAC6 reverses cognitive impairment and tau pathology as a result of cisplatin treatment

Fig. 4

Effect of cisplatin and ACY-1083 on synaptosomal mitochondrial deficits. After completion of all behavioral tests, synaptosomes were isolated from brains of mice treated with (a) PBS + vehicle, (b) cisplatin + vehicle, (c) PBS + ACY-1083, or (d) cisplatin + ACY-1083. Mitochondrial morphology was assessed on electron microscopic images. Mitochondria were indicated by arrows. e Percentage of atypical mitochondria was quantified (n = 4 mice (25–35 mitochondria) per group; two-way ANOVA with Tukey’s post-hoc analysis: F (1, 120) = 7.57; PBS vs. Cisplatin, p = 0.0256; Cisplatin vs. Cisplatin + ACY-1083, p = 0.0060). Oxygen consumption rates were analyzed in isolated synaptosomes using the Seahorse XFe24 Flux Analyzer. f Maximum respiratory capacity (MRC) (n = 6; two-way ANOVA with Tukey’s post-hoc analysis: F (1, 20) = 6.243; PBS vs. Cisplatin, p = 0.0416; Cisplatin vs. Cisplatin + ACY-1083, p = 0.0345), (g) spare respiratory capacity (SRC) (n = 6; two-way ANOVA with Tukey’s post-hoc analysis: F (1, 20) = 5.296; PBS vs. Cisplatin, p = 0.0147; Cisplatin vs. Cisplatin + ACY-1083, p = 0.0291; n = 6), (h) basal respiration (n = 6; two-way ANOVA, F (1, 20) = 0.6219, p = 0.4396), and (i) ATP-coupled respiration (n = 6; two-way ANOVA, F (1, 20) = 0.02046, p = 0.8877) were calculated. Results are expressed as means ± SEM; *p < 0.05, **p < 0.01

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