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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Microbial BMAA elicits mitochondrial dysfunction, innate immunity activation, and Alzheimer’s disease features in cortical neurons

Fig. 2

BMAA affects neuronal mitochondria oxygen consumption rate (OCR) and mitochondrial calcium uptake. The fundamental parameters of mitochondrial function namely ability to uptake calcium, basal respiration, ATP synthesis, and maximal respiration can be evaluated in isolated mitochondria. a Mitochondrial ability to uptake calcium was evaluated by Ca2+-sensitive fluorescent dye Calcium Green 5N, in isolated mitochondria treated or not with BMAA (0.5–3 mM), subjected to 10 μM Ca2+ pulses applied until the Ca2+ retention capacity was reached as shown by the upward deflection of the trace. b OCR representative curve and respective histograms of basal respiration, maximal respiration, and ATP synthesis were determined in isolated mitochondria from cortical tissue treated with different BMAA concentrations. The assay was performed in MAS containing 10 mM succinate plus 2 μM rotenone under sequentially injection of mitochondrial inhibitors and substrates (final concentration, 4 mM ADP; 2.5 μg/mL oligomycin; 4 μM FCCP and 4 μM antimycin A) as shown in representative traces using Seahorse XF24 extracellular flux analyzer. Data represent the mean ± SEM derived from six independent experiments and are expressed as pmol of O2/min/μg of isolated mitochondria. The statistical significance was determined using one-way ANOVA followed by Dunnett’s test *p < 0.05 versus untreated mitochondria

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