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Fig. 1 | Journal of Neuroinflammation

Fig. 1

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

Fig. 1

BMAA targets the mitochondria in cells lacking functional glutamate receptors. a SHSY-5Y cells, which do not express functional NMDA receptors, were exposed to 3 mM BMAA for 48 h. After this period, mitochondrial membrane potential was measured using TMRM+ dye. After baseline reading neurons were exposed to 1 μM of CCCP + 2.5 μM oligomycin to prevent reversal of ATP synthase. Bars depict maximum RFU after CCCP + oligomycin minus basal RFU reading. Data represent the mean ± SEM derived from six independent experiments and are expressed relative to untreated neurons. The statistical significance was determined using unpaired t test and *p < 0.05 when compared to untreated SHSY-5Y cells. b After 48 h of exposure to increasing concentrations of BMAA (250 μM; 500 μM; 1 mM and 3 mM), the MTT assay was performed to assess cell metabolic activity by measuring the formation of insoluble formazan. Data represent mean ± SEM values derived from three independent determinations and results are expressed relative to untreated neurons

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