Figure 5. Acute hypoxia induces MOAS in WT mice.

(a,c) Elongated mitochondria were observed using TEM (a) or super-resolution fluorescence microscopy with Tom20 (red) and Drp1 (green) antibodies (c) in the CA1 hippocampi of a WT mouse 10 weeks of age sacrificed by cervical dislocation without prior use of anesthetics. (b,d) Exposure of a WT mouse 10 weeks of age to CO₂ for 5 min produced MOAS observed by TEM (b) or super-resolution fluorescence microscopy with Tom20 (red) and Drp1 (green) antibodies (d). (e) MOAS in the CA1 hippocampi in a WT mouse 88 weeks of age sacrificed by cervical dislocation. (f) Exposure of a WT mouse 88 weeks of age to CO₂ for 5 min caused MOAS formation. Exposure of a WT mouse 10 weeks of age to CO₂ for 5 min produced mitochondria with increased size (g, FSC histogram, median intensity of control 109.19 and hypoxia 203.0) and granularity (h, SSC histogram, median intensity of control 138.56 and hypoxia 268.44), and resulted in enhanced mitochondrial recruitment of Drp1 phosphorylated at S616 (53.8%, S616-Tom20 plots) in the CA1 hippocampal region compared to age-matched control. (h–j) Flow cytometry analysis of mitochondria isolated from hippocampi of mice exposed to hypoxic conditions compared to control mice (g,h) confirmed that enhanced recruitment of the activated Drp1 to mitochondria results in elongated organelles (i,j). Scale bars, 2 μm (a,e,b,f). Scale bars, 1 μm (c,d). Three to four female mice per each group were examined.