FIGURE 2.

Ru360 promotes propagation of stress-induced Ca²⁺ release events beyond the defective mitochondrial region. The G93A fiber was loaded with both TMRE (panel 1) and fluo-4 AM (panels 2-5). Following a brief (2-min) hypotonic shock, the stress-induced Ca²⁺ release events stay mainly in the fiber segment with depolarized mitochondria (panels 2 and 3). Perfusion of Ru360, an inhibitor of mitochondrial uniporter, caused propagation of those osmotic stress-induced Ca²⁺ release events beyond the defective mitochondrial region (panels 4 and 5).