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. 2016 Apr 30;111(3):287–294. doi: 10.1093/cvr/cvw093

Figure 5.

Figure 5

[Ca2+]Cleft is increased in myocytes from AnkB+/− mice. (A) Working hypothesis. NCX and NKA density in the T-tubules is reduced in myocytes from AnkB+/− mice, which may result in slower Ca2+ extrusion from the junctional cleft and consequently elevated [Ca2+]Cleft compared with WT myocytes. This higher [Ca2+]Cleft may activate RyR through direct sensitization and indirectly by activating local CaMKII. (B) Example of [Ca2+]Cleft measurements with GCaMP2.2-FKBP12.6. (C) Mean decrease in fluorescence intensity upon application of 0Na+/0Ca2+ external solution and tetracaine for AnkB+/− and WT myocytes. (D) [Ca2+]Cleft calculated from data in panel C using the in situ characteristics of GCaMP2.2-FKBP12.6. (E) Mean decrease in GCaMP2.2-FKBP12.6 fluorescence upon inhibition of sarcolemmal Ca2+ transport in 0Na+/0Ca2+ solution (Sarc) and blockade of SR Ca2+ leak with tetracaine (SR). Data in panels C–E are from 24 cells from three different AnkB+/− mice and 20 cells from three WT mice. Statistical differences between groups were determined using Student's t-test. *P < 0.05 and ***P < 0.001.