MICROSENSOR TECHNOLOGY TO MEASURE FAST EXTRACELLULAR EVENTS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Calcium (Ca2+)-induced calcium-release (CICR) within the dyadic space of cardiac myocytes displays gradedness and high gain. Disruption of this Ca2+ signalling in the myocyte can activate pathological hypertrophy and thus heart disease. While CICR at the cellular level has been extensively modeled, the correlation between single openings of the L-type Ca2+ channel and the quantal intracellular release of Ca2+ (sparks) in cardiac myocytes remains unsubstantiated. Studies of ion channels have benefited greatly from patch-clamping, allowing single channel currents to be measured with unparalleled resolution. Even so, patch clamping is relatively invasive to the cell, disrupting intracellular signal transduction, particularly local CICR pathways.