Abstract
Since our observation that T-tubules can fail to propagate action potentials in diseased hearts (1), our studies have focused on understanding the consequences of these electrical defects for local Ca2+ release (2) and force production (3). More recently, we have started to explore the causes of electrical defects (4), focusing on the presence of electrical conduction failures, seemingly associated with a local drop in membrane excitability (5). The methodology developed through our work has allowed us to quantitatively assess T-tubular conductivity, thus permitting evaluation of the efficiency of passive spread of voltage changes across the cardiac cell. Although these passive … [↵][1]2To whom correspondence should be addressed. Email: sacconi{at}lens.unifi.it. [1]: #xref-corresp-1-1
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