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Functional role of L-type Cav1.3 Ca2+ channels in cardiac pacemaker activity

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      Most cited references 16

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      Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches

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        Congenital deafness and sinoatrial node dysfunction in mice lacking class D L-type Ca2+ channels.

        Voltage-gated L-type Ca2+ channels (LTCCs) containing a pore-forming alpha1D subunit (D-LTCCs) are expressed in neurons and neuroendocrine cells. Their relative contribution to total L-type Ca2+ currents and their physiological role and significance as a drug target remain unknown. Therefore, we generated D-LTCC deficient mice (alpha1D-/-) that were viable with no major disturbances of glucose metabolism. alpha1D-/-mice were deaf due to the complete absence of L-type currents in cochlear inner hair cells and degeneration of outer and inner hair cells. In wild-type controls, D-LTCC-mediated currents showed low activation thresholds and slow inactivation kinetics. Electrocardiogram recordings revealed sinoatrial node dysfunction (bradycardia and arrhythmia) in alpha1D-/- mice. We conclude that alpha1D can form LTCCs with negative activation thresholds essential for normal auditory function and control of cardiac pacemaker activity.
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          Pacemaker mechanisms in cardiac tissue.

           D DiFrancesco (1992)
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            Author and article information

            Journal
            Proceedings of the National Academy of Sciences
            Proceedings of the National Academy of Sciences
            Proceedings of the National Academy of Sciences
            0027-8424
            1091-6490
            April 29 2003
            April 16 2003
            April 29 2003
            : 100
            : 9
            : 5543-5548
            10.1073/pnas.0935295100
            © 2003
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