Ca2+/Calmodulin-Dependent Facilitation and Inactivation of P/Q-Type Ca2+ Channels
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چکیده
منابع مشابه
Calmodulin Is the Ca2+ Sensor for Ca2+-Dependent Inactivation of L-Type Calcium Channels
Elevated intracellular Ca2+ triggers inactivation of L-type calcium channels, providing negative Ca2+ feedback in many cells. Ca2+ binding to the main alpha1c channel subunit has been widely proposed to initiate such Ca2+ -dependent inactivation. Here, we find that overexpression of mutant, Ca2+ -insensitive calmodulin (CaM) ablates Ca2+ -dependent inactivation in a "dominant-negative" manner. ...
متن کاملCa/Calmodulin-Dependent Facilitation and Inactivation of P/Q-Type Ca Channels
Trains of action potentials cause Ca-dependent facilitation and inactivation of presynaptic P/Q-type Ca channels that can alter synaptic efficacy. A potential mechanism for these effects involves calmodulin, which associates in a Ca-dependent manner with the pore-forming a1A subunit. Here, we report that Ca and calmodulin dramatically enhance inactivation and facilitation of P/Q-type Ca channel...
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Alternative splicing of the P/Q-type channel (Ca(V)2.1) promises customization of the computational repertoire of neurons. Here we report that concerted splicing of its main alpha1A subunit, at both an EF-hand-like domain and the channel C terminus, controls the form of Ca2+-dependent facilitation (CDF), an activity-dependent enhancement of channel opening that is triggered by calmodulin. In re...
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Inactivation of currents carried by Ba2+ and Ca2+, as well as intramembrane charge movement from L-type Ca2+ channels were studied in guinea pig ventricular myocytes using the whole-cell patch clamp technique. Prolonged (2 s) conditioning depolarization caused substantial reduction of charge movement between -70 and 10 mV (charge 1, or charge from noninactivated channels). In parallel, the char...
متن کاملCa2+- and voltage-dependent inactivation of Ca2+ channels in nerve terminals of the neurohypophysis.
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ژورنال
عنوان ژورنال: The Journal of Neuroscience
سال: 2000
ISSN: 0270-6474,1529-2401
DOI: 10.1523/jneurosci.20-18-06830.2000