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The Journal of Neuroscience, July 9, 2003, 23(14):6041-6049

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Cav1.4{alpha}1 Subunits Can Form Slowly Inactivating Dihydropyridine-Sensitive L-Type Ca2+ Channels Lacking Ca2+-Dependent Inactivation

Alexandra Koschak,1 Daniel Reimer,1,2 Doris Walter,1 Jean-Charles Hoda,1 Thomas Heinzle,2 Manfred Grabner,2 and Jörg Striessnig1

1Institut für Pharmazie, Abteilung Pharmakologie und Toxikologie, A-6020 Innsbruck, Austria,2Institut für Biochemische Pharmakologie, A-6020 Innsbruck, Austria

The neuronal L-type calcium channels (LTCCs) Cav1.2{alpha}1 and Cav1.3{alpha}1 are functionally distinct. Cav1.3{alpha}1 activates at lower voltages and inactivates more slowly than Cav1.2{alpha}1, making it suitable to support sustained L-type Ca2+ inward currents (ICa,L) and serve in pacemaker functions. We compared the biophysical and pharmacological properties of human retinal Cav1.4{alpha}1 using the whole-cell patch-clamp technique after heterologous expression in tsA-201 cells with other L-type {alpha}1 subunits. Cav1.4{alpha}1-mediated inward Ba2+ currents (IBa) required the coexpression of {alpha}2{delta}1 and {beta}3 or {beta}2a subunits and were detected in a lower proportion of transfected cells than Cav1.3{alpha}1. IBa activated at more negative voltages (5% activation threshold; -39mV; 15 mM Ba2+) than Cav1.2{alpha}1 and slightly more positive than Cav1.3{alpha}1. Voltage-dependent inactivation of IBa was slower than for Cav1.2{alpha}1 and Cav1.3{alpha}1(~50% inactivation after 5 sec; {alpha}2{delta}1 + {beta}3 coexpression). Inactivation was not increased with Ca2+ as the charge carrier, indicating the absence of Ca2+-dependent inactivation. Cav1.4{alpha}1 exhibited voltage-dependent, G-protein-independent facilitation by strong depolarizing pulses. The dihydropyridine (DHP)-antagonist isradipine blocked Cav1.4{alpha}1 with ~15-fold lower sensitivity than Cav1.2{alpha}1 and in a voltage-dependent manner. Strong stimulation by the DHP BayK 8644 was found despite the substitution of an otherwise L-type channel-specific tyrosine residue in position 1414 (repeat IVS6) by a phenylalanine. Cav1.4{alpha}1 + {alpha}2{delta}1 + {beta} channel complexes can form LTCCs with intermediate DHP antagonist sensitivity lacking Ca2+-dependent inactivation. Their biophysical properties should enable them to contribute to sustained ICa,L at negative potentials, such as required for tonic neurotransmitter release in sensory cells and plateau potentials in spiking neurons.

Key words: calcium channels; calcium-dependent inactivation; retina; calcium channel blockers; dihydropyridines; congenital stationary night blindness

Received Jan. 21, 2003; revised Apr. 16, 2003; accepted Apr. 24, 2003.




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