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The Journal of Neuroscience, August 15, 2001, 21(16):5944-5951

Neuronal Ca_V1.3₁ L-Type Channels Activate at Relatively Hyperpolarized Membrane Potentials and Are Incompletely Inhibited by Dihydropyridines

Weifeng Xu and Diane Lipscombe

Department of Neuroscience, Brown University, Providence, Rhode Island 02912

L-type calcium channels regulate a diverse array of cellular functions within excitable cells. Of the four molecularly defined subclasses of L-type Ca channels, two are expressed ubiquitously in the mammalian nervous system (Ca_V1.2₁ and Ca_V1.3₁). Despite diversity at the molecular level, neuronal L-type channels are generally assumed to be functionally and pharmacologically similar, i.e., high-voltage activated and highly sensitive to dihydropyridines. We now show that Ca_V1.3₁ L-type channels activate at membrane potentials ~25 mV more hyperpolarized, compared with Ca_V1.2₁. This unusually negative activation threshold for Ca_V1.3₁ channels is independent of the specific auxiliary subunits coexpressed, of alternative splicing in domains I-II, IVS3-IVS4, and the C terminus, and of the expression system. The use of high concentrations of extracellular divalent cations has possibly obscured the unique voltage-dependent properties of Ca_V1.3₁ in certain previous studies. We also demonstrate that Ca_V1.3₁ channels are pharmacologically distinct from Ca_V1.2₁. The IC₅₀ for nimodipine block of Ca_V1.3₁ L-type calcium channel currents is 2.7 ± 0.3 µM, a value 20-fold higher than the concentration required to block Ca_V1.2₁. The relatively low sensitivity of the Ca_V1.3₁ subunit to inhibition by dihydropyridine is unaffected by alternative splicing in the IVS3-IVS4 linker. Our results suggest that functional and pharmacological criteria used commonly to distinguish among different Ca currents greatly underestimate the biological importance of L-type channels in cells expressing Ca_v1.3₁.

Key words: Ca_V1.3₁; L-type; voltage-gated calcium channel; dihydropyridine; low threshold; R-type; clone; Xenopus oocytes; HEK 293

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21165944-08$05.00/0

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