Figure 4.
Steady-state inactivation of human CaV2.1 channels occurs at more negative voltages in the fast than in the slow gating mode, independently of the β subtype. Single channel recordings as in Fig. 1 on HEK293 cells stably coexpressing human CaV2.1α1 (α1A-2), α2bδ-1, and β1b, β2e, β3a, or β4a subunits. (A) Open probability in successive depolarizations at +30 mV as a function of time during recordings in which the holding potential was changed as indicated above the horizontal bars, from two representative patches containing a single CaV2.1 (α1A-2–β4a–α2bδ-1) channel in either the fast (left) or the slow gating mode (right). (B) Normalized open probability, (po)n, at +30 mV of CaV2.1 channels gating in the fast and slow modes containing either the β1b or the β4a subunits as a function of holding potential, Vh, obtained from patches containing a single channel showing only, or mainly, one gating mode or two clearly separated periods in the two modes. Po at different holding potentials was obtained by averaging the open probability of all consecutive sweeps at a given Vh in experiments (n = 3–8) like those in A. In each experiment, the open probability was normalized to the value at Vh = −80 mV. (C) Normalized open probability, (po)n, at +30 mV of CaV2.1 channels containing different β subunits all gating in the fast mode as a function of Vh. β1b (Δ), β2e (○), β3a (□), β4a (⋄). Most of the patches contained a single channel. Part of the data for CaV2.1 channels containing the β2e subunit were obtained from HEK293 cells transiently coexpressing human CaV2.1α1, α2bδ-1, and β2e subunits. Most of the data for CaV2.1 channels containing the β3a subunit were obtained from PB1-14 cells transfected with β3a cDNA.