Erratum to: Isoform- and receptor-specific channel property of canonical transient receptor potential (TRPC)1/4 channels

Erratum to: Pflugers Arch - Eur J Physiol

DOI 10.1007/s00424-013-1332-y

The authors would like to apologize for inadvertently using Fig. 1d also for Fig. 5 h in the printed version of this paper.

The correct versions of Fig. 1d and Fig. 5 h are given below.

Fig. 1 G_q/11-coupled receptor stimulation and TRPC1α, TRPC1α/4, TRPC4 channel activity. From a to h, all left panels indicate I–V relationship and right panels indicate corresponding current traces. Inset legends at upper left area of I–V curves demonstrate heterologously expressed proteins. a, b In cells expressing M1 or M3 receptor, receptor stimulation by extracellular carbachol (100 μM) did not induced significant whole-cell current. c, d Cells expressing TRPC1α channels showed indistinguishable current increment in response to M1 or M3 stimulation achieved by extracellular carbachol (CCh, 100 μM). e, f Heteromeric TRPC1α/4 channel showed typical outward-rectifying I–V curves in response to M1 or M3 stimulation. g, h Genuine TRPC4 homomeric currents (without co-expression of TRPC1α) in response to M1 or M3 receptor stimulation. i Left panel indicates summarized current density measured above and right panel indicates rectification factor (|I _{+80 mV}/I_{−60 mV}|) analysis which was devised in order to show the sheer difference in I–V curve signature. j Left panel compares double-rectifying I–V curves of CCh-activated TRPC4 (light gray) and outward-rectifying I–V curves of CCh-activated TRPC1α/4 (black). In order to quantify the order of outward rectification, another rectification factor ρ (Rho) was devised which parameterizes two different slope conductance: ρ ≡ | g_{+10~+50 mV}|/|g _{− 120 ~ −80 mV}|. Two different I–V curves show stark difference in ρ value

Fig. 5. TRPC1α, TRPC1α/4, and TRPC4 channel activities in response to G_i/o-coupled receptor (M2) stimulation and overexpression of Gα _i2 ^Q205L protein. a, b Genuine TRPC4 homomeric channel activity in response to M2 receptor stimulation and overexpression of Gα _i2 ^Q205L (intrinsic GTPase activity deficient mutant) protein. Extracellular carbachol (CCh, 100 μM) and Cs⁺ -rich solution ([Cs⁺]_o = 140 mM) was treated for each activation systems, respectively. TRPC4 channels activated by each condition showed typical double-rectifying I–V curves. c, d TRPC1α homomeric channel activities in response to M2 receptor and Gα _i2 ^Q205L protein. Neither M2 receptor stimulation nor Gα _i2 ^Q205L protein activated TRPC1α channels. e, f TRPC1α/4 heteromeric channel activities in response to M2 receptor and Gα _i2 ^Q205L protein. Each activation system was insufficient to induce TRPC1α/4 channel currents but selectively activated TRPC4 homomeric channels. g, h TRPC1β homomeric channel activities in response to M2 receptor and Gα _i2 ^Q205L protein. Both systems could not induce channel activation. i, j TRPC1β/4 heteromeric channel activities in response toM2 receptor and Gα _i2 ^Q205L protein. Like TRPC1α/4, TRPC1β/4 did not permit their activation to those stimulators but only TRPC4 did permit their activation