FIGURE 6.

Snails express two cardiac cation currents, the highly sodium-permeant T-type channel LCa_v3 and the calcium-selective L-type channel LCa_v1. A–C, quantitative RT-PCR standardized to Lymnaea HPRT1 control gene. A, relative mRNA expression levels of exon 12a and 12b in juvenile (juv) and adult (ad) snails, reflecting the almost exclusive expression of exon 12a in the snail heart and exon 12b in prostate and albumen glands. B, dramatic decline in LCa_v3 channel expression in whole animals can mostly be attributed to the decline of LCa_v3-12a expression in the developing heart. C, snail hearts lack mRNA expression of any sodium channel gene (LNa_v1 and LNa_v2). Snail hearts also lack any expression of the LCa_v2 synaptic non-L-type channel or the Ca_v3 T-type channel gene with exon 12b. Note the break in the y axis scale, illustrating that the range of expression of the sodium channel gene of LNa_v1 in the snail brain is ∼30-fold higher than the control HPRT1 gene, compared with the low levels of expression of the other calcium channel genes (which vary up to ∼3-fold higher than the control HPRT1 gene). D–G, ramp protocols (−110 to +100 mV in 1 s) carried out in the presence of external solutions as follows: 2 mm Ba²⁺ and 100 mm Na⁺ ions or 2 mm Ba²⁺ and 100 mm NMDG⁺ reveal a covert sodium-permeant, T-type current superimposed on the Ba²⁺ current in cardiomyocytes in the presence of a sodium-impermeant, L-type current (F). The sodium-permeant T-type currents in cardiomyocytes are indistinguishable from mammalian HEK-293T cells transfected with LCa_v3 with exon 12a with co-expression of LCa_v1 and accessory subunits (α₂δ and β_2a) (D). E, LCa_v3 with exon 12b; G, human Ca_v3.1 has some Na⁺ permeability but is not as Na⁺-permeant as the LCa_v3-12a variant expressed in cardiomyocytes. H, bar graph ± S.E., including sample data in D–G.