Figure 7.
Effects of bkip-1 mutation on neurotransmitter release. A, At 5 mm [Ca2+]o, the amplitude of ePSCs at the neuromuscular junction was significantly smaller in worms expressing SLO-1(gf), which could be reversed by bkip-1(lf) (zw10 allele). ePSC amplitude in bkip-1(lf) alone was comparable with that in wild-type animal. B, At 500 μm [Ca2+]o, ePSC amplitude of bkip-1(lf) was significantly larger than that of the wild type but similar to that of slo-1(md1745) [a putative null (Wang et al., 2001)] or the double-mutant slo-1(md1745);bkip-1(zw10). In both A and B, the neuromuscular transmission phenotype of bkip-1(lf) was rescued by neuronal but not muscle expression of wild-type BKIP-1. The holding potential was −60 mV. * indicates a statistically significant difference compared with the wild-type (p < 0.01, one-way ANOVA with Bonferroni's post hoc test). Error bars represent SE. The number of samples analyzed is indicated inside each column.