Dale B, Yazaki I, Tosti E
Stazione Zoologica, Naples, Italy.
Am J Physiol. 1997 Sep;273(3 Pt 1):C822-5. doi: 10.1152/ajpcell.1997.273.3.C822.
Using the whole cell clamp technique, we have measured calcium-dependent currents and steady-state conductance in early sea urchin blastomeres. The calcium currents in M phase decreased from 8.5 microA/cm2 at the four-cell stage to 5.4 microA/cm2 at the eight-cell stage. In 16-cell stage embryos, calcium currents were 7.4 microA/cm2 in the mesomeres, 2.3 microA/cm2 in the macromeres, and were not detected in the micromeres. In contrast, the micromeres had a two- to threefold higher steady-state conductance than the mesomeres or macromeres, which may be due to potassium ion conductivity. Nifedipine, an L-type channel antagonist, delays cleavage division at a concentration of 0.05-0.1 mM and causes developmental defects, such as poor skeletal differentiation in later sea urchin embryos.
运用全细胞钳技术,我们测量了海胆早期卵裂球中钙依赖性电流和稳态电导。M期的钙电流在四细胞期为8.5微安/平方厘米,在八细胞期降至5.4微安/平方厘米。在16细胞期胚胎中,中体的钙电流为7.4微安/平方厘米,大卵裂球为2.3微安/平方厘米,而小卵裂球未检测到钙电流。相比之下,小卵裂球的稳态电导比中体或大卵裂球高两到三倍,这可能是由于钾离子传导性所致。硝苯地平,一种L型通道拮抗剂,在浓度为0.05 - 0.1毫摩尔时会延迟卵裂,并导致发育缺陷,如后期海胆胚胎中骨骼分化不良。