Tatsumi H, Katayama Y
Department of Autonomic Physiology, Tokyo Medical and Dental University, Japan.
Neurosci Lett. 1995 Aug 18;196(1-2):9-12. doi: 10.1016/0304-3940(95)11823-f.
Neurons were acutely dissociated from the rat nucleus basalis, and whole-cell patch clamp recordings were made. Voltage dependent calcium currents (ICa) were recorded and fura-2 microfluorimetric recordings of intracellular free Ca2+ concentration ([Ca2+]i) were made at the same time. In Na(+)-containing solution, a depolarization from -60 to +40 mV evoked the maximal increase in [Ca2+]i, and this decreased to 43% of the maximal with a large depolarization to +120 mV. The [Ca2+]i increase induced by the large depolarization (+20 to +120 mV) was inhibited by perfusion of Na(+)-free external solution, and was less when the recording pipette contained a peptide (PRLLFYKYVYKRYRAGKQRG, named XIP) known to inhibit Na/Ca exchange. These results suggest that the [Ca2+]i increase by the large depolarization is mediated by reverse operation of Na/Ca exchange (Ca2+ inward and Na+ outward).
从大鼠基底核中急性分离出神经元，并进行全细胞膜片钳记录。记录电压依赖性钙电流（ICa），同时用fura-2微荧光法记录细胞内游离Ca2+浓度（[Ca2+]i）。在含Na+的溶液中，从-60 mV去极化到+40 mV可引起[Ca2+]i的最大增加，而当去极化到+120 mV时，这种增加下降到最大值的43%。大去极化（+20到+120 mV）诱导的[Ca2+]i增加可被无Na+的细胞外溶液灌注所抑制，并且当记录电极内含有一种已知可抑制Na/Ca交换的肽（PRLLFYKYVYKRYRAGKQRG，命名为XIP）时，增加幅度较小。这些结果表明，大去极化引起的[Ca2+]i增加是由Na/Ca交换的反向运作（Ca2+内流和Na+外流）介导的。
