Eckert R, Ewald D
J Physiol. 1983 Dec;345:549-65. doi: 10.1113/jphysiol.1983.sp014996.
Calcium tail currents, recorded at -40 mV after repolarization from 7 or 10 ms voltage-clamp depolarizations in axotomized Aplysia neurones in the presence of tetrodotoxin and tetraethylammonium, were used to investigate the inactivation of the calcium conductance without interference from contaminating potassium currents. Prior depolarization with a prepulse (V1) resulted in a reduction in size of the tail currents recorded following the test pulse (V2). The reduction occurred in both the fast (tau 1 less than 0.4 ms) and slow (tau 2 approximately equal to 2.0 ms) components of the tail current. The degree of inactivation remained constant when tail currents were measured at potentials ranging up to 30 mV on either side of the potassium equilibrium potential. Thus, any changes in potassium current must have contributed virtually nothing to the changes in tail current amplitude seen following presentation of the prepulse. Inactivation was greatest following prepulses to potentials (+10 to +40 mV) that produce maximal entry of calcium ions, and declined to about zero as the prepulse approached the calcium equilibrium potential. For V1 potentials above +50 mV, the prepulse caused an apparent short-term facilitation of V2 tail currents in EGTA-injected neurones. This effect, detected up to 50 ms following the pulse, is of uncertain origin. Pressure injection of calcium ions caused reduction in the size of the tail current, which was restored by subsequent injection of EGTA. Tail current amplitude was reduced by presentation of the prepulse for all test pulse voltages, but the measured inactivation declined exponentially towards a minimum with test pulses of increasingly positive potential. Removal of inactivation following a 200 ms prepulse was greatly accelerated by injection of EGTA. The EGTA-resistant inactivation remaining at short times decayed with a time constant of about 0.12 s. The relation of tail current reduction to prepulse voltage is consistent with the interpretation that the EGTA-resistant inactivation remaining at short times depends on entry of calcium ions during the prepulse, as does the EGTA-sensitive inactivation remaining at later times. It is proposed that the 'EGTA-resistant' phase of inactivation results from loading of EGTA with calcium ions near the inner surface of the membrane during sustained calcium entry, allowing the intracellular calcium concentration to rise. The results provide further evidence for a calcium-mediated inactivation of the calcium conductance.(ABSTRACT TRUNCATED AT 400 WORDS)
在存在河豚毒素和四乙铵的情况下，对切断轴突的海兔神经元进行7或10毫秒电压钳去极化后复极化至-40 mV时记录的钙尾电流，用于研究钙电导的失活，而不受污染钾电流的干扰。用预脉冲（V1）进行先前的去极化导致在测试脉冲（V2）之后记录的尾电流大小减小。这种减小发生在尾电流的快速成分（τ1小于0.4毫秒）和慢速成分（τ2约等于2.0毫秒）中。当在钾平衡电位两侧高达30 mV的电位下测量尾电流时，失活程度保持恒定。因此，钾电流的任何变化对预脉冲呈现后观察到的尾电流幅度变化几乎没有贡献。在预脉冲到产生最大钙离子内流的电位（+10至+40 mV）后失活最大，并且当预脉冲接近钙平衡电位时失活降至约零。对于高于+50 mV的V1电位，预脉冲在注射EGTA的神经元中引起V2尾电流明显的短期易化。这种效应在脉冲后长达50毫秒时被检测到，其起源尚不确定。压力注射钙离子导致尾电流大小减小，随后注射EGTA可使其恢复。对于所有测试脉冲电压，预脉冲的呈现都会使尾电流幅度减小，但随着测试脉冲电位越来越正，测量到的失活呈指数下降至最小值。注射EGTA可大大加速200毫秒预脉冲后的失活去除。短时间内剩余的EGTA抗性失活以约0.12秒的时间常数衰减。尾电流减小与预脉冲电压的关系与以下解释一致，即短时间内剩余的EGTA抗性失活取决于预脉冲期间钙离子的内流，就像稍后剩余的EGTA敏感失活一样。有人提出，失活的“EGTA抗性”阶段是由于在持续钙内流期间EGTA在膜内表面附近与钙离子结合，从而使细胞内钙浓度升高所致。这些结果为钙介导的钙电导失活提供了进一步的证据。（摘要截断于400字）
