Gähwiler B H, Brown D A
Neuroscience. 1987 Mar;20(3):731-8. doi: 10.1016/0306-4522(87)90236-3.
Slow inward Ca-currents were recorded from CA3 pyramidal cells in rat hippocampus slice cultures when these cells were voltage-clamped at -40 mV and depolarizing commands applied. Ca-currents were increased in amplitude by the dihydropyridine Ca-agonist BAY K8644 (0.1-1 microM) and reduced by the Ca-antagonists nifedipine and PY 108-068 (0.1-1 microM). Ca-current inhibition by the latter could be temporarily relieved by membrane hyperpolarization. In unclamped cells, dihydropyridines did not alter membrane potential, Ca-spike amplitude, excitatory or inhibitory synaptic current amplitude, or spontaneous synaptic activity. Their principal effects were to alter the threshold for Ca/Ba spike generation and for pitrazepin-induced burst-depolarization. BAY K8644 also induced an after-spike following the normal Na spike, which was reduced by PY 108-068. It is concluded that the slow inward Ca-current in hippocampal neurones is sensitive to dihydropyridine drugs and that the absence of functional effects of antagonists is due to other causes such as the voltage-dependence of dihydropyridine block and the presence of an additional transient Ca-current which may be less sensitive to block.
当将大鼠海马切片培养物中的CA3锥体细胞电压钳制在-40 mV并施加去极化指令时，记录到了缓慢内向钙电流。二氢吡啶类钙激动剂BAY K8644（0.1 - 1 microM）可增加钙电流幅度，而钙拮抗剂硝苯地平和PY 108 - 068（0.1 - 1 microM）则使其降低。后者对钙电流的抑制作用可通过膜超极化暂时解除。在未钳制的细胞中，二氢吡啶类药物不会改变膜电位、钙峰幅度、兴奋性或抑制性突触电流幅度或自发突触活动。它们的主要作用是改变钙/钡峰产生的阈值以及匹莫齐定诱导的爆发性去极化的阈值。BAY K8644还会在正常钠峰之后诱导一个后峰，而PY 108 - 068可使其降低。得出的结论是，海马神经元中的缓慢内向钙电流对二氢吡啶类药物敏感，拮抗剂缺乏功能效应是由于其他原因，如二氢吡啶类阻断的电压依赖性以及可能对阻断不太敏感的额外瞬时钙电流的存在。
