PERSISTENT SLOW INWARD CALCIUM CURRENT IN VOLTAGE-CLAMPED HIPPOCAMPAL-NEURONS OF THE GUINEA-PIG
PERSISTENT SLOW INWARD CALCIUM CURRENT IN VOLTAGE-CLAMPED HIPPOCAMPAL-NEURONS OF THE GUINEA-PIG
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DOI：
10.1113/jphysiol.1983.sp014625
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发表时间：
1983-01-01
影响因子：
5.5
通讯作者：
GRIFFITH, WH
中科院分区：
文献类型：
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作者：
BROWN, DA;GRIFFITH, WH
通过单个微电极对豚鼠海马横切片中的CA 1和CA 3神经元进行电压钳位，并在（正常）24 - 26 ℃下用含有0.5 μ M-河豚毒素和10 μ M-四乙基铵的Krebs溶液灌注。C.缓慢的内向电流≤0.5在去极化电压命令至膜电位为正至-40和-30 mV之间期间记录nA。这些电流在去极化命令开始后的100 - 300 ms达到峰值，然后在继续去极化期间下降。这种下降可以归因于一个发展外向电流，因为复极内向电流的尾巴显示没有减少到700毫秒。没有明确的证据，时间依赖性失活的内向电流可以得到。当膜电位维持在内向电流阈值以上时，可以检测到内向电流的持续成分，使得小的超极化命令诱导向外松弛，并且大的超极化产生内向尾电流。去钙或加入0.2 - 0.5mM-Cd或0.1mM-Verapamil均抑制内向电流，而加入1mM-Ba则使内向电流增加。这种持续的内向电流在产生低膜去极化的基础上在这些神经元的爆发放电的可能作用进行了讨论。在一些神经元（主要是CA 1），一个额外的快速尖峰样电流记录，这是由镉或锰和抑郁症的去极化预脉冲阻断。这是先前报道的树突状Ca峰的表现。
CA1 and CA3 neurons in transverse slices of guinea pig hippocampus were voltage clamped through a single micro-electrode, and perfused with Krebs solution containing 0.5 .mu.M-tetrodotoxin and 10 .mu.M-tetraethylammonium at (normally) 24-26.degree. C. Slow inward currents of .ltoreq. 0.5 nA were recorded during depolarizing voltage commands to membrane potentials positive to between -40 and -30 mV. These currents peaked at 100-300 ms after the onset of the depolarizing command, then subsequently declined during continuing depolarization. This decline could be ascribed to a developing outward current since repolarizing inward current tails showed no diminution up to 700 ms. No clear evidence for time-dependent inactivation of the inward current could be obtained. A persistent component of inward current could be detected when the membrane potential was maintained above the inward current threshold, such that small hyperpolarizing commands induced an outward relaxation and large hyperpolarizations produced an inward tail current. The inward current was depressed by removing external Ca, or by adding 0.2-0.5 mM-Cd, or 0.1 mM-verapamil, and was increased by adding 1 mm-Ba. A possible role for this persistent inward current in generating the low membrane depolarization underlying burst discharges in these neurons is discussed. In some neurons (primarily CA1), an additional fast spike-like current was recorded, which was blocked by Cd or Mn and depressed by a depolarizing pre-pulse. This was a manifestation of the previously-reported dendritic Ca spike.