Properties of persistent sodium conductance and calcium conductance of layer V neurons from cat sensorimotor cortex in vitro.
Properties of persistent sodium conductance and calcium conductance of layer V neurons from cat sensorimotor cortex in vitro.
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DOI：
10.1152/jn.1985.53.1.153
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发表时间：
1985
影响因子：
2.5
通讯作者：
C. Stafstrom;P. Schwindt;M. C. Chubb;W. Crill
中科院分区：
文献类型：
--
作者：
C. Stafstrom;P. Schwindt;M. C. Chubb;W. Crill
猫感觉运动皮层第V层神经元的持续钠电导和钙电导的特性进行了研究，在体外切片制备使用一个单一的微电极，体细胞电压钳，电流钳，内和细胞外的应用程序的阻断剂，和细胞外离子取代。持续钠电流（INaP）在每个电位下电压阶跃变化的2-4 ms内达到稳定水平，可直接检查[至静息电位（RP）正向约40 mV]。由于INaP起效快，它可在单个兴奋性突触后电位（EPSP）过程中被激活，并可影响随后的电压时程和细胞兴奋性。应用大于或等于RP正20 mV的去极化保持电位可以抑制尖峰，从而允许在尖峰阈值正电压下检查INaP。在INaP可见的每个电位处，它与缓慢的外向电流混合。在用阻断剂抑制钾电流后，在去极化至RP正向约40 mV期间可以观察到INaP，其中它通常被较大的外向电流所隐藏。间接证据表明，INaP是存在的，并在长期的去极化大于50 mV的RP积极的大。通过细胞内注射利多卡因衍生物QX-314以及细胞外河豚毒素（TTX）阻断INaP。INaP对QX-314的敏感性远高于穗高和穗上升速率。上述观察结果和第3段中的结果可通过单独的INaP和尖峰钠通道得到最好的解释。在阻断INaP和钠峰后，只有首先抑制钾电流，才能诱发Ca 2+峰。再生电位的Ca 2+依赖性的消失时，Co 2+或Mn 2+取代的灌注液中的Ca 2+和由类似形式的大大增强的电位时，Ba 2+取代的Ca 2+的外观表示。Ba ~（2+）替代显著增强诱发电位和自发突触电位。TTX和Ba ~（2+）均可诱发延长的高原动作电位。Ca ~（2+）峰电位阈值为30-40 mV，与Na ~+峰电位阈值相比，RP的峰电位阈值更高。在正常灌注液中以及在存在Ca 2+阻断剂或Ba 2+的情况下的电压钳结果表明，在25 mV正向RP的电压范围内很少或没有Ca 2+电导被激活，其中INaP是主导离子电流。（400字处截断摘要）
Properties of the persistent sodium conductance and the calcium conductance of layer V neurons from cat sensorimotor cortex were examined in an in vitro slice preparation by use of a single microelectrode, somatic voltage clamp, current clamp, intra- and extracellular application of blocking agents, and extracellular ion substitution. The persistent sodium current (INaP) attained its steady level within 2-4 ms of a step change in voltage at every potential where it could be examined directly [to about 40 mV positive to resting potential (RP)]. Because of its fast onset INaP can be activated during a single excitatory postsynaptic potential (EPSP) and can influence the subsequent voltage time course and cell excitability. Application of a depolarizing holding potential greater than or equal to 20 mV positive to RP could inactivate spikes, thus allowing examination of INaP at voltages positive to spike threshold. At every potential where INaP was visible, it was mixed with a slow outward current. After depressing potassium currents with blocking agents, INaP could be observed during depolarizations to about 40 mV positive to RP where it is normally hidden by the larger outward currents. Indirect evidence suggests that INaP is present and large during prolonged depolarizations greater than 50 mV positive to RP. INaP was blocked by intracellular injection of the lidocaine derivative QX-314, as well as by extracellular tetrodotoxin (TTX). INaP was much more sensitive to QX-314 than was the height and rate of rise of the spike. This observation and the results in paragraph 3 above are best explained by separate INaP and spike sodium channels. After blockade of INaP and sodium spikes, Ca2+ spikes could be evoked only if potassium currents were first depressed. The Ca2+-dependent nature of the regenerative potentials was indicated by their disappearance when Co2+ or Mn2+ was substituted for Ca2+ in the perfusate and by the appearance of greatly enhanced potentials of similar form when Ba2+ was substituted for Ca2+. Ba2+ substitution greatly enhanced evoked and spontaneous synaptic potentials. Prolonged-plateau action potentials could be evoked in the presence of TTX and Ba2+. Ca2+ spike threshold was 30-40 mV positive to RP, which is significantly more positive than sodium spike threshold. Results of voltage clamp in the normal perfusate and in the presence of Ca2+-blockers or Ba2+ indicated that little or no Ca2+ conductance is activated in the voltage range 25 mV positive to RP where INaP is the dominant ionic current.(ABSTRACT TRUNCATED AT 400 WORDS)