Properties of subthreshold response and action potential recorded in layer V neurons from cat sensorimotor cortex in vitro.
Properties of subthreshold response and action potential recorded in layer V neurons from cat sensorimotor cortex in vitro.
复制标题
体外猫感觉运动皮层 V 层神经元记录的阈下反应和动作电位的特性。
DOI：
10.1152/jn.1984.52.2.244
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发表时间：
1984
影响因子：
2.5
通讯作者：
Crill,WE
中科院分区：
文献类型：
--
作者：
Stafstrom,CE;Schwindt,PC;Flatman,JA;Crill,WE
使用细胞内记录和刺激，应用阻断主动电导的药物和单微电极电压钳（SEVC），在猫感觉运动皮层的体外切片中研究了大V层神经元的动作电位和阈下反应的特性。各种测量的参数，包括动作电位持续时间，后电位，输入电阻，基强度，和膜时间常数，是类似的大的神经元从这个区域的皮层在体内报告的相同参数。在体外条件下，微电极电位振幅和静息电位均较大。大多数测量的参数分布单峰，这表明这些参数是相似的，在所有大的V层神经元，无论其轴突终止。亚阈值恒流脉冲的电压响应表现出时间和电压的依赖性，在绝大多数细胞。超极化或阈下去极化方向的电流脉冲使膜电位达到早期峰值，然后衰减（下降）至稳定水平。在脉冲终止时，膜响应瞬时超过静息电位。电流-电压关系图显示了静息电位两侧极化过程中的内向整流。在去极化方向的阈下内向整流被河豚毒素（TTX）所消除。使用SEVC检查负责阈下整流和凹陷的离子电流。持续的阈下钠电流（INaP）引起去极化方向的稳定内向整流（54）。响应于去极化电流脉冲而观察到的下垂是由于缓慢外向电流的激活，其叠加并部分抵消持续钠电流。响应于超极化电流脉冲的凹陷和超极化方向上的整流都是由缓慢向内的“凹陷电流”引起的，该凹陷电流由超极化电压阶跃激活。TTX、四乙基铵（TEA）、Co 2+、Ba 2+或4-氨基吡啶均不改变凹陷电流。快速上升，短持续时间的动作电位可以通过细胞内电流脉冲或通过顺向或逆向刺激引起。峰电位被TTX阻断。在具有相似静息电位的细胞之间，直接诱发的尖峰之后的后电位的形式不同。双相后超极化（AHPs）的快，慢成分最常见。约30%的细胞显示去极化后电位（DAP），这往往是由AHP。其他细胞显示出纯双相AHP。（400字处截断摘要）
Properties of the action potential and subthreshold response were studied in large layer V neurons in in vitro slices of cat sensorimotor cortex using intracellular recording and stimulation, application of agents that block active conductances, and a single-microelectrode voltage clamp (SEVC). A variety of measured parameters, including action-potential duration, afterpotentials, input resistance, rheobase, and membrane time constant, were similar to the same parameters reported for large neurons from this region of cortex in vivo. Action-potential amplitudes and resting potentials were greater in vitro. Most measured parameters were distributed unimodally, suggesting that these parameters are similar in all large layer V neurons irrespective of their axonal termination. The voltage response to subthreshold constant-current pulses exhibited both time and voltage dependence in the great majority of cells. Current pulses in either the hyperpolarizing or subthreshold depolarizing direction cause the membrane potential to attain an early peak and then decay (sag) to a steady level. On termination of the pulse, the membrane response transiently overshoots resting potential. Plots of current-voltage relations demonstrate inward rectification during polarization on either side of resting potential. Subthreshold inward rectification in the depolarizing direction is abolished by tetrodotoxin (TTX). The ionic currents responsible for subthreshold rectification and sag were examined using the SEVC. Steady inward rectification in the depolarizing direction is caused by a persistent, subthreshold sodium current (INaP) (54). Sag observed in response to a depolarizing current pulse is due to activation of a slow outward current, which superimposes on and partially counters the persistent sodium current. Both sag in response to hyperpolarizing current pulses and rectification in the hyperpolarizing direction are caused by a slow inward "sag current" that is activated by hyperpolarizing voltage steps. The sag current is unaltered by TTX, tetraethylammonium, (TEA), Co2+, Ba2+, or 4-aminopyridine. Fast-rising, short-duration action potentials can be elicited by an intracellular current pulse or by orthodromic or antidromic stimulation. Spikes are blocked by TTX. The form of the afterpotential following a directly evoked spike varies among cells with similar resting potentials. Biphasic afterhyperpolarizations (AHPs) with fast and slow components were most frequently seen. About 30% of the cells displayed a depolarizing afterpotential (DAP), which was often followed by an AHP. Other cells displayed a purely monophasic AHP.(ABSTRACT TRUNCATED AT 400 WORDS)