ANOMALOUS RECTIFICATION IN NEURONS FROM CAT SENSORIMOTOR CORTEX INVITRO
ANOMALOUS RECTIFICATION IN NEURONS FROM CAT SENSORIMOTOR CORTEX INVITRO
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DOI：
10.1152/jn.1987.57.5.1555
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发表时间：
1987-05-01
影响因子：
2.5
通讯作者：
CRILL, WE
中科院分区：
文献类型：
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作者：
SPAIN, WJ;SCHWINDT, PC;CRILL, WE
在离体脑片上研究了猫感觉运动皮层V层大神经元异常整流的离子机制。异常整流是明显的，在膜超极化过程中的斜率电导的增加，和异常整流的发展过程中的超极化电流脉冲的信号通过去极化下垂的膜电位向静息电位（RP）。电压钳分析揭示了产生异常整流的时间和电压依赖性内向电流（IAR）。根据线性、瞬时、电流-电压关系的外推，IAR逆转电位（IAR）估计约为-50 mV。IAR（GAR）的电导具有S形稳态激活特征。GAR随着超极化从-55 mV增加到-105 mV，在约-82 mV时半激活。在电压阶跃期间，GAR和IAR的时间过程由两个指数描述。较快指数的时间常数（τ F）约为40 ms;较慢时间常数（τ S）约为300 ms。在-60 mV至-110 mV范围内，τ F和τ S均不随电压变化。在每个电位下，快成分约占IAR的80%。IAR和GAR均随细胞外钾[（K+）]o升高而增加，且随电压轴向正移，但GAR激活曲线不沿电压轴向沿着移动。含有不可渗透的Na+替代品的解决方案引起了IAR的初始瞬时下降，随后IAR的缓慢增加。用K+敏感的微电极测量，浸泡在Na+取代溶液中的脑切片的[K+]o逐渐增加。我们的结论是，GAR是渗透的Na+和K+，但Na+的全部贡献被掩盖的缓慢增加的[K+]o发生在Na+取代的解决方案。氯化物似乎对IAR没有显着贡献，因为在用氯化钾或硫酸甲酯填充的微电极刺穿的神经元中，ECl的估计值相似，而用KCl填充的微电极，ECl（从GABA诱导的离子电流的逆转估计）的正性约为30 mV。细胞外Cs+引起可逆的剂量和电压依赖性减少GAR，而细胞内Cs+是无效的。电压钳位过程中测量的参数被用来制定IAR的定量经验模型。（400字处截断摘要）
The ionic mechanisms underlying anomalous rectification in large neurons from layer V of cat sensorimotor cortex were studied in an in vitro brain slice. The anomalous rectification was apparent as an increase of slope conductance during membrane hyperpolarization, and the development of anomalous rectification during a hyperpolarizing current pulse was signaled by a depolarizing sag of membrane potential toward resting potential (RP). Voltage-clamp analysis revealed the time- and voltage-dependent inward current (IAR) that produced anomalous rectification. IAR reversal potential (EAR) was estimated to be approximately -50 mV from extrapolation of linear, instantaneous, current-voltage relations. The conductance underlying IAR (GAR) had a sigmoidal steady-state activation characteristic. GAR increased with hyperpolarization from -55 to -105 mV with half-activation at approximately -82 mV. The time course of both GAR and IAR during a voltage step was described by two exponentials. The faster exponential had a time constant (tau F) of approximately 40 ms; the slow time constant (tau S) was approximately 300 ms. Neither tau F nor tau S changed with voltage in the range -60 mV to -110 mV. The fast component constituted approximately 80% of IAR at each potential. Both IAR and GAR increased in raised extracellular potassium [( K+]o) and EAR shifted positive, but the GAR activation curve did not shift along the voltage axis. Solutions containing an impermeable Na+ substitute caused an initial transient decrease in IAR followed by a slower increase of IAR. Brain slices bathed in Na+-substituted solution developed a gradual increase in [K+]o as measured with K+-sensitive microelectrodes. We conclude that GAR is permeable to both Na+ and K+, but the full contribution of Na+ was masked by the slow increase of [K+]o that occurred in Na+ substituted solutions. Chloride did not appear to contribute significantly to IAR since estimates of EAR were similar in neurons impaled with microelectrodes filled with potassium chloride or methylsulfate, whereas, ECl (estimated from reversal of a GABA-induced ionic current) was approximately 30 mV more positive with the KCl-filled microelectrodes. Extracellular Cs+ caused a reversible dose- and voltage-dependent reduction of GAR, whereas intracellular Cs+ was ineffective. The parameters measured during voltage clamp were used to formulate a quantitative empirical model of IAR.(ABSTRACT TRUNCATED AT 400 WORDS)