Hyperpolarization-activated currents in neurons of the rat basolateral amygdala.

Hyperpolarization-activated currents in neurons of the rat basolateral amygdala.
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DOI:
10.1152/jn.1993.70.5.2056
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发表时间:
1993-11
影响因子:
2.5
通讯作者:
M. Womble;H. C. Moises
M. Womble;H. C. Moises
中科院分区:
医学3区
文献类型:
--
作者:
M. Womble;H. C. Moises

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1. 使用单个微电极获得大鼠腹侧前脑切片中杏仁核基底外侧核 (BLA) 中两种神经元细胞类型(锥体细胞和晚发神经元)的电流钳或电压钳记录。确定了由 -70 mV 保持电位的超极化电压阶跃激活的电导,并使用卡巴胆碱浴灌注确定了它们对毒蕈碱调节的敏感性。 2.未钳制的锥体神经元表现出异常整流,被视为响应超极化电流脉冲而缓慢发展的电势去极化凹陷。 3. 步进电压钳位锥体神经元以控制 -70 至 -100 mV 之间的电位,激活了缓慢发展的内向电流 (ISlow),该电流遵循单一指数时间过程。较大的超极化电压阶跃会引发快速发展的内向电流 (IFast),该电流先于 ISlow 的发展。 4. ISlow 分量在 -70 mV 保持电位的正电平处反转。当超极化电压阶跃变得更负时,其激活速率加快。 ISlow 的电导激活阈值约为 -60 mV,半激活发生在 -90 mV。 5. 细胞外 Cs+ (2 mM) 阻断 ISlow 并消除未夹紧的锥体神经元中的异常整流。 Cs+ 对 ISlow 的抑制也与膜超极化和超极化后介质减少有关。 ISlow 不受细胞外 Ba2+ (100 microM) 的影响。该电流的特性与先前在其他神经元中发现的混合阳离子 H 电流的特性相似。 6. 与锥体细胞相比,未钳制的晚放电神经元表现出较小但发展较快的异常整流,以响应休息时的大超极化。在电压钳中,超极化步骤命令电位比 -100 mV 更负,从而引发 IFast。晚放电神经元很少或不表达ISlow。 7. IFast 的特性在锥体神经元和晚放电神经元中是相同的。该电流在负电位至-70 mV 时反转。其电流激活速率随着超极化电压阶跃的幅度而增加。该速率比相同膜电位下记录的 ISlow 激活速度大约快七倍。 IFast 被 2 mM 细胞外 Cs+ 阻断,并被 100 microM 细胞外 Ba2+ 还原。基础电导激活的阈值约为-85 mV,半激活发生在-112 mV。 IFast 的特性与之前在其他中枢神经元中发现的内向整流电流的特性相似。 8. Carbachol (40 microM) 很大程度上阻断了 IFast,但不影响其激活率。(摘要截断为 400 字)
1. A single microelectrode was used to obtain current-clamp or voltage-clamp recordings from two neuronal cell types (pyramidal and late-firing neurons) in the basolateral nucleus of the amygdala (BLA) in slices of the rat ventral forebrain. Conductances activated by hyperpolarizing voltage steps from a holding potential of -70 mV were identified and their sensitivity to muscarinic modulation was determined using bath superfusion of carbachol. 2. Unclamped pyramidal neurons exhibited anomalous rectification, seen as a slowly developing depolarizing sag in the electronic potential in response to a hyperpolarizing current pulse. 3. Stepping voltage-clamped pyramidal neurons to command potentials of between -70 and -100 mV activated a slowly developing inward current (ISlow) that followed a single exponential time course. Larger hyperpolarizing voltage steps evoked a rapidly developing inward current (IFast) that preceded the development of ISlow. 4. The ISlow component reversed at a level positive to the -70 mV holding potential. Its rate of activation accelerated as the hyperpolarizing voltage step was made more negative. The threshold for activation of the conductance underlying ISlow was approximately -60 mV, with half-activation occurring at -90 mV. 5. Extracellular Cs+ (2 mM) blocked ISlow and eliminated anomalous rectification in unclamped pyramidal neurons. The inhibition of ISlow by Cs+ was also associated with membrane hyperpolarization and reduction of the medium afterhyperpolarization. ISlow was unaffected by extracellular Ba2+ (100 microM). The properties of this current appeared similar to that of the mixed cationic H-current previously identified in other neurons. 6. In comparison with pyramidal cells, unclamped late-firing neurons displayed a lesser but more rapidly developing anomalous rectification in response to large hyperpolarizations from rest. In voltage clamp, hyperpolarizing steps to command potentials more negative than -100 mV elicited IFast. Late-firing neurons expressed little or no ISlow. 7. The properties of IFast were identical in both pyramidal and late-firing neurons. This current reversed at a potential negative to -70 mV. Its rate of current activation increased with the magnitude of the hyperpolarizing voltage step. This rate was approximately sevenfold faster than ISlow activation recorded at the same membrane potential. IFast was blocked by 2 mM extracellular Cs+ and reduced by 100 microM extracellular Ba2+. The threshold for activation of the underlying conductance was approximately -85 mV, with half-activation occurring at -112 mV. The properties of IFast were similar to those of the inward rectifier current previously identified in other central neurons. 8. Carbachol (40 microM) largely blocked IFast without affecting its rate of activation.(ABSTRACT TRUNCATED AT 400 WORDS)