Subthreshold inactivation of Na+ and K+ channels supports activity-dependent enhancement of back-propagating action potentials in hippocampal CA1.

Subthreshold inactivation of Na+ and K+ channels supports activity-dependent enhancement of back-propagating action potentials in hippocampal CA1.
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Na 和 K 通道的阈下失活支持海马 CA1 中反向传播动作电位的活动依赖性增强。

DOI:
10.1152/jn.2001.85.2.1013
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发表时间:
2001
期刊:
Journal of neurophysiology.
影响因子:
--
通讯作者:
Colbert,CM
Colbert,CM
中科院分区:
--
文献类型:
--
作者:
Pan,E;Colbert,CM

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CA 1区锥体神经元的反向传播动作电位可能提供诱导长时程突触可塑性所必需的突触后树突去极化。反向传播动作电位的幅度不是全部或没有,而是受到树突状A型K+通道的限制。以前的反向传播动作电位的研究表明,树突状细胞膜的预先去极化通过失活降低了A型通道的可用性,从而导致树突状细胞动作电位的增强或增强。然而,在阈下电位范围内的失活动力学尚未直接测量。此外,还没有考虑Na+通道失活与去极化的相应速率。我们在细胞贴附贴片(距离索马150-220 μm,32°C)中报告,在20 mV正向静息时,A型K+通道以6 ms的单指数时间常数失活,而Na+通道以37 ms的时间常数失活。可用Na+与K+电流的比率随着去极化持续时间的增加而增加。因此,Na+和A型K+通道的亚阈值特性提供了一种机制,通过该机制,关于突触活动水平的信息可以编码在反向传播动作电位的幅度中。
Back-propagating action potentials in CA1 pyramidal neurons may provide the postsynaptic dendritic depolarization necessary for the induction of long-term synaptic plasticity. The amplitudes of back-propagating action potentials are not all or none but are limited in amplitude by dendritic A-type K+channels. Previous studies of back-propagating action potentials have suggested that prior depolarization of the dendritic membrane reduces A-type channel availability through inactivation, resulting in an enhanced, or boosted, dendritic action potential. However, inactivation kinetics in the subthreshold potential range have not been directly measured. Furthermore, the corresponding rates of Na+channel inactivation with depolarization have not been considered. Here we report in cell-attached patches (150–220 μm from the soma, 32°C) that at 20-mV positive to rest, A-type K+channels inactivated with a single exponential time constant of 6 ms, whereas Na+channels inactivated with a time constant of 37 ms. The ratio of available Na+to K+current increased as the duration of the depolarization increased. Thus the subthreshold properties of Na+and A-type K+channels provide a mechanism by which information about the level of synaptic activity may be encoded in the amplitude of back-propagating action potentials.