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:
影响因子:
--
通讯作者:
Colbert,CM
中科院分区:
文献类型:
--
作者:
Pan,E;Colbert,CM
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.