Selective shunting of the NMDA EPSP component by the slow afterhyperpolarization in rat CA1 pyramidal neurons
Selective shunting of the NMDA EPSP component by the slow afterhyperpolarization in rat CA1 pyramidal neurons
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DOI：
10.1152/jn.00422.2006
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发表时间：
2007-05-01
影响因子：
2.5
通讯作者：
Buno, Washington
中科院分区：
文献类型：
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作者：
Fernandez de Sevilla, David;Fuenzalida, Marco;Buno, Washington
锥体神经元树突表达控制突触整合和可塑性的电压门控电导，但尚未充分了解Ca 2+激活的K+介导的电流对树突功能的贡献。采用大鼠海马CA 1区锥体神经元的树突和体细胞记录技术，研究了由穿通通路-Schaffer侧支刺激诱发的兴奋性突触后电位（EPSP）的动作电位爆发产生的缓慢Ca 2+激活的K+介导的后超极化（sAHP）引起的变化。在体细胞记录中，sAHP降低了EPSP的振幅和衰减时间常数（tau（EPSP））。相反，树突状EPSP振幅保持不变，而tau蛋白（EPSP）减少。时间总和减少和空间总和线性化的sAHP。孤立的N-甲基-D-天冬氨酸组分的EPSPs（EPSPNMDA）的幅度降低，而tau（NMDA）不受sAHP。相比之下，sAHP没有修改孤立的EPSPAMPA的振幅，但减少了tau（AMPA）在树突和体细胞记录。这些变化是由于电导增加，主要是通过选择性的“分流”的EPSPNMDA，因为他们是不存在的电压钳下，不存在与施加超极化模拟sAHP，失踪时，sAHP被抑制与异丙肾上腺素，并减少下块的EPSPNMDA。EPSPs在基底树突产生类似修改的sAHP，这表明体细胞和顶端树突位置的sAHP通道。因此，sAHP可能通过调节突触效能和时空总和在树突中起决定性作用。
Pyramidal neuron dendrites express voltage-gated conductances that control synaptic integration and plasticity, but the contribution of the Ca2+-activated K+-mediated currents to dendritic function is not well understood. Using dendritic and somatic recordings in rat hippocampal CA1 pyramidal neurons in vitro, we analyzed the changes induced by the slow Ca2+-activated K+-mediated afterhyperpolarization (sAHP) generated by bursts of action potentials on excitatory postsynaptic potentials (EPSPs) evoked at the apical dendrites by perforant path-Schaffer collateral stimulation. Both the amplitude and decay time constants of EPSPs (tau(EPSP)) were reduced by the sAHP in somatic recordings. In contrast, the dendritic EPSP amplitude remained unchanged, whereas tau(EPSP) was reduced. Temporal summation was reduced and spatial summation linearized by the sAHP. The amplitude of the isolated N-methyl-D-aspartate component of EPSPs (EPSPNMDA) was reduced, whereas tau(NMDA) was unaffected by the sAHP. In contrast, the sAHP did not modify the amplitude of the isolated EPSPAMPA but reduced tau(AMPA) both in dendritic and somatic recordings. These changes are attributable to a conductance increase that acted mainly via a selective "shunt" of EPSPNMDA because they were absent under voltage clamp, not present with imposed hyperpolarization simulating the sAHP, missing when the sAHP was inhibited with isoproterenol, and reduced under block of EPSPNMDA. EPSPs generated at the basal dendrites were similarly modified by the sAHP, suggesting both a somatic and apical dendritic location of the sAHP channels. Therefore the sAHP may play a decisive role in the dendrites by regulating synaptic efficacy and temporal and spatial summation.