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树突状钙离子激活钾离子电导调节无脊椎动物神经元中的电信号传播。

Dendritic Ca(2+)-activated K(+) conductances regulate electrical signal propagation in an invertebrate neuron.

作者信息

Wessel R, Kristan W B, Kleinfeld D

机构信息

Department of Physics, University of California at San Diego, La Jolla, California 92093, USA.

出版信息

J Neurosci. 1999 Oct 1;19(19):8319-26. doi: 10.1523/JNEUROSCI.19-19-08319.1999.

Abstract

Activity-dependent changes in the short-term electrical properties of neurites were investigated in the anterior pagoda (AP) cell of leech. Imaging studies revealed that backpropagating Na(+) spikes and synaptically evoked EPSPs caused Ca(2+) entry through low-voltage-activated Ca(2+) channels that are distributed throughout the neurites. Voltage-clamp recordings from the soma revealed a TEA-sensitive outward current that was reduced when Ca(2+) entry was blocked with Co(2+) or when the intracellular concentration of free Ca(2+) was reduced by a high-affinity Ca(2+) buffer. Ca(2+) released in the neurite from a caged Ca(2+) compound caused a hyperpolarization of the membrane potential. These data imply that the AP cell expresses Ca(2+)-activated K(+) conductances, and that these conductances are present in the neurites. When the Ca(2+)-activated K(+) current was reduced through the block of Ca(2+) entry, backpropagating Na(+) spikes and synaptically evoked EPSPs increased in amplitude. Hence, the activity-dependent changes in the intracellular [Ca(2+)] together with the Ca(2+)-activated K(+) conductances participate in the regulation of dendritic signal propagation.

摘要

研究了水蛭前塔(AP)细胞中神经突短期电特性的活动依赖性变化。成像研究表明,反向传播的Na(+) 峰电位和突触诱发的兴奋性突触后电位(EPSPs)通过分布于整个神经突的低电压激活Ca(2+) 通道引起Ca(2+) 内流。从胞体进行的电压钳记录显示出一种对四乙铵(TEA)敏感的外向电流,当用Co(2+) 阻断Ca(2+) 内流或用高亲和力Ca(2+) 缓冲液降低细胞内游离Ca(2+) 浓度时,该电流减小。从笼装Ca(2+) 化合物在神经突中释放的Ca(2+) 导致膜电位超极化。这些数据表明AP细胞表达Ca(2+) 激活的K(+) 电导,并且这些电导存在于神经突中。当通过阻断Ca(2+) 内流降低Ca(2+) 激活的K(+) 电流时,反向传播的Na(+) 峰电位和突触诱发的EPSPs幅度增加。因此,细胞内[Ca(2+)] 的活动依赖性变化以及Ca(2+) 激活的K(+) 电导参与树突信号传播的调节。

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