Wessel R, Kristan W B, Kleinfeld D
Department of Physics, University of California at San Diego, La Jolla, California 92093, USA.
J Neurosci. 1999 Oct 1;19(19):8319-26. doi: 10.1523/JNEUROSCI.19-19-08319.1999.
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.
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。