Korogod S M, Kopysova I L, Bras H, Gogan P, Tyc-Dumont S
Research Laboratory of Biophysics and Bioelectronics, Dniepropetrovsk State University, Ukraine.
Neuroscience. 1996 Dec;75(4):1153-63. doi: 10.1016/0306-4522(96)00265-5.
Intracellular recording of abducens motoneurons in vivo has shown that ionophoretic applications of N-methyl-D-aspartate produced long-lasting membrane potential oscillations including a slow depolarization plateau with a burst of fast action potentials. This complex N-methyl-D-aspartate pattern was reproduced in the model of abducens motoneuron in vivo identified, intracellularly stained with horseradish peroxidase and reconstructed at high spatial resolution. The excitable soma of the simulated cell contained voltage-gated Ca, Na and K conductances, N-methyl-D-aspartate-gated voltage-sensitive Ca-Na-K conductance and Ca-dependent K conductance. The dendrite was passive either completely or with the exception of branching nodes containing N-methyl-D-aspartate conductances of the same slow kinetics but of lower values than at the soma. In the completely passive case, the N-methyl-D-aspartate pattern decayed with different rates along different dendritic paths depending on the geometry and topology of the reconstructed dendrite. The branches formed four clusters discriminated in somatofugal attenuations of steady voltages, and were correspondingly discriminated in attenuation of the complex N-methyl-D-aspartate pattern. Fast spikes decayed more than the slow depolarization plateau so that the prevalence of slow over fast components in the transformed pattern increased with somatofugal path distance. As a consequence, the lower the electrotonic effectiveness of a branch in the cluster or in the whole arborization, the lower both the voltage level and the frequency range of its voltage modulation by N-methyl-D-aspartate oscillations. In the case of active branching points, the somatic pattern changed depending on the level of activation of dendritic N-methyl-D-aspartate conductances with slow kinetics of voltage sensitivity. The higher this level, the longer the plateau and burst, and the greater the discharge rate; and the spikes in the burst were smaller. When the pattern spread in the dendrite, the fast spikes decayed and the slow plateau was boosted, with a greater effect along the somatofugal path containing more branching points. These results show how the somatofugal back-invasion along the dendrites by activity patterns generated at the soma can tune voltage-sensitive dendritic conductances. The dendritic back-invasion is geometry- and topology-dependent. It is proposed as a subtle feedback mechanism for the neuron to control its own synaptic inputs.
体内展神经运动神经元的细胞内记录表明，离子电泳施加N-甲基-D-天冬氨酸可产生持久的膜电位振荡，包括缓慢去极化平台期并伴有一阵快速动作电位。这种复杂的N-甲基-D-天冬氨酸模式在通过辣根过氧化物酶进行细胞内染色并以高空间分辨率重建的体内展神经运动神经元模型中得到了重现。模拟细胞的可兴奋胞体包含电压门控的钙、钠和钾电导、N-甲基-D-天冬氨酸门控的电压敏感钙-钠-钾电导以及钙依赖性钾电导。树突要么完全被动，要么除了包含具有相同缓慢动力学但值低于胞体处的N-甲基-D-天冬氨酸电导的分支节点外是被动的。在完全被动的情况下，N-甲基-D-天冬氨酸模式沿着不同的树突路径以不同速率衰减，这取决于重建树突的几何形状和拓扑结构。这些分支形成了四个簇，在稳定电压的向胞体递减衰减中得以区分，并且在复杂的N-甲基-D-天冬氨酸模式的衰减中也相应地得以区分。快速尖峰的衰减比缓慢去极化平台期更明显，因此在转换模式中缓慢成分相对于快速成分的占比随着向胞体路径距离的增加而增加。结果，簇中或整个树突分支中一个分支的电紧张有效性越低，其由N-甲基-D-天冬氨酸振荡进行电压调制的电压水平和频率范围就越低。在存在活跃分支点的情况下，胞体模式会根据具有缓慢电压敏感性动力学的树突N-甲基-D-天冬氨酸电导的激活水平而改变。该激活水平越高，平台期和爆发期就越长，放电率就越大；并且爆发中的尖峰就越小。当模式在树突中传播时，快速尖峰衰减而缓慢平台期增强，沿着包含更多分支点的向胞体路径效果更明显。这些结果表明，由胞体产生的活动模式沿着树突向胞体的反向入侵如何能够调节电压敏感的树突电导。树突反向入侵取决于几何形状和拓扑结构。它被认为是神经元控制自身突触输入的一种微妙反馈机制。
