Koizumi Amane, Hayashida Yuki, Kiuchi Teppei, Yamada Yoshitake, Fujii Atsunori, Yagi Tetsuya, Kaneko Akimichi
Keio University School of Medicine, Department of Physiology, Shinjuku, Tokyo, Japan.
J Integr Neurosci. 2005 Sep;4(3):363-80. doi: 10.1142/s0219635205000859.
Previously we reported that cultured rat GABAergic amacrine cells can evoke subthreshold graded depolarization and action potentials. Both types of electrical signals are thought to contribute to neurotransmitter release from their dendrites, because Ca(2+) channels in amacrine cells can be activated at a subthreshold level (around -50 mV). The aim of the present study is to describe the spatiotemporal pattern of the spread of these electrical signals in an amacrine cell, using a computer simulation study. The simulation is based on physiological data, obtained by dual whole-cell patch-clamp recordings on the soma and the dendrites of cultured rat GABAergic amacrine cells. We determined passive and active properties of amacrine cells from the physiological recordings. Then, using the NEURON simulator, we conducted computer simulations on a reconstructed model of amacrine cells. We show that graded potentials and action potentials spread through amacrine cells with distinct patterns, and discuss the electrical interrelationship among the dendrites of an amacrine cell. Subthreshold graded potentials applied to a distal dendrite were sufficiently localized, so that each dendrite could behave independently (dendritic independence). However, at a suprathreshold level, once action potentials were triggered, they propagated into every dendrite, exciting the entire cell (dendritic interdependence). We also showed that GABAergic inhibitory inputs on the dendrites suppress the dendritic interdependence of amacrine cells. These results suggest that an inhibitory amacrine cell can mediate both local and wide-field lateral inhibition, regulated by the spatiotemporal pattern of excitatory and inhibitory synaptic inputs on its dendrites.
我们之前报道过,培养的大鼠γ-氨基丁酸能无长突细胞可诱发阈下分级去极化和动作电位。这两种电信号都被认为有助于从其树突释放神经递质,因为无长突细胞中的钙离子通道可在阈下水平(约-50 mV)被激活。本研究的目的是通过计算机模拟研究来描述这些电信号在无长突细胞中传播的时空模式。该模拟基于通过对培养的大鼠γ-氨基丁酸能无长突细胞的胞体和树突进行双全细胞膜片钳记录获得的生理数据。我们从生理记录中确定了无长突细胞的被动和主动特性。然后,使用NEURON模拟器,我们对无长突细胞的重建模型进行了计算机模拟。我们发现分级电位和动作电位以不同模式在无长突细胞中传播,并讨论了无长突细胞树突之间的电相互关系。施加到远端树突的阈下分级电位足够局限,使得每个树突能够独立发挥作用(树突独立性)。然而,在阈上水平,一旦触发动作电位,它们就会传播到每个树突,使整个细胞兴奋(树突相互依赖性)。我们还表明,树突上的γ-氨基丁酸能抑制性输入会抑制无长突细胞的树突相互依赖性。这些结果表明,抑制性无长突细胞可以介导局部和广域侧向抑制,这是由其树突上兴奋性和抑制性突触输入的时空模式调节的。