Wilson C J
Department of Anatomy and Neurobiology, University of Tennessee, Memphis 38163, USA.
J Comput Neurosci. 1995 Jun;2(2):91-115. doi: 10.1007/BF00961882.
Computer simulations of a dendrite possessing voltage-sensitive potassium conductances were used to determine the effects of these conductances on synaptic transmission and on the propagation of synaptic signals within the dendritic tree. Potassium conductances had two principal effects on voltage transients generated by current injections or synaptic conductances. Locally (near the source of the transient), voltage-gated potassium channels produced a potassium shunt current that reduced the amplitude of voltage transient increased and so acted to prevent large synaptic transients from reaching levels that would saturate due to a reduction in driving force. In the presence of rapidly activating potassium currents, excitatory synapses produced larger synaptic currents that were more linearly related to synaptic conductance, but these produced smaller voltage transients. The maximum amplitudes of the voltage transients were limited by the voltage sensitivity of the K+ conductance and the rate at which it could activate. Sufficiently rapid synaptic currents could outrun the K+ conductance and thus achieve high local peak amplitudes. These effects of K+ conductances were unrelated to whether they were located on dendrites or not, being related only to their proximity to the source of synaptic current. The second class of effects of K+ conductances depended on their alteration of the electronic structure of the postsynaptic cell and so were observed only when they were located on postsynaptic dendrites. Voltage-gated K+ conductances produced voltage-dependent electronic expansion of depolarized dendrites, which had the effect of isolating synaptic inputs on depolarized dendrites from events on the rest of the neuron. Thus, synapses on the same dendrite interacted destructively to a degree much greater than that expected from the classical driving force nonlinearity. Synapses located proximally to a depolarized dendritic region were less effected than those located distally, and the range of the nonlinear interaction between synapses was dependent on the kinetics of activation and deactivation of the conductance. When present in conjunction with rapidly activating dendritic sodium conductance, the potassium conductance sharpened the requirement for spatial and temporal coincidence to produce synaptic boosting by inward currents, and suppressed out-of-synchrony synaptic inputs.
利用具有电压敏感性钾电导的树突的计算机模拟，来确定这些电导对突触传递以及突触信号在树突树内传播的影响。钾电导对电流注入或突触电导产生的电压瞬变有两个主要影响。在局部（瞬变源附近），电压门控钾通道产生钾分流电流，该电流降低了电压瞬变的幅度，从而起到防止大的突触瞬变达到因驱动力降低而饱和的水平。在存在快速激活的钾电流时，兴奋性突触产生更大的突触电流，这些电流与突触电导更呈线性相关，但产生的电压瞬变更小。电压瞬变的最大幅度受钾电导的电压敏感性及其激活速率的限制。足够快速的突触电流可以超过钾电导，从而达到较高的局部峰值幅度。钾电导的这些影响与它们是否位于树突上无关，仅与它们与突触电流源的接近程度有关。钾电导的第二类影响取决于它们对突触后细胞电子结构的改变，因此只有当它们位于突触后树突上时才会被观察到。电压门控钾电导产生去极化树突的电压依赖性电子扩展，这使得去极化树突上的突触输入与神经元其余部分的事件隔离开来。因此，同一树突上的突触相互作用的破坏性程度远大于经典驱动力非线性所预期的程度。位于去极化树突区域近端的突触比远端的突触受影响小，突触之间非线性相互作用的范围取决于电导激活和失活的动力学。当与快速激活的树突钠电导同时存在时，钾电导提高了产生内向电流突触增强所需的空间和时间一致性要求，并抑制了不同步的突触输入。
