Computer study of presynaptic inhibition controlling the spread of action potentials into axonal terminals.
Computer study of presynaptic inhibition controlling the spread of action potentials into axonal terminals.
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突触前抑制控制动作电位向轴突末梢传播的计算机研究。
DOI：
10.1152/jn.1990.63.5.987
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发表时间：
1990
影响因子：
2.5
通讯作者：
Segev,I
中科院分区：
文献类型：
--
作者：
Segev,I
1.计算分析了突触前轴突抑制对突触后轴突终末动作电位行为的影响。考虑了突触前抑制的位置和强度的意义，以及轴突终末的形态和膜特性。2.在保持末端膜和轴浆特性不变的情况下，阻碍传播的临界“沉默”稳态电导变化(GCRIT)与末端直径的3/2次方成线性关系。在一个5波长长，直径1微米的轴突的中点，在18摄氏度下具有标准的Hodgkin和Huxley(1952)动力学(输入电导为8.7 ns)，Gcrit为72 ns。在0摄氏度时，Gcrit=200毫微秒，而在30摄氏度时，Gcrit=30毫微秒。3.阻止传播的临界电导变化与终端可激发通道(GNA)的密度密切相关。对于18℃下几何均匀的终端，当GNA大于600ms/cm2时，动作电位不能被局部分流所阻断。4.突触后释放部位附近的轴突突触对该部位的峰波幅度(因此，对突触后输出)具有逐渐的控制作用。远离释放部位的突触前抑制在释放部位有全有或无的影响。5.抑制对冲击被动终端而不是可兴奋终端时的终端尖峰的衰减更为有效。6.与突触前抑制相关的电导增加和动作电位幅度变化的可探测性较差，仅在距离轴突突触较近的地方。一些轴突终末的瓶颈和曲张的存在更加强了这种去偶联效应。因此，突触前抑制可以显著降低受影响轴突输出部位附近的电位，而不会在距离受影响轴突几十微米(空间常数的十分之几)处产生任何明显的电导或电压变化。7.突触前抑制最有效地减弱终末动作电位的最佳部位是轴突终末的曲张和瓶颈。即使有高密度的可兴奋通道，这种终端几何结构的传播也是不安全的，一个或几个量子的抑制性发射器(几个纳米级的电导变化)可以阻止那里的传播。
1. The effect of presynaptic, axoaxonal inhibition, that exerts its action by producing a local conductance increase, on the behavior of action potentials at postsynaptic axon terminals is analyzed computationally. The significance of the location and strength of the presynaptic inhibition, as well as the morphology and membrane properties of the axonal terminals, are considered. 2. Keeping the specific properties of terminal membrane and axoplasm constant, the critical "silent" steady-state conductance change (gcrit) that blocks propagation is linearly scaled with the terminal diameter raised to the 3/2 power. At the midpoint of a 5 lambda long, 1 micron diameter axon that has the standard Hodgkin and Huxley (1952) kinetics at 18 degrees C (and an input conductance of 8.7 nS), gcrit is 72 nS. At 0 degrees C, gcrit = 200 nS, whereas at 30 degrees C gcrit = 30 nS. 3. The critical conductance change that blocks propagation depends steeply on the density of excitable channels (gNa) at the terminal. For a geometrically uniform terminal at 18 degrees C, the action potential can not be blocked by a local shunt when gNa greater than 600 mS/cm2. 4. An axoaxonal synapse in the proximity of the postsynaptic release site has graded control over the spike amplitude (and, therefore, over the postsynaptic output) at that site. Presynaptic inhibition located remotely from the release site has an all-or-none effect at the release site. 5. Inhibition is more effective in attenuating the spike at the terminal when it impinges onto a passive terminal rather than on an excitable one. 6. The detectability of the conductance increase as well as the change in action potential amplitude associated with the presynaptic inhibition is poor at only a short distance from the axoaxonal synapse. The presence of bottlenecks and varicosities at some axonal terminals enhances this decoupling effect even more. Thus presynaptic inhibition may reduce the potential near the output site of the affected axon significantly, without producing any noticeable conductance or voltage change at a distance of only several tens of micrometers (a few tenths of a space constant) away from it. 7. Varicosities and bottlenecks typically found along axonal terminals are the optimal loci for presynaptic inhibition to be most effective in attenuating the action potential at the terminal. Even with high density of excitable channels, propagation with such terminal geometry is insecure, and one, or few, quanta of inhibitory transmitter (a conductance change of several nanosiemens) can block propagation there.(ABSTRACT TRUNCATED AT 400 WORDS)