Calvin W H
Brain Res. 1975 Jan 24;84(1):1-22. doi: 10.1016/0006-8993(75)90796-9.
The membrane potential waveforms to be expected from many asynchronous inputs to CNS neurons are described, along with modes for repetitive firing through which the input waveforms are converted into spike trains. Area beneath a postsynaptic potential (PSP), rather than PSP peak height, is shown to be an important parameter susceptible to modification. Occasional crossings of threshold produce occasional spikes, but a sustained depolarizing waveform which attempts to hold the membrane potential above threshold elicits rhythmic firing. Firing rate is graded with the amount by which the synaptic depolarizing currents exceed the minimum current for rhythmic firing (approximately rheobase). A systematic sequence of alterations in the membrane potential trajectory between spikes, quite different from those of receptors and invertebrate neurons, may control the firing rate and give rise to sudden changes in the "gain" of this conversion of depolarizing current into firing rate. The different implications of synaptic location during the occasional spike mode and the rhythmic firing mode are discussed, as is the role of the antidromic invasion of the soma-dendritic region during rhythmic firing. Less frequently an"extra spike mode" is seen where depolarizing afterpotentials following a spike themselves cross threshold to elicit an extra spike, which may similarly elicit another extra spike, etc., in a regenerative cycle. The character of the underlying depolarizing afterpotentials (or "delayed depolarizations") is reviewed, along with theories for their origin from the antidromic invasion of the dendritic tree. The stereotyped burst firing patterns characteristic of the extra spike mode can also be seen in deafferented neurons and neurons studied in chronic syndromes such as epilepsy and central pain. This raises the question as to whether some disease states may augment extra spike firing, thus multiplying many-fold the response to a normal input.
描述了中枢神经系统神经元许多异步输入所预期的膜电位波形，以及通过重复放电模式将输入波形转换为脉冲序列的方式。结果表明，突触后电位（PSP）下方的面积而非PSP峰值高度是一个易受修饰影响的重要参数。偶尔的阈值穿越会产生偶尔的脉冲，但试图将膜电位维持在阈值以上的持续去极化波形会引发节律性放电。放电频率随突触去极化电流超过节律性放电最小电流（近似基强度）的量而分级。脉冲之间膜电位轨迹的一系列系统性变化与感受器和无脊椎动物神经元的变化截然不同，可能控制放电频率，并导致去极化电流向放电频率转换的“增益”突然变化。讨论了偶尔脉冲模式和节律性放电模式期间突触位置的不同影响，以及节律性放电期间轴突逆行侵入胞体 - 树突区域的作用。较少见的是“额外脉冲模式”，即一个脉冲后的去极化后电位本身穿越阈值引发一个额外脉冲，该额外脉冲可能类似地引发另一个额外脉冲等，形成一个再生循环。回顾了潜在的去极化后电位（或“延迟去极化”）的特征，以及关于其起源于树突树轴突逆行侵入的理论。在去传入神经的神经元以及在慢性综合征（如癫痫和中枢性疼痛）中研究的神经元中也可以看到额外脉冲模式特有的刻板爆发放电模式。这就提出了一个问题，即某些疾病状态是否可能增强额外脉冲放电，从而使对正常输入的反应增加许多倍。
