Guinan J J, Li R Y
Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge.
Hear Res. 1990 Nov;49(1-3):321-34. doi: 10.1016/0378-5955(90)90111-2.
In the medial nucleus of the trapezoid body (MNTB), each principal neuron receives one large axonal ending (a calyx of Held) and many small endings. In this same region, microelectrode recordings show unusual 'unit' waveforms which have two components separated by about 0.5 ms. We show that the first component (C1) of such a waveform corresponds to a spike from the calyx of Held and that the second component (C2) corresponds to a spike from the MNTB principal neuron. There are two kinds of evidence for these correspondences. First, electrical stimulation of calyciferous axons in the contralateral trapezoid body evokes C1 spikes with latencies of 0.1-0.3 ms. These latencies are too short for there to be an intervening synapse and are consistent with C1 being a presynaptic spike. Second, shocks in the lateral superior olive (which receives projections from MNTB principal-neurons) evoke 'A' spikes in the MNTB which can be shown by their waveshapes and mutual refractoriness with C2 spikes to result from antidromic activation of the neurons producing C2 spikes. Spontaneous and sound-evoked responses in dozens of cats anesthetized by barbiturates or Ketamine always had a C2 spike following each C1 spike. This implies that there is normally one-to-one spike transmission from the calyx of Held input to the MNTB principal neuron output. The small endings on MNTB principal neurons are also capable of evoking spikes. Electric shocks (and in one case, sound), evoked long latency (1-3 ms) 'LC2' spikes, which (by mutual refractoriness and waveshape) are from the same neural elements as C2 and 'A' spikes. Since LC2 spikes are not preceded by C1 spikes, LC2 spikes must be mediated by small axonal endings on MNTB principal neurons. We found some evidence of inhibition, possibly recurrent inhibition, in MNTB principal neurons. In a few neurons, sound or shocks inhibited 'A' spikes or LC2 spikes. In some cases, after each C2 spike, LC2 spikes were blocked or reduced in amplitude for several milliseconds. Our data firmly establish that there is fast, secure spike transmission from calyces of Held to MNTB principal neurons and suggest that under some circumstances there is additional signal processing in MNTB principal neurons.
在梯形体内侧核（MNTB）中，每个主神经元接收一个大的轴突终末（Held壶腹）和许多小终末。在同一区域，微电极记录显示出异常的“单位”波形，该波形有两个成分，间隔约0.5毫秒。我们发现，这种波形的第一个成分（C1）对应于来自Held壶腹的一个锋电位，第二个成分（C2）对应于来自MNTB主神经元的一个锋电位。有两类证据支持这些对应关系。第一，对侧梯形体中含壶腹轴突的电刺激会诱发潜伏期为0.1 - 0.3毫秒的C1锋电位。这些潜伏期太短，不可能存在中间突触，这与C1是一个突触前锋电位一致。第二，外侧上橄榄核（它接收来自MNTB主神经元的投射）中的电刺激会在MNTB中诱发“A”锋电位，通过其波形和与C2锋电位的相互不应期可以表明，这些“A”锋电位是由产生C2锋电位的神经元的逆向激活所致。在几十只经巴比妥类药物或氯胺酮麻醉的猫中，自发反应和声诱发反应总是在每个C1锋电位之后出现一个C2锋电位。这意味着通常存在从Held壶腹输入到MNTB主神经元输出的一对一锋电位传递。MNTB主神经元上的小终末也能够诱发锋电位。电刺激（在一个例子中是声音）诱发长潜伏期（1 - 3毫秒）的“LC2”锋电位，通过相互不应期和波形判断，这些锋电位与C2和“A”锋电位来自相同的神经元件。由于LC2锋电位之前没有C1锋电位，LC2锋电位必定是由MNTB主神经元上的小轴突终末介导的。我们发现了一些MNTB主神经元存在抑制的证据，可能是回返性抑制。在少数神经元中，声音或电刺激会抑制“A”锋电位或LC2锋电位。在某些情况下，在每个C2锋电位之后，LC2锋电位会被阻断或幅度降低数毫秒。我们的数据确凿地证实了从Held壶腹到MNTB主神经元存在快速、可靠的锋电位传递，并表明在某些情况下MNTB主神经元中存在额外的信号处理。
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