In the medial nucleus of the trapezoid body (MNTB), each principal neuron receives one large axon... more 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.
In the medial nucleus of the trapezoid body (MNTB), each principal neuron receives one large axon... more 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.
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