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J Physiol Vol 483, Issue Pt 1 pp 167-182
Copyright © 1995 by The Physiological Society
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Cellular basis of temporal synaptic signalling: an in vitro electrophysiological study in rat auditory thalamus.

B Hu

Neuroscience Unit, Loeb Research Institute, Ottawa Civic Hospital, University of Ottawa, Ontario, Canada.

1. The cellular mechanisms underlying temporal synaptic signalling of tectothalamic pathways were investigated in rat medial geniculate body (MGB) maintained in vitro. Stimulation of the brachium of the inferior colliculus elicited either a short latency, single- (or dual-) spike or a long latency (10-80 ms) burst in MGB neurones. The delayed burst response was found in most non-lemniscal or caudodorsal MGB (MGd) neurones, whereas single-spike units were mainly seen in the lemniscal ventral MGB (MGv). Population latency analysis revealed that the overall relay time of tectothalamic transmission is approximately 50 ms, with at least two excitation peaks occurring around 8 and 15 ms, respectively. 2. Intracellular recordings showed that the delayed burst responses in MGd neurones were mediated by an EPSP-triggered low threshold spike (LTS). Small variations in either the membrane voltage or in EPSP amplitude induced significant shifts of LTS latency. 3. Compared with MGv cells, MGd neurones exhibited a more negative resting membrane potential and a prolonged EPSP; they lacked an apparent hyperpolarization-activated inward rectifier (Ih). These factors seem to lead collectively to a dominant occurrence of long latency burst response in the MGd. In the majority of single-spiking MGv cells that expressed a clear Ih, application of Cs+ consistently hyperpolarized the cell, which transformed a single-spike synaptic response into an EPSP-LTS burst or a subthreshold EPSP. 4. Taken together, these data suggest that the monosynaptic tectothalamic pathways are capable of introducing a ventrodorsal gradient in auditory response time. This synaptic activity pattern is probably dominantly regulated by a set of membrane conductances expressed endogenously in thalamocortical neurones.




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