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18 - Synaptic transduction in neocortical neurones

from Part III - Control of central nervous system output

Published online by Cambridge University Press:  04 August 2010

Hugh Bostock
Affiliation:
Institute of Neurology, London
P. A. Kirkwood
Affiliation:
Institute of Neurology, London
A. H. Pullen
Affiliation:
Institute of Neurology, London
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Summary

Introduction

Neurotransmitters mediate information transfer between neurones and in most cell types synaptic activity evokes slow potentials that are transduced into all-or-nothing action potentials. The primary site for integration of neuronal activity is on the soma and dendrites where input from many different sources converge and generate spike trains in neurones by summed synaptic currents. The molecular events during synaptic communication also provide many sites for modulation. Here I consider only the last step of the postsynaptic transduction operation where slow synaptic potentials are transduced into nerve impulses. This process is controlled by the type and density of voltage and chemically gated ion channels in the postsynaptic neurone. The model system discussed here is the pyramidal neurones in layer V of rat and cat somatosensory cortex. The pattern of evoked repetitive firing in pyramidal neurones has functional significance. Lemon & Mantel (1989) found that even a single spike in a corticospinal neurone produced a measurable facilitation of the target muscle electromyogram.

Types of channels in neocortical neurones

Central neurones uniformly have many types of ion channels. No one type occurs only in a single class of neurones. The collection of ion channel types provides great diversity in the voltage dependence, kinetics and modulation by neurotransmitters. In a specific neurone type modest changes in density, location or modulation of ion channels can markedly alter neurone behaviour. The paper physiologist can easily generate models with many different response patterns.

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The Neurobiology of Disease
Contributions from Neuroscience to Clinical Neurology
, pp. 201 - 209
Publisher: Cambridge University Press
Print publication year: 1996

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