Skip to main content Accessibility help
×
Hostname: page-component-78c5997874-t5tsf Total loading time: 0 Render date: 2024-11-19T23:59:00.738Z Has data issue: false hasContentIssue false

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
Get access

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.

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

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×