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How the cortico-thalamic feedback affects the EEG power spectrum over frontal and occipital regions during propofol-induced anaesthetic sedation

Identifieur interne : 000848 ( Main/Exploration ); précédent : 000847; suivant : 000849

How the cortico-thalamic feedback affects the EEG power spectrum over frontal and occipital regions during propofol-induced anaesthetic sedation

Auteurs : Meysam Hashemi [France] ; Axel Hutt [France] ; Jamie Sleigh [Nouvelle-Zélande]

Source :

RBID : Hal:hal-01091503

Abstract

Increasing concentrations of the anaesthetic agent propofol initially induces sedation before achieving full general anaesthesia. The characteristic changes in electroencephalographic (EEG) rhythms include increased activity in the δ− (1-4 Hz) and α− (8-12 Hz) frequency bands over the frontal region, but increased δ− and decreased α−activity over the occipital region. It is known that the cortex, the thalamus, and the thalamo-cortical feedback loop contribute to some degree to the propofol-induced changes in the EEG power spectrum. However the precise role of each structure to the dynamics of the EEG is unknown. In this paper we apply a neuronal population model of a single thalamo-cortical module to repro-duce the power spectrum changes in EEG during propofol-induced anaesthesia sedation. Based on recent experimental data, the effect of propofol is modelled as an increase in inhibitory synaptic response amplitude and decay time constant in thalamo-cortical relay cells while cortical inhibition is neglected. The model reproduces the power spectrum features observed experimentally both in frontal and occipital electrodes. Moreover a detailed analysis of the model indicates the importance of multiple resting states in brain activity. The work suggests that the α−activity originates from the cortico-thalamic relay interaction, whereas the emergence of δ−activity results from the full cortico-reticular-relay-cortical feedback loop with a prominent enforced thalamic reticular-relay interac-tion. This model suggests an essential role of synaptic GABAergic receptors at relay neurons and, more generally, for the thalamus in the generation of both the α− and the δ−EEG patterns that are seen during propofol anaesthesia sedation.

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<orgName type="acronym">LORIA</orgName>
<date type="start">2012-01-01</date>
<desc>
<address>
<addrLine>Campus Scientifique BP 239 54506 Vandoeuvre-lès-Nancy Cedex</addrLine>
<country key="FR"></country>
</address>
<ref type="url">http://www.loria.fr</ref>
</desc>
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<relation active="#struct-413289" type="direct"></relation>
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</org>
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<org type="institution" xml:id="struct-413289" status="VALID">
<idno type="IdRef">157040569</idno>
<idno type="IdUnivLorraine">[UL]100--</idno>
<orgName>Université de Lorraine</orgName>
<orgName type="acronym">UL</orgName>
<date type="start">2012-01-01</date>
<desc>
<address>
<addrLine>34 cours Léopold - CS 25233 - 54052 Nancy cedex</addrLine>
<country key="FR"></country>
</address>
<ref type="url">http://www.univ-lorraine.fr/</ref>
</desc>
</org>
</tutelle>
<tutelle name="UMR7503" active="#struct-441569" type="indirect">
<org type="institution" xml:id="struct-441569" status="VALID">
<idno type="ISNI">0000000122597504</idno>
<idno type="IdRef">02636817X</idno>
<orgName>Centre National de la Recherche Scientifique</orgName>
<orgName type="acronym">CNRS</orgName>
<date type="start">1939-10-19</date>
<desc>
<address>
<country key="FR"></country>
</address>
<ref type="url">http://www.cnrs.fr/</ref>
</desc>
</org>
</tutelle>
</tutelles>
</hal:affiliation>
<country>France</country>
<placeName>
<settlement type="city">Nancy</settlement>
<settlement type="city">Metz</settlement>
<region type="region" nuts="2">Grand Est</region>
<region type="old region" nuts="2">Lorraine (région)</region>
</placeName>
<orgName type="university">Université de Lorraine</orgName>
</affiliation>
</author>
<author>
<name sortKey="Sleigh, Jamie" sort="Sleigh, Jamie" uniqKey="Sleigh J" first="Jamie" last="Sleigh">Jamie Sleigh</name>
<affiliation wicri:level="1">
<hal:affiliation type="laboratory" xml:id="struct-261683" status="INCOMING">
<orgName>Department of Anaesthetics</orgName>
<desc>
<address>
<addrLine>Department of Anaesthetics, Waikato Hospital, Hamilton, New Zealand</addrLine>
<country key="NZ"></country>
</address>
</desc>
<listRelation>
<relation active="#struct-362126" type="direct"></relation>
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<tutelle active="#struct-362126" type="direct">
<org type="institution" xml:id="struct-362126" status="INCOMING">
<orgName>Waikato Hospital</orgName>
<desc>
<address>
<country key="FR"></country>
</address>
</desc>
</org>
</tutelle>
</tutelles>
</hal:affiliation>
<country>Nouvelle-Zélande</country>
</affiliation>
</author>
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<front>
<div type="abstract" xml:lang="en">Increasing concentrations of the anaesthetic agent propofol initially induces sedation before achieving full general anaesthesia. The characteristic changes in electroencephalographic (EEG) rhythms include increased activity in the δ− (1-4 Hz) and α− (8-12 Hz) frequency bands over the frontal region, but increased δ− and decreased α−activity over the occipital region. It is known that the cortex, the thalamus, and the thalamo-cortical feedback loop contribute to some degree to the propofol-induced changes in the EEG power spectrum. However the precise role of each structure to the dynamics of the EEG is unknown. In this paper we apply a neuronal population model of a single thalamo-cortical module to repro-duce the power spectrum changes in EEG during propofol-induced anaesthesia sedation. Based on recent experimental data, the effect of propofol is modelled as an increase in inhibitory synaptic response amplitude and decay time constant in thalamo-cortical relay cells while cortical inhibition is neglected. The model reproduces the power spectrum features observed experimentally both in frontal and occipital electrodes. Moreover a detailed analysis of the model indicates the importance of multiple resting states in brain activity. The work suggests that the α−activity originates from the cortico-thalamic relay interaction, whereas the emergence of δ−activity results from the full cortico-reticular-relay-cortical feedback loop with a prominent enforced thalamic reticular-relay interac-tion. This model suggests an essential role of synaptic GABAergic receptors at relay neurons and, more generally, for the thalamus in the generation of both the α− and the δ−EEG patterns that are seen during propofol anaesthesia sedation.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>France</li>
<li>Nouvelle-Zélande</li>
</country>
<region>
<li>Grand Est</li>
<li>Lorraine (région)</li>
</region>
<settlement>
<li>Metz</li>
<li>Nancy</li>
</settlement>
<orgName>
<li>Université de Lorraine</li>
</orgName>
</list>
<tree>
<country name="France">
<region name="Grand Est">
<name sortKey="Hashemi, Meysam" sort="Hashemi, Meysam" uniqKey="Hashemi M" first="Meysam" last="Hashemi">Meysam Hashemi</name>
</region>
<name sortKey="Hutt, Axel" sort="Hutt, Axel" uniqKey="Hutt A" first="Axel" last="Hutt">Axel Hutt</name>
</country>
<country name="Nouvelle-Zélande">
<noRegion>
<name sortKey="Sleigh, Jamie" sort="Sleigh, Jamie" uniqKey="Sleigh J" first="Jamie" last="Sleigh">Jamie Sleigh</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

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