ParkinsonFranceV1, Hal, Corpus, bibRecord, 000A59

Subthalamic nucleus electrical stimulation modulates calcium activity of nigral astrocytes.

Identifieur interne : 000A59 ( Hal/Corpus ); précédent : 000A58; suivant : 000A60

Subthalamic nucleus electrical stimulation modulates calcium activity of nigral astrocytes.

Auteurs : Elodie Barat ; Sylvie Boisseau ; Céline Bouyssières ; Florence Appaix ; Marc Savasta ; Mireille Albrieux

Source :

PLoS ONE [ 1932-6203 ] ; 2012.

RBID : Hal:inserm-00742194

Abstract

BACKGROUND: The substantia nigra pars reticulata (SNr) is a major output nucleus of the basal ganglia, delivering inhibitory efferents to the relay nuclei of the thalamus. Pathological hyperactivity of SNr neurons is known to be responsible for some motor disorders e.g. in Parkinson's disease. One way to restore this pathological activity is to electrically stimulate one of the SNr input, the excitatory subthalamic nucleus (STN), which has emerged as an effective treatment for parkinsonian patients. The neuronal network and signal processing of the basal ganglia are well known but, paradoxically, the role of astrocytes in the regulation of SNr activity has never been studied. PRINCIPAL FINDINGS: In this work, we developed a rat brain slice model to study the influence of spontaneous and induced excitability of afferent nuclei on SNr astrocytes calcium activity. Astrocytes represent the main cellular population in the SNr and display spontaneous calcium activities in basal conditions. Half of this activity is autonomous (i.e. independent of synaptic activity) while the other half is dependent on spontaneous glutamate and GABA release, probably controlled by the pace-maker activity of the pallido-nigral and subthalamo-nigral loops. Modification of the activity of the loops by STN electrical stimulation disrupted this astrocytic calcium excitability through an increase of glutamate and GABA releases. Astrocytic AMPA, mGlu and GABA(A) receptors were involved in this effect. SIGNIFICANCE: Astrocytes are now viewed as active components of neural networks but their role depends on the brain structure concerned. In the SNr, evoked activity prevails and autonomous calcium activity is lower than in the cortex or hippocampus. Our data therefore reflect a specific role of SNr astrocytes in sensing the STN-GPe-SNr loops activity and suggest that SNr astrocytes could potentially feedback on SNr neuronal activity. These findings have major implications given the position of SNr in the basal ganglia network.

Url:

http://www.hal.inserm.fr/inserm-00742194

DOI: 10.1371/journal.pone.0041793

Links to Exploration step

Hal:inserm-00742194

Le document en format XML

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<idno type="DOI">10.1371/journal.pone.0041793</idno>
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<front><div type="abstract" xml:lang="en">BACKGROUND: The substantia nigra pars reticulata (SNr) is a major output nucleus of the basal ganglia, delivering inhibitory efferents to the relay nuclei of the thalamus. Pathological hyperactivity of SNr neurons is known to be responsible for some motor disorders e.g. in Parkinson's disease. One way to restore this pathological activity is to electrically stimulate one of the SNr input, the excitatory subthalamic nucleus (STN), which has emerged as an effective treatment for parkinsonian patients. The neuronal network and signal processing of the basal ganglia are well known but, paradoxically, the role of astrocytes in the regulation of SNr activity has never been studied. PRINCIPAL FINDINGS: In this work, we developed a rat brain slice model to study the influence of spontaneous and induced excitability of afferent nuclei on SNr astrocytes calcium activity. Astrocytes represent the main cellular population in the SNr and display spontaneous calcium activities in basal conditions. Half of this activity is autonomous (i.e. independent of synaptic activity) while the other half is dependent on spontaneous glutamate and GABA release, probably controlled by the pace-maker activity of the pallido-nigral and subthalamo-nigral loops. Modification of the activity of the loops by STN electrical stimulation disrupted this astrocytic calcium excitability through an increase of glutamate and GABA releases. Astrocytic AMPA, mGlu and GABA(A) receptors were involved in this effect. SIGNIFICANCE: Astrocytes are now viewed as active components of neural networks but their role depends on the brain structure concerned. In the SNr, evoked activity prevails and autonomous calcium activity is lower than in the cortex or hippocampus. Our data therefore reflect a specific role of SNr astrocytes in sensing the STN-GPe-SNr loops activity and suggest that SNr astrocytes could potentially feedback on SNr neuronal activity. These findings have major implications given the position of SNr in the basal ganglia network.</div>
</front>
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            <author role="aut">              <persName>                <forename type="first">Elodie</forename>
                <surname>Barat</surname>
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            <author role="aut">              <persName>                <forename type="first">Sylvie</forename>
                <surname>Boisseau</surname>
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              <idno type="halauthorid">399298</idno>
              <affiliation ref="#struct-391045"></affiliation>
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            <author role="aut">              <persName>                <forename type="first">Céline</forename>
                <surname>Bouyssières</surname>
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              <idno type="halauthorid">773136</idno>
              <affiliation ref="#struct-391045"></affiliation>
            </author>
            <author role="aut">              <persName>                <forename type="first">Florence</forename>
                <surname>Appaix</surname>
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              <idno type="halauthorid">230946</idno>
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            </author>
            <author role="aut">              <persName>                <forename type="first">Marc</forename>
                <surname>Savasta</surname>
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              <idno type="halauthorid">201370</idno>
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            </author>
            <author role="crp">              <persName>                <forename type="first">Mireille</forename>
                <surname>Albrieux</surname>
              </persName>
              <email type="md5">0f1dbf4d3a7cbcdb92b4dfcbf6f2e842</email>
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            </author>
            <editor role="depositor">              <persName>                <forename>Marc</forename>
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              <email type="md5">17a3ed21e3dd17a996152da3d29e00bb</email>
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            <funder>Funding provided by the Institut National de la Santé et de la Recherche Médicale; Université Joseph Fourier; France Parkinson; Fondation de France</funder>
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                <author role="aut">                  <persName>                    <forename type="first">Elodie</forename>
                    <surname>Barat</surname>
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                <author role="aut">                  <persName>                    <forename type="first">Sylvie</forename>
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                <author role="aut">                  <persName>                    <forename type="first">Céline</forename>
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                  <affiliation ref="#struct-391045"></affiliation>
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                <author role="aut">                  <persName>                    <forename type="first">Florence</forename>
                    <surname>Appaix</surname>
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                  <affiliation ref="#struct-391045"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Marc</forename>
                    <surname>Savasta</surname>
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                  <idno type="halauthorid">201370</idno>
                  <affiliation ref="#struct-391045"></affiliation>
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                <author role="crp">                  <persName>                    <forename type="first">Mireille</forename>
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            <abstract xml:lang="en">BACKGROUND: The substantia nigra pars reticulata (SNr) is a major output nucleus of the basal ganglia, delivering inhibitory efferents to the relay nuclei of the thalamus. Pathological hyperactivity of SNr neurons is known to be responsible for some motor disorders e.g. in Parkinson's disease. One way to restore this pathological activity is to electrically stimulate one of the SNr input, the excitatory subthalamic nucleus (STN), which has emerged as an effective treatment for parkinsonian patients. The neuronal network and signal processing of the basal ganglia are well known but, paradoxically, the role of astrocytes in the regulation of SNr activity has never been studied. PRINCIPAL FINDINGS: In this work, we developed a rat brain slice model to study the influence of spontaneous and induced excitability of afferent nuclei on SNr astrocytes calcium activity. Astrocytes represent the main cellular population in the SNr and display spontaneous calcium activities in basal conditions. Half of this activity is autonomous (i.e. independent of synaptic activity) while the other half is dependent on spontaneous glutamate and GABA release, probably controlled by the pace-maker activity of the pallido-nigral and subthalamo-nigral loops. Modification of the activity of the loops by STN electrical stimulation disrupted this astrocytic calcium excitability through an increase of glutamate and GABA releases. Astrocytic AMPA, mGlu and GABA(A) receptors were involved in this effect. SIGNIFICANCE: Astrocytes are now viewed as active components of neural networks but their role depends on the brain structure concerned. In the SNr, evoked activity prevails and autonomous calcium activity is lower than in the cortex or hippocampus. Our data therefore reflect a specific role of SNr astrocytes in sensing the STN-GPe-SNr loops activity and suggest that SNr astrocytes could potentially feedback on SNr neuronal activity. These findings have major implications given the position of SNr in the basal ganglia network.</abstract>
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Subthalamic nucleus electrical stimulation modulates calcium activity of nigral astrocytes.

Subthalamic nucleus electrical stimulation modulates calcium activity of nigral astrocytes.

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