Altered expression of vesicular glutamate transporters VGLUT1 and VGLUT2 in Parkinson disease.
Identifieur interne : 000596 ( Ncbi/Curation ); précédent : 000595; suivant : 000597Altered expression of vesicular glutamate transporters VGLUT1 and VGLUT2 in Parkinson disease.
Auteurs : Alireza Kashani [France] ; Catalina Betancur ; Bruno Giros ; Etienne Hirsch ; Salah El MestikawySource :
- Neurobiology of aging [ 1558-1497 ] ; 2007.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Autoradiography (methods), Blotting, Western (methods), Brain (metabolism), Case-Control Studies, Female, Gene Expression Regulation (physiology), Humans, Male, Middle Aged, Nerve Tissue Proteins (metabolism), Parkinson Disease (metabolism), Parkinson Disease (pathology), Postmortem Changes, Vesicular Glutamate Transport Protein 1 (metabolism), Vesicular Glutamate Transport Protein 2 (metabolism).
- MESH :
- chemical , metabolism : Nerve Tissue Proteins, Vesicular Glutamate Transport Protein 1, Vesicular Glutamate Transport Protein 2.
- metabolism : Brain, Parkinson Disease.
- methods : Autoradiography, Blotting, Western.
- pathology : Parkinson Disease.
- physiology : Gene Expression Regulation.
- Aged, Aged, 80 and over, Case-Control Studies, Female, Humans, Male, Middle Aged, Postmortem Changes.
Abstract
Glutamatergic pathways play a key role in the functional organization of neuronal circuits involved in Parkinson disease (PD). Recently, three vesicular glutamate transporters (VGLUT1-3) were identified. VGLUT1 and VGLUT2 are responsible for the uploading of glutamate into synaptic vesicles and are the first specific markers of glutamatergic neurons available. Here, we analyzed the expression of VGLUT1 and VGLUT2 in autopsy tissues of PD patients and matched controls using Western blot and immunoautoradiography. VGLUT1 and VGLUT2 expression was increased in the Parkinsonian putamen by 24% and 29%, respectively (p<0.01). In contrast, only VGLUT1 was dramatically decreased in the prefrontal and temporal cortex of PD patients (approximately 50%, p<0.01 and p<0.001, respectively). These findings demonstrate the existence of profound alterations of glutamatergic transmission in PD, which are likely to contribute to the motor and cognitive impairments associated with the disease, and should thus be taken into account in the treatment of PD.
DOI: 10.1016/j.neurobiolaging.2006.02.010
PubMed: 16563567
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sort="Giros, Bruno" uniqKey="Giros B" first="Bruno" last="Giros">Bruno Giros</name></author><author><name sortKey="Hirsch, Etienne" sort="Hirsch, Etienne" uniqKey="Hirsch E" first="Etienne" last="Hirsch">Etienne Hirsch</name></author><author><name sortKey="El Mestikawy, Salah" sort="El Mestikawy, Salah" uniqKey="El Mestikawy S" first="Salah" last="El Mestikawy">Salah El Mestikawy</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:16563567</idno><idno type="pmid">16563567</idno><idno type="doi">10.1016/j.neurobiolaging.2006.02.010</idno><idno type="wicri:Area/PubMed/Corpus">000D97</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000D97</idno><idno type="wicri:Area/PubMed/Curation">000D57</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000D57</idno><idno type="wicri:Area/PubMed/Checkpoint">000D57</idno><idno 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type="city">Créteil</settlement></placeName></affiliation></author><author><name sortKey="Betancur, Catalina" sort="Betancur, Catalina" uniqKey="Betancur C" first="Catalina" last="Betancur">Catalina Betancur</name></author><author><name sortKey="Giros, Bruno" sort="Giros, Bruno" uniqKey="Giros B" first="Bruno" last="Giros">Bruno Giros</name></author><author><name sortKey="Hirsch, Etienne" sort="Hirsch, Etienne" uniqKey="Hirsch E" first="Etienne" last="Hirsch">Etienne Hirsch</name></author><author><name sortKey="El Mestikawy, Salah" sort="El Mestikawy, Salah" uniqKey="El Mestikawy S" first="Salah" last="El Mestikawy">Salah El Mestikawy</name></author></analytic><series><title level="j">Neurobiology of aging</title><idno type="eISSN">1558-1497</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Autoradiography (methods)</term><term>Blotting, Western (methods)</term><term>Brain (metabolism)</term><term>Case-Control Studies</term><term>Female</term><term>Gene Expression Regulation (physiology)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Nerve Tissue Proteins (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Postmortem Changes</term><term>Vesicular Glutamate Transport Protein 1 (metabolism)</term><term>Vesicular Glutamate Transport Protein 2 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nerve Tissue Proteins</term><term>Vesicular Glutamate Transport Protein 1</term><term>Vesicular Glutamate Transport Protein 2</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Autoradiography</term><term>Blotting, Western</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Case-Control Studies</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Postmortem Changes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glutamatergic pathways play a key role in the functional organization of neuronal circuits involved in Parkinson disease (PD). Recently, three vesicular glutamate transporters (VGLUT1-3) were identified. VGLUT1 and VGLUT2 are responsible for the uploading of glutamate into synaptic vesicles and are the first specific markers of glutamatergic neurons available. Here, we analyzed the expression of VGLUT1 and VGLUT2 in autopsy tissues of PD patients and matched controls using Western blot and immunoautoradiography. VGLUT1 and VGLUT2 expression was increased in the Parkinsonian putamen by 24% and 29%, respectively (p<0.01). In contrast, only VGLUT1 was dramatically decreased in the prefrontal and temporal cortex of PD patients (approximately 50%, p<0.01 and p<0.001, respectively). These findings demonstrate the existence of profound alterations of glutamatergic transmission in PD, which are likely to contribute to the motor and cognitive impairments associated with the disease, and should thus be taken into account in the treatment of PD.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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