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- Publisher Website: 10.1002/cne.21852
- Scopus: eid_2-s2.0-58149277182
- PMID: 18831527
- WOS: WOS:000260842000001
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Article: Downregulation of glial glutamate transporters after dopamine denervation in the striatum of 6-hydroxydopamine-lesioned rats
Title | Downregulation of glial glutamate transporters after dopamine denervation in the striatum of 6-hydroxydopamine-lesioned rats |
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Authors | |
Keywords | Animal model of Parkinson's disease Degeneration of dopaminergic neurons GLAST Glial glutamate transporters GLT1 Neuronal glutamate transporter; EAAC1; basal ganglia Neurotoxin |
Issue Date | 2008 |
Publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31248 |
Citation | Journal Of Comparative Neurology, 2008, v. 511 n. 4, p. 421-437 How to Cite? |
Abstract | Overactivity of glutamatergic neurotransmission in the basal ganglia is known to be closely related to the onset and pathogenesis of Parkinson's disease. Glutamate homeostasis around glutamatergic synapses is tightly regulated by two groups of glutamate transporters: glial glutamate transporters GLT1 (EAAT2) and GLAST (EAAT1), and neuronal glutamate transporter EAAC1. In order to investigate the changes of glutamate transporters after the onset of Parkinson's disease, unilateral 6-hydroxydopamine-lesioned rat, an animal model of Parkinson's disease, was employed. By immunofluorescence and Western blot analyses, GLT1 and GLAST proteins were significantly reduced in the striatum with lesion. No change in GLT1 and GLAST protein was found in the substantia nigra. The reduction of GLT1 protein in the striatum was more prominent than that of GLAST protein (∼40% vs. 20%). In addition, EAAC1 protein was found to be increased in the substantia nigra pars reticulata of the lesioned rats but not in the striatum. The present results indicate that reductions of GLT1 and GLAST may impair glutamate homeostasis around glutamatergic synapses in the striatum and contribute to over-spills of glutamate in the system. An increase in the EAAC1 level in the substantia nigra pars reticulata may increase GABA synthesis and enhance GABAergic neurotransmission. These results indicate that there are differential and distinct modulations of glutamate transporters after dopamine denervation in the 6-hydroxydopamine-lesioned rat. © 2008 Wiley-Liss, Inc. |
Persistent Identifier | http://hdl.handle.net/10722/171776 |
ISSN | 2023 Impact Factor: 2.3 2023 SCImago Journal Rankings: 1.218 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chung, EKY | en_US |
dc.contributor.author | Chen, LW | en_US |
dc.contributor.author | Chan, YS | en_US |
dc.contributor.author | Yung, KKL | en_US |
dc.date.accessioned | 2012-10-30T06:16:59Z | - |
dc.date.available | 2012-10-30T06:16:59Z | - |
dc.date.issued | 2008 | en_US |
dc.identifier.citation | Journal Of Comparative Neurology, 2008, v. 511 n. 4, p. 421-437 | en_US |
dc.identifier.issn | 0021-9967 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171776 | - |
dc.description.abstract | Overactivity of glutamatergic neurotransmission in the basal ganglia is known to be closely related to the onset and pathogenesis of Parkinson's disease. Glutamate homeostasis around glutamatergic synapses is tightly regulated by two groups of glutamate transporters: glial glutamate transporters GLT1 (EAAT2) and GLAST (EAAT1), and neuronal glutamate transporter EAAC1. In order to investigate the changes of glutamate transporters after the onset of Parkinson's disease, unilateral 6-hydroxydopamine-lesioned rat, an animal model of Parkinson's disease, was employed. By immunofluorescence and Western blot analyses, GLT1 and GLAST proteins were significantly reduced in the striatum with lesion. No change in GLT1 and GLAST protein was found in the substantia nigra. The reduction of GLT1 protein in the striatum was more prominent than that of GLAST protein (∼40% vs. 20%). In addition, EAAC1 protein was found to be increased in the substantia nigra pars reticulata of the lesioned rats but not in the striatum. The present results indicate that reductions of GLT1 and GLAST may impair glutamate homeostasis around glutamatergic synapses in the striatum and contribute to over-spills of glutamate in the system. An increase in the EAAC1 level in the substantia nigra pars reticulata may increase GABA synthesis and enhance GABAergic neurotransmission. These results indicate that there are differential and distinct modulations of glutamate transporters after dopamine denervation in the 6-hydroxydopamine-lesioned rat. © 2008 Wiley-Liss, Inc. | en_US |
dc.language | eng | en_US |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31248 | en_US |
dc.relation.ispartof | Journal of Comparative Neurology | en_US |
dc.subject | Animal model of Parkinson's disease | - |
dc.subject | Degeneration of dopaminergic neurons | - |
dc.subject | GLAST | - |
dc.subject | Glial glutamate transporters | - |
dc.subject | GLT1 | - |
dc.subject | Neuronal glutamate transporter; EAAC1; basal ganglia | - |
dc.subject | Neurotoxin | - |
dc.subject.mesh | Adrenergic Agents - Toxicity | en_US |
dc.subject.mesh | Amino Acid Transport System X-Ag - Metabolism | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Blotting, Western | en_US |
dc.subject.mesh | Corpus Striatum - Drug Effects - Metabolism | en_US |
dc.subject.mesh | Denervation | en_US |
dc.subject.mesh | Dopamine - Metabolism | en_US |
dc.subject.mesh | Down-Regulation | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Fluorescent Antibody Technique | en_US |
dc.subject.mesh | Immunohistochemistry | en_US |
dc.subject.mesh | Neuroglia - Metabolism | en_US |
dc.subject.mesh | Oxidopamine - Toxicity | en_US |
dc.subject.mesh | Parkinsonian Disorders - Metabolism | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Rats, Sprague-Dawley | en_US |
dc.title | Downregulation of glial glutamate transporters after dopamine denervation in the striatum of 6-hydroxydopamine-lesioned rats | en_US |
dc.type | Article | en_US |
dc.identifier.email | Chan, YS:yschan@hkucc.hku.hk | en_US |
dc.identifier.authority | Chan, YS=rp00318 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1002/cne.21852 | en_US |
dc.identifier.pmid | 18831527 | en_US |
dc.identifier.scopus | eid_2-s2.0-58149277182 | en_US |
dc.identifier.hkuros | 164088 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-58149277182&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 511 | en_US |
dc.identifier.issue | 4 | en_US |
dc.identifier.spage | 421 | en_US |
dc.identifier.epage | 437 | en_US |
dc.identifier.isi | WOS:000260842000001 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Chung, EKY=16315234600 | en_US |
dc.identifier.scopusauthorid | Chen, LW=25937158100 | en_US |
dc.identifier.scopusauthorid | Chan, YS=7403676627 | en_US |
dc.identifier.scopusauthorid | Yung, KKL=13605496000 | en_US |
dc.identifier.issnl | 0021-9967 | - |