RGD Reference Report - Up-regulation in expression of vesicular glutamate transporter 3 in substantia nigra but not in striatum of 6-hydroxydopamine-lesioned rats. - Rat Genome Database

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Up-regulation in expression of vesicular glutamate transporter 3 in substantia nigra but not in striatum of 6-hydroxydopamine-lesioned rats.

Authors: Chung, EK  Chen, LW  Chan, YS  Yung, KK 
Citation: Chung EK, etal., Neurosignals. 2006-2007;15(5):238-48. Epub 2007 Apr 13.
RGD ID: 9999153
Pubmed: PMID:17435391   (View Abstract at PubMed)
DOI: DOI:10.1159/000101704   (Journal Full-text)

Overactivity of the glutamatergic system is suggested to be closely related to the onset and pathogenesis of Parkinson's disease. Vesicular glutamate transporters (VGLUT1, T2 and T3) are a group of glutamate transporters in neurons that are responsible for transporting glutamate into synaptic vesicles and they are key elements for homeostasis of glutamate neurotransmission. The present study was aimed to investigate the expression of VGLUT1, T2 and T3 proteins after the onset of Parkinson's disease. A rat model of Parkinson's disease, the 6-hydroxydopamine-lesioned rat, was employed. Immunocytochemistry revealed that VGLUT1, T2 and T3 immunoreactivity was not modulated in the striatum of the lesioned rat. Western blotting analyses also showed that there was no change in the expression of T1, T2 and T3 proteins in the striatum. In contrast, no VGLUT1 protein was detected in the substantia nigra. After the lesion, levels of VGLUT2 immunoreactivity and protein were not modulated. Significant increase of VGLUT3 immunoreactivity was observed in the perikarya of GABAergic substantia nigra pars reticulata neurons (+14.7%) although VGLUT3 protein was not modulated in the nigral tissues. VGLUT3 in GABAergic neurons is suggested to play a role in GABA synthesis. The present results may therefore implicate that VGLUT1 and T2 are not modulated in the striatum and the substantia nigra of the 6-hydroxydopamine-lesioned rat and only VGLUT3 plays a role in pathogenesis of Parkinson's disease.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
SLC17A8HumanParkinsonism  ISOSlc17a8 (Rattus norvegicus)protein:increased expression:substantia nigra pars reticulata more ...RGD 
Slc17a8RatParkinsonism  IEP protein:increased expression:substantia nigra pars reticulata more ...RGD 
Slc17a8MouseParkinsonism  ISOSlc17a8 (Rattus norvegicus)protein:increased expression:substantia nigra pars reticulata more ...RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Cellular Component

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Slc17a8Ratperikaryon  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Slc17a8  (solute carrier family 17 member 8)

Genes (Mus musculus)
Slc17a8  (solute carrier family 17 (sodium-dependent inorganic phosphate cotransporter), member 8)

Genes (Homo sapiens)
SLC17A8  (solute carrier family 17 member 8)


Additional Information