RGD Reference Report - The roles of striatal serotonin and L -amino-acid decarboxylase on L-DOPA-induced Dyskinesia in a Hemiparkinsonian rat model. - Rat Genome Database

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The roles of striatal serotonin and L -amino-acid decarboxylase on L-DOPA-induced Dyskinesia in a Hemiparkinsonian rat model.

Authors: Gil, S  Park, C  Lee, J  Koh, H 
Citation: Gil S, etal., Cell Mol Neurobiol. 2010 Aug;30(6):817-25. Epub 2010 Mar 16.
RGD ID: 5128860
Pubmed: PMID:20232137   (View Abstract at PubMed)
DOI: DOI:10.1007/s10571-010-9509-9   (Journal Full-text)

The administration of L: -DOPA is the standard treatment for Parkinson's disease (PD). However, the symptomatic relief provided by long-term administration may be compromised by L: -DOPA-induced dyskinesia (LID) that presents as adverse fluctuations in motor responsiveness and progressive loss of motor control. In the later stages of PD, raphestriatal serotonin neurons compensate for the loss of nigrostriatal dopamine (DA) neurons by converting and releasing DA derived from exogenous L: -DOPA. Since the serotonin system does not have an autoregulatory mechanism for DA, raphe-mediated striatal DA release may fluctuate dramatically and precede the development of LID. The 6-hydroxydopamine lesioned rats were treated with L: -DOPA (6 mg/kg) and benserazide (15 mg/kg) daily for 3 weeks to allow for the development of abnormal involuntary movement score (AIMs). In rats with LID, chronic treatment with L: -DOPA increased striatal DA levels compared with control rats. We also observed a relative increase in the expression of striatal L: -amino-acid decarboxylase (AADC) in LID rats, even though tyrosine hydroxylase (TH) expression did not increase. The administration of L: -DOPA also increased striatal serotonin immunoreactivity in LID rats compared to control rats. Striatal DA and 5-hydroxytryptamine (5-HT) levels were negatively correlated in L: -DOPA-treated rats. These results of this study reveal that 5-HT contributes to LID. Striatal DA positively influences LID, while 5-HT is negatively associated with LID. Finally, we suggest that by strategic modification of the serotonin system it may be possible to attenuate the adverse effects of chronic L: -DOPA therapy in PD patients.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
DDCHumanDrug-Induced Dyskinesia  ISODdc (Rattus norvegicus)associated with Parkinson Disease and protein:decreased expression:striatum (rat)RGD 
DdcRatDrug-Induced Dyskinesia  IEP associated with Parkinson Disease and protein:decreased expression:striatum (rat)RGD 
DdcMouseDrug-Induced Dyskinesia  ISODdc (Rattus norvegicus)associated with Parkinson Disease and protein:decreased expression:striatum (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ddc  (dopa decarboxylase)

Genes (Mus musculus)
Ddc  (dopa decarboxylase)

Genes (Homo sapiens)
DDC  (dopa decarboxylase)


Additional Information