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Deletion of adenosine A1 or A2A receptors reduces l-3,4-dihydroxyphenylalanine-induced dyskinesia in a model of Parkinson's disease
- Source :
- Brain Research. 1367:310-318
- Publication Year :
- 2011
- Publisher :
- Elsevier BV, 2011.
-
Abstract
- Adenosine A(₂A) receptor antagonism provides a promising approach to developing nondopaminergic therapy for Parkinson's disease (PD). Clinical trials of A(₂A) antagonists have targeted PD patients with L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia (LID) in an effort to improve parkinsonian symptoms. The role of adenosine in the development of LID is little known, especially regarding its actions via A₁ receptors. We aimed to examine the effects of genetic deletion and pharmacological blockade of A₁ and/or A(₂A) receptors on the development of LID, on the induction of molecular markers of LID including striatal preprodynorphin and preproenkephalin (PPE), and on the integrity of dopaminergic nigrostriatal neurons in hemiparkinsonian mice. Following a unilateral 6-hydroxydopamine lesion A₁, A(₂A) and double A₁-A(₂A) knockout (KO) and wild-type littermate mice, and mice pretreated with caffeine (an antagonist of both A₁ and A(₂A) receptors) or saline were treated daily for 18-21 days with a low dose of L-DOPA. Total abnormal involuntary movements (AIMs, a measure of LID) were significantly attenuated (p
- Subjects :
- medicine.medical_specialty
General Neuroscience
Dopaminergic
Biology
Adenosine receptor antagonist
Adenosine receptor
Adenosine
Abnormal involuntary movement
chemistry.chemical_compound
Endocrinology
chemistry
Dyskinesia
Internal medicine
medicine
Neurology (clinical)
medicine.symptom
Receptor
Molecular Biology
Oxidopamine
Developmental Biology
medicine.drug
Subjects
Details
- ISSN :
- 00068993
- Volume :
- 1367
- Database :
- OpenAIRE
- Journal :
- Brain Research
- Accession number :
- edsair.doi...........6bba19f5b7091f54b1046d512779ca08