Journal
NEUROBIOLOGY OF DISEASE
Volume 18, Issue 2, Pages 323-335Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2004.10.005
Keywords
arrestin; G protein-coupled receptor kinase; dyskinesia; Parkinson disease
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Funding
- NEI NIH HHS [EY11500] Funding Source: Medline
- NIGMS NIH HHS [GM44944, GM63097, GM47417] Funding Source: Medline
- NIMH NIH HHS [MH62654] Funding Source: Medline
- NINDS NIH HHS [NS045117] Funding Source: Medline
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Dysregulation of dopamine receptors (DARs) is believed to contribute to Parkinson disease (PD) pathology. G protein-coupled receptors (GPCR) undergo desensitization via activation-dependent phosphorylation by G protein-coupled receptor kinases (GRKs) followed by arrestin binding. Using quantitative Western blotting, we detected profound differences in the expression of arrestin2 and GRKs among four experimental groups of nonhuman primates: (1) normal, (2) parkinsonian, (3) parkinsonian treated with levodopa without or (4) with dyskinesia. Arrestin2 and GRK6 expression was significantly elevated in the MPTP-lesioned group in most brain regions; GRK2 was increased in caudal caudate and internal globus pallidus. Neither levodopa-treated group differed significantly from control. The only dyskinesia-specific change was an elevation of GRK3 in the ventral striatum of the dyskinetic group. Changes in arrestin and GRK expression in the MPTP group were accompanied by enhanced ERK activation and elevated total ERK expression, which were also reversed by L-DOPA. The data suggest the involvement of arrestins and GRKs in Parkinson disease pathology and the effects of levodopa treatment. (C) 2004 Elsevier Inc. All rights reserved.
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