D1 dopamine receptor stimulation impairs striatal proteasome activity in Parkinsonism through 26S proteasome disassembly

Neurobiology of Disease
Pedro Barroso-ChineaMarie-Laure Martin-Négrier

Abstract

Among the mechanisms underlying the development of L-dopa-induced dyskinesia (LID) in Parkinson's disease, complex alterations in dopamine signaling in D1 receptor (D1R)-expressing medium spiny striatal neurons have been unraveled such as, but not limited to, dysregulation of D1R expression, lateral diffusion, intraneuronal trafficking, subcellular localization and desensitization, leading to a pathological anchorage of D1R at the plasma membrane. Such anchorage is partly due to a decreased proteasomal activity that is specific of the L-dopa-exposed dopamine-depleted striatum, results from D1R activation and feeds-back the D1R exaggerated cell surface abundance. The precise mechanisms by which L-dopa affects striatal proteasome activity remained however unknown. We here show, in a series of in vitro ex vivo and in vivo models, that such rapid modulation of striatal proteasome activity intervenes through D1R-mediated disassembly of the 26S proteasome rather than change in transcription or translation of proteasome or proteasome subunits intraneuronal relocalization.

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Citations

Jul 26, 2015·Progress in Neurobiology·Matthieu F BastideErwan Bézard
Feb 6, 2018·Journal of Neural Transmission·Giada Spigolon, Gilberto Fisone
May 8, 2019·International Journal of Molecular Sciences·Fiona LimanaqiFrancesco Fornai
Jan 17, 2019·Oxidative Medicine and Cellular Longevity·Gloria LazzeriFrancesco Fornai
Jan 27, 2019·Molecular Psychiatry·Madeline R Scott, James H Meador-Woodruff
May 17, 2019·Neuroscience and Biobehavioral Reviews·Fiona LimanaqiFrancesco Fornai

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