Dopamine D3 Receptor Plasticity in Parkinson’s Disease and L-DOPA-Induced Dyskinesia

Parkinson’s Disease (PD) is characterized by primary and secondary plasticity that occurs in response to progressive degeneration and long-term L-DOPA treatment. Some of this plasticity contributes to the detrimental side effects associated with chronic L-DOPA treatment, namely L-DOPA-induced dyskin...
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Autor*in:	Kathryn Lanza [verfasserIn] Christopher Bishop [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	dopamine D3 receptor dopamine D1 receptor D1R–D3R Parkinson’s Disease L-DOPA-induced dyskinesia striatum

Übergeordnetes Werk:	In: Biomedicines - MDPI AG, 2014, 9(2021), 3, p 314
Übergeordnetes Werk:	volume:9 ; year:2021 ; number:3, p 314

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/biomedicines9030314

Katalog-ID:	DOAJ062565397

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520			\|a Parkinson’s Disease (PD) is characterized by primary and secondary plasticity that occurs in response to progressive degeneration and long-term L-DOPA treatment. Some of this plasticity contributes to the detrimental side effects associated with chronic L-DOPA treatment, namely L-DOPA-induced dyskinesia (LID). The dopamine D3 receptor (D3R) has emerged as a promising target in LID management as it is upregulated in LID. This upregulation occurs primarily in the D1-receptor-bearing (D1R) cells of the striatum, which have been repeatedly implicated in LID manifestation. D3R undergoes dynamic changes both in PD and in LID, making it difficult to delineate D3R’s specific contributions, but recent genetic and pharmacologic tools have helped to clarify its role in LID. The following review will discuss these changes, recent advances to better clarify D3R in both PD and LID and potential steps for translating these findings.
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callnumber-first	Q - Science
author	Kathryn Lanza
spellingShingle	Kathryn Lanza misc QH301-705.5 misc dopamine D3 receptor misc dopamine D1 receptor misc D1R–D3R misc Parkinson’s Disease misc L-DOPA-induced dyskinesia misc striatum misc Biology (General) Dopamine D3 Receptor Plasticity in Parkinson’s Disease and L-DOPA-Induced Dyskinesia
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topic_title	QH301-705.5 Dopamine D3 Receptor Plasticity in Parkinson’s Disease and L-DOPA-Induced Dyskinesia dopamine D3 receptor dopamine D1 receptor D1R–D3R Parkinson’s Disease L-DOPA-induced dyskinesia striatum
topic	misc QH301-705.5 misc dopamine D3 receptor misc dopamine D1 receptor misc D1R–D3R misc Parkinson’s Disease misc L-DOPA-induced dyskinesia misc striatum misc Biology (General)
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title	Dopamine D3 Receptor Plasticity in Parkinson’s Disease and L-DOPA-Induced Dyskinesia
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title_sort	dopamine d3 receptor plasticity in parkinson’s disease and l-dopa-induced dyskinesia
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title_auth	Dopamine D3 Receptor Plasticity in Parkinson’s Disease and L-DOPA-Induced Dyskinesia
abstract	Parkinson’s Disease (PD) is characterized by primary and secondary plasticity that occurs in response to progressive degeneration and long-term L-DOPA treatment. Some of this plasticity contributes to the detrimental side effects associated with chronic L-DOPA treatment, namely L-DOPA-induced dyskinesia (LID). The dopamine D3 receptor (D3R) has emerged as a promising target in LID management as it is upregulated in LID. This upregulation occurs primarily in the D1-receptor-bearing (D1R) cells of the striatum, which have been repeatedly implicated in LID manifestation. D3R undergoes dynamic changes both in PD and in LID, making it difficult to delineate D3R’s specific contributions, but recent genetic and pharmacologic tools have helped to clarify its role in LID. The following review will discuss these changes, recent advances to better clarify D3R in both PD and LID and potential steps for translating these findings.
abstractGer	Parkinson’s Disease (PD) is characterized by primary and secondary plasticity that occurs in response to progressive degeneration and long-term L-DOPA treatment. Some of this plasticity contributes to the detrimental side effects associated with chronic L-DOPA treatment, namely L-DOPA-induced dyskinesia (LID). The dopamine D3 receptor (D3R) has emerged as a promising target in LID management as it is upregulated in LID. This upregulation occurs primarily in the D1-receptor-bearing (D1R) cells of the striatum, which have been repeatedly implicated in LID manifestation. D3R undergoes dynamic changes both in PD and in LID, making it difficult to delineate D3R’s specific contributions, but recent genetic and pharmacologic tools have helped to clarify its role in LID. The following review will discuss these changes, recent advances to better clarify D3R in both PD and LID and potential steps for translating these findings.
abstract_unstemmed	Parkinson’s Disease (PD) is characterized by primary and secondary plasticity that occurs in response to progressive degeneration and long-term L-DOPA treatment. Some of this plasticity contributes to the detrimental side effects associated with chronic L-DOPA treatment, namely L-DOPA-induced dyskinesia (LID). The dopamine D3 receptor (D3R) has emerged as a promising target in LID management as it is upregulated in LID. This upregulation occurs primarily in the D1-receptor-bearing (D1R) cells of the striatum, which have been repeatedly implicated in LID manifestation. D3R undergoes dynamic changes both in PD and in LID, making it difficult to delineate D3R’s specific contributions, but recent genetic and pharmacologic tools have helped to clarify its role in LID. The following review will discuss these changes, recent advances to better clarify D3R in both PD and LID and potential steps for translating these findings.
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title_short	Dopamine D3 Receptor Plasticity in Parkinson’s Disease and L-DOPA-Induced Dyskinesia
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