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Interactions of CaMKII with dopamine D2 receptors: roles in levodopa-induced dyskinesia in 6-hydroxydopamine lesioned Parkinson's rats

Ca2+ /calmodulin-dependent protein kinase II is a synapse-enriched kinase in mammalian brains. This kinase interacts with various synaptic proteins to regulate expression and function of interacting proteins and thereby modulates synaptic transmission. CaMKII and its interacting partners are also be... Full description

Journal Title: Scientific Reports (Nature Publisher Group) Oct 2014, Vol.4, p.6811
Main Author: Zhang, Sufang
Other Authors: Xie, Chenglong , Wang, Qiang , Liu, Zhenguo
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 20452322 ; DOI: 10.1038/srep06811
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title: Interactions of CaMKII with dopamine D2 receptors: roles in levodopa-induced dyskinesia in 6-hydroxydopamine lesioned Parkinson's rats
format: Article
creator:
  • Zhang, Sufang
  • Xie, Chenglong
  • Wang, Qiang
  • Liu, Zhenguo
subjects:
  • Dopamine
  • Kinases
  • Proteins
  • Synaptic Transmission
  • Neurons
  • 6-Hydroxydopamine
  • Parkinson'S Disease
  • Calcium-Binding Protein
  • Dyskinesia
  • Movement Disorders
  • Dopamine D2 Receptors
  • Levodopa
  • Neurological Diseases
  • Neurodegenerative Diseases
  • Neostriatum
  • Ca2+/Calmodulin-Dependent Protein Kinase II
ispartof: Scientific Reports (Nature Publisher Group), Oct 2014, Vol.4, p.6811
description: Ca2+ /calmodulin-dependent protein kinase II is a synapse-enriched kinase in mammalian brains. This kinase interacts with various synaptic proteins to regulate expression and function of interacting proteins and thereby modulates synaptic transmission. CaMKII and its interacting partners are also believed to play a pivotal role in the pathogenesis of various neurological and neurodegenerative disorders, such as Parkinson's disease (PD). In this study, we found that CaMKIIα binds to dopamine D2 receptors (D2R) in vitro. A distal region in the D2R third intracellular loop harbors CaMKIIα binding. Endogenous CaMKIIα was also found to interact with native D2Rs in rat striatal neurons in which D2Rs are expressed at a high level. In addition, in a rat 6-hydroxydopamine lesioned model of PD, chronic levodopa administration induced characteristic dyskinesia. In parallel, levodopa induced an increase in CaMKIIα-D2R interactions in striatal neurons. Intrastriatal injection of a Tat-fusion and CaMKIIα-D2R...
language: eng
source:
identifier: E-ISSN: 20452322 ; DOI: 10.1038/srep06811
fulltext: fulltext_linktorsrc
issn:
  • 20452322
  • 2045-2322
url: Link


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titleInteractions of CaMKII with dopamine D2 receptors: roles in levodopa-induced dyskinesia in 6-hydroxydopamine lesioned Parkinson's rats
creatorZhang, Sufang ; Xie, Chenglong ; Wang, Qiang ; Liu, Zhenguo
ispartofScientific Reports (Nature Publisher Group), Oct 2014, Vol.4, p.6811
identifierE-ISSN: 20452322 ; DOI: 10.1038/srep06811
subjectDopamine ; Kinases ; Proteins ; Synaptic Transmission ; Neurons ; 6-Hydroxydopamine ; Parkinson'S Disease ; Calcium-Binding Protein ; Dyskinesia ; Movement Disorders ; Dopamine D2 Receptors ; Levodopa ; Neurological Diseases ; Neurodegenerative Diseases ; Neostriatum ; Ca2+/Calmodulin-Dependent Protein Kinase II
descriptionCa2+ /calmodulin-dependent protein kinase II is a synapse-enriched kinase in mammalian brains. This kinase interacts with various synaptic proteins to regulate expression and function of interacting proteins and thereby modulates synaptic transmission. CaMKII and its interacting partners are also believed to play a pivotal role in the pathogenesis of various neurological and neurodegenerative disorders, such as Parkinson's disease (PD). In this study, we found that CaMKIIα binds to dopamine D2 receptors (D2R) in vitro. A distal region in the D2R third intracellular loop harbors CaMKIIα binding. Endogenous CaMKIIα was also found to interact with native D2Rs in rat striatal neurons in which D2Rs are expressed at a high level. In addition, in a rat 6-hydroxydopamine lesioned model of PD, chronic levodopa administration induced characteristic dyskinesia. In parallel, levodopa induced an increase in CaMKIIα-D2R interactions in striatal neurons. Intrastriatal injection of a Tat-fusion and CaMKIIα-D2R...
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titleInteractions of CaMKII with dopamine D2 receptors: roles in levodopa-induced dyskinesia in 6-hydroxydopamine lesioned Parkinson's rats
descriptionCa2+ /calmodulin-dependent protein kinase II is a synapse-enriched kinase in mammalian brains. This kinase interacts with various synaptic proteins to regulate expression and function of interacting proteins and thereby modulates synaptic transmission. CaMKII and its interacting partners are also believed to play a pivotal role in the pathogenesis of various neurological and neurodegenerative disorders, such as Parkinson's disease (PD). In this study, we found that CaMKIIα binds to dopamine D2 receptors (D2R) in vitro. A distal region in the D2R third intracellular loop harbors CaMKIIα binding. Endogenous CaMKIIα was also found to interact with native D2Rs in rat striatal neurons in which D2Rs are expressed at a high level. In addition, in a rat 6-hydroxydopamine lesioned model of PD, chronic levodopa administration induced characteristic dyskinesia. In parallel, levodopa induced an increase in CaMKIIα-D2R interactions in striatal neurons. Intrastriatal injection of a Tat-fusion and CaMKIIα-D2R...
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titleInteractions of CaMKII with dopamine D2 receptors: roles in levodopa-induced dyskinesia in 6-hydroxydopamine lesioned Parkinson's rats
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abstractCa2+ /calmodulin-dependent protein kinase II is a synapse-enriched kinase in mammalian brains. This kinase interacts with various synaptic proteins to regulate expression and function of interacting proteins and thereby modulates synaptic transmission. CaMKII and its interacting partners are also believed to play a pivotal role in the pathogenesis of various neurological and neurodegenerative disorders, such as Parkinson's disease (PD). In this study, we found that CaMKIIα binds to dopamine D2 receptors (D2R) in vitro. A distal region in the D2R third intracellular loop harbors CaMKIIα binding. Endogenous CaMKIIα was also found to interact with native D2Rs in rat striatal neurons in which D2Rs are expressed at a high level. In addition, in a rat 6-hydroxydopamine lesioned model of PD, chronic levodopa administration induced characteristic dyskinesia. In parallel, levodopa induced an increase in CaMKIIα-D2R interactions in striatal neurons. Intrastriatal injection of a Tat-fusion and CaMKIIα-D2R...
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