Dopamine receptor 3 might be an essential molecule in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity

Chen, Yan; Ni, Ying-yin; Liu, Jie; Lu, Jiawei; Wang, Fang; Wu, Xiaolin; Gu, Min; Lu, Zhenyu; Wang, Zhugang; Ren, Zhihua

doi:10.1186/1471-2202-14-76

Cited by 16 publications

(14 citation statements)

References 23 publications

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“…Importantly, we have recently demonstrated that dopamine receptor D3 (D3R), expressed in CD4 + T-cells, is fundamental in inducing the loss of dopaminergic neurons in the SN pc of a PD mouse model [ 17 ]. In this regard, we and others have reported that D3R-deficient (D3RKO) mice are resistant to MPTP-induced PD [ 17 , 56 ]. Interestingly, when wild type (WT) CD4 + T-cells were transferred to D3RKO mice, the animals acquired the capability to respond to MPTP-induced neurodegeneration.…”

Section: Introductionmentioning

confidence: 99%

T-cell-mediated regulation of neuroinflammation involved in neurodegenerative diseases

González

Pacheco

2014

J Neuroinflammation

203

152

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Neuroinflammation is involved in several neurodegenerative disorders and emerging evidence indicates that it constitutes a critical process that is required for the progression of neurodegeneration. Microglial activation constitutes a central event in neuroinflammation. Furthermore, microglia can not only be activated with an inflammatory and neurotoxic phenotype (M1-like phenotype), but they also can acquire a neurosupportive functional phenotype (M2-like phenotype) characterised by the production of anti-inflammatory mediators and neurotrophic factors. Importantly, during the past decade, several studies have shown that CD4+ T-cells infiltrate the central nervous system (CNS) in many neurodegenerative disorders, in which their participation has a critical influence on the outcome of microglial activation and consequent neurodegeneration. In this review, we focus on the analysis of the interplay of the different sub-populations of CD4+ T-cells infiltrating the CNS and how they participate in regulating the outcome of neuroinflammation and neurodegeneration in the context of Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis and multiple sclerosis. In this regard, encephalitogenic inflammatory CD4+ T-cells, such as Th1, Th17, GM-CSF-producer CD4+ T-cells and γδT-cells, strongly contribute to chronic neuroinflammation, thus perpetuating neurodegenerative processes. In contrast, encephalitogenic or meningeal Tregs and Th2 cells decrease inflammatory functions in microglial cells and promote a neurosupportive microenvironment. Moreover, whereas some neurodegenerative disorders such as multiple sclerosis, Parkinson’s disease and Alzheimer’s disease involve the participation of inflammatory CD4+ T-cells 'naturally', the physiopathology of other neurodegenerative diseases, such as amyotrophic lateral sclerosis, is associated with the participation of anti-inflammatory CD4+ T-cells that delay the neurodegenerative process. Thus, current evidence supports the hypothesis that the involvement of CD4+ T-cells against CNS antigens constitutes a key component in regulating the progression of the neurodegenerative process.

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Section: Introductionmentioning

confidence: 99%

T-cell-mediated regulation of neuroinflammation involved in neurodegenerative diseases

González

Pacheco

2014

J Neuroinflammation

203

152

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“…The rotarod test was conducted to assess the movement equilibrium function (Chen et al, 2013). Mice were trained on a rotarod (YLS-4C type, Biological Research Apparatus, Shandong, China) at several different rod-rotation speeds.…”

Section: Rotarod Test For Movement Function Measurementmentioning

confidence: 99%

Tetrahydroxystilbene glucoside ameliorates memory and movement functions, protects synapses and inhibits α-synuclein aggregation in hippocampus and striatum in aged mice

Shen

Sun

Zhang

et al. 2015

RNN

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“…Increases in brain derived neurotrophic factor (BDNF) have been found to enhance endogenous neurogenesis in the SVZ and the SGZ (Zhao et al, 2008 ), while the release of neurotrophic factors such as glial cell-derived neurotrophic factor (GDNF) has been shown to promote neurogenesis and synaptic connectivity (Borta and Höglinger, 2007 ). In addition to neurotrophic factors, dopamine receptor D3 (DRD3) and dopamine receptor D5 (DRD5) are known to be involved in adult neurogenesis as well as the pathophysiology of PD (Borta and Höglinger, 2007 ; Chen et al, 2013 ; Chetrit et al, 2013 ; Lao et al, 2013 ; Elgueta et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Korean Red Ginseng Enhances Neurogenesis in the Subventricular Zone of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Treated Mice

Ryu

Jeon

Koo

et al. 2018

Front. Aging Neurosci.

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Regulation of adult neurogenesis plays an important role in therapeutic strategies for various neurodegenerative diseases. Recent studies have suggested that the enhancement of adult neurogenesis can be helpful in the treatment of Parkinson’s disease (PD). In this study, we investigated whether Korean red ginseng (KRG) can enhance neurogenesis in the subventricular zone (SVZ) of a PD mouse model. To accomplish this, male 8-week-old C57BL/6 mice were injected with vehicle or 20 mg/kg of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) four times at 2 h intervals. After the final injection, they were administered water or 100 mg/kg of KRG extract and injected intraperitoneally with 50 mg/kg of 5’-bromo-2’-deoxyuridine-monophosphate (BrdU) once a day for 14 consecutive days. After the last pole test, dopaminergic neuronal survival in the striatum and the substantia nigra (SN), cell proliferation in the SVZ and mRNA expression of neurotrophic factors and dopamine receptors in the striatum were evaluated. KRG administration suppressed dopaminergic neuronal death induced by MPTP in the striatum as well as the SN, augmented the number of BrdU- and BrdU/doublecortin (Dcx)-positive cells in the SVZ and enhanced the expression of proliferation cell nuclear antigen, brain derived neurotrophic factor (BDNF), glial cell derived neurotrophic factor (GDNF), cerebral dopamine neurotrophic factor (CDNF), ciliary neurotrophic factor (CNTF), dopamine receptor D3 (DRD3) and D5 mRNAs. These results suggest that KRG administration augments neurogenesis in the SVZ of the PD mouse model.

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Dopamine receptor 3 might be an essential molecule in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity

Cited by 16 publications

References 23 publications

T-cell-mediated regulation of neuroinflammation involved in neurodegenerative diseases

T-cell-mediated regulation of neuroinflammation involved in neurodegenerative diseases

Tetrahydroxystilbene glucoside ameliorates memory and movement functions, protects synapses and inhibits α-synuclein aggregation in hippocampus and striatum in aged mice

Korean Red Ginseng Enhances Neurogenesis in the Subventricular Zone of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Treated Mice

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