Effects of intrastriatal injection of the dopamine receptor agonist SKF38393 and quinpirole on locomotor behavior in hemiparkinsonism rats

Guo, Mengnan; Xiang, Tianyu; Li, Min; Sun, Yue; Sun, Shuang; Chen, Dadian; Jia, Qingmei; Li, Yuchuan; Yao, Xiaomeng; Wang, Xiaojun; Zhang, Xiao; He, Feng; Wang, Min

doi:10.1016/j.bbr.2021.113339

Cited by 3 publications

(2 citation statements)

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“…Numerous studies have shown that dopaminergic deficiency in the CPu contributes to cognitive decline and motor deficits in PD (McCoy et al, 2019). For instance, intra-CPu infusion of a D1R agonist or D2R agonist efficiently improved motor dysfunction in 6-OHDA-induced PD rats (M. Guo et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

“…Numerous studies have shown that dopaminergic deficiency in the CPu contributes to cognitive decline and motor deficits in PD (McCoy et al, 2019 ). For instance, intra‐CPu infusion of a D1R agonist or D2R agonist efficiently improved motor dysfunction in 6‐OHDA‐induced PD rats (M. Guo et al, 2021 ). Additionally, the enhancement of dopaminergic signals in the CPu was consistent with improvements in both motor function and cognition of PD participants (Darvas et al, 2014 ; McCoy et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

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Regulation of Cdc42 signaling by the dopamine D2 receptor in a mouse model of Parkinson’s disease

Liu

Zhao

et al. 2022

Aging Cell

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Substantial spine loss in striatal medium spiny neurons (MSNs) and abnormal behaviors are common features of Parkinson's disease (PD). The caudate putamen (CPu) mainly contains MSNs expressing dopamine D1 receptor (dMSNs) and dopamine D2 receptor (iMSNs) exerting critical effects on motor and cognition behavior. However, the molecular mechanisms contributing to spine loss and abnormal behaviors in dMSNs and iMSNs under parkinsonian state remain unknown. In the present study, we revealed that Cell division control protein 42 (Cdc42) signaling was significantly decreased in the caudate putamen (CPu) in parkinsonian mice. In addition, overexpression of constitutively active Cdc42 in the CPu reversed spine abnormalities and improved the behavior deficits in parkinsonian mice. Utilizing conditional dopamine D1 receptor (D1R) or D2 receptor (D2R) knockout mice, we found that such a decrease under parkinsonian state was further reduced by conditional knockout of the D2R but not D1R. Moreover, the thin spine loss in iMSNs and deficits in motor coordination and cognition induced by conditional knockout of D2R were reversed by overexpression of constitutively active Cdc42 in the CPu. Additionally, conditional knockout of Cdc42 from D2R‐positive neurons in the CPu was sufficient to induce spine and behavior deficits similar to those observed in parkinsonian mice. Overall, our results indicate that impaired Cdc42 signaling regulated by D2R plays an important role in spine loss and behavioral deficits in PD.

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Section: Introductionmentioning

confidence: 99%