The oscillatory boundary conditions of different frequency bands in Parkinson’s disease

Hu, Bing; Shi, Qianqian; Guo, Yu; Diao, Xiyezi; Guo, Hongzhu; Zhang, Jinsong; Yu, Liang; Dai, Hao; Chen, Luonan

doi:10.1016/j.jtbi.2018.04.040

Cited by 3 publications

(2 citation statements)

References 92 publications

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“…Oscillation activities, mainly including alpha (8–12 Hz), beta (11–30 Hz), delta (1–3 Hz), and theta (2–7 Hz)-frequency bands, are prominent features of the neuronal network and are closely related to many brain behavioral and functional states (Hutchison et al, 2004). Theta activity has been reported to lead to a paroxysmal increase in freezing behavior in PD patients (Follett and Torresrussotto, 2012; Hu et al, 2018). HCN channels reportedly contribute to theta frequency membrane resonance in hyperpolarized mammalian SNc neurons, which may be involved in theta oscillation (Xue et al, 2012).…”

Section: Hcn Channels Regulate the Electrical Activities Of Neurons Imentioning

confidence: 99%

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels: An Emerging Role in Neurodegenerative Diseases

Chang

Wang

Jiang

et al. 2019

Front. Mol. Neurosci.

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Neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and spinal muscular atrophy (SMA) are chronic, progressive, and age-associated neurological disorders characterized by neuronal deterioration in specific brain regions. Although the specific pathological mechanisms underlying these disorders have remained elusive, ion channel dysfunction has become increasingly accepted as a potential mechanism for neurodegenerative diseases. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are encoded by the HCN1-4 gene family and conduct the hyperpolarization-activated current ( I h ). These channels play important roles in modulating cellular excitability, rhythmic activity, dendritic integration, and synaptic transmission. In the present review, we first provide a comprehensive picture of the role of HCN channels in PD by summarizing their role in the regulation of neuronal activity in PD-related brain regions. Dysfunction of I h may participate in 1-methyl-4-phenylpyridinium (MPP + )-induced toxicity and represent a pathogenic mechanism in PD. Given current reports of the critical role of HCN channels in neuroinflammation and depression, we also discussed the putative contribution of HCN channels in inflammatory processes and non-motor symptoms in PD. In the second section, we summarize how HCN channels regulate the formation of β-amyloid peptide in AD and the role of these channels in learning and memory. Finally, we briefly discuss the effects of HCN channels in ALS and SMA based on existing discoveries.

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Section: Hcn Channels Regulate the Electrical Activities Of Neurons Imentioning

confidence: 99%

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels: An Emerging Role in Neurodegenerative Diseases

Chang

Wang

Jiang

et al. 2019

Front. Mol. Neurosci.

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“…Currently, the pathogenesis of PD is still unclear (Carnwath et al, 2018), with a lack of an ideal therapeutic regimen in the clinic. According to most researchers, the primary pathologic changes of PD are that the degeneration and loss of dopaminergic neurons in the midbrain substantia nigra (SNc) cause the reduction of the dopamine (DA) release in the SNc—striatum pathway, the decrease of the direct pathway activity and the increase of the indirect pathway activity in the basal ganglia (BG), and the over-inhibition of thalamic and cortical neurons, which therefore lead to a clinical syndrome characterized by motor dysfunctions, such as bradykinesia, muscular rigidity, static tremor, gait disturbance, and postural instability (Ali and Morris, 2015; Hu et al, 2018; Stephano et al, 2018; Chen et al, 2019). Therefore, the main target for the treatment of PD is to deactivate the indirect pathway by enhancing dopaminergic neurotransmission or reducing glutamatergic neurotransmission.…”

Section: Introductionmentioning

confidence: 99%

Study on Effect of Striatal mGluR2/3 in Alleviating Motor Dysfunction in Rat PD Model Treated by Exercise Therapy

Chen

2019

Front. Aging Neurosci.

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Background: Exercise therapy has been widely applied in clinical rehabilitation as an important practical and side effect—free adjuvant therapy, with a significant effect in alleviating motor dysfunction of patients with Parkinson’s disease (PD) or animal PD models. This study focuses on the effect of exercise therapy in reducing the concentration of extracellular glutamate (Glu) in the striatum in a rat PD model by upregulating the expression of group II metabotropic Glu receptor (mGluR2/3), so as to alleviate motor dysfunction in the rat PD model.Methods: Neurotoxin 6-hydroxydopamine (6-OHDA) was injected into the right medial forebrain bundle (MFB) of the rats to establish the semi-lateral cerebral damage PD model. The sham-operated group was given an equal amount of normal saline at the same site and taken as the control group. The apomorphine (APO)-induced rotational behavior test combined with immunohistochemical staining with tyrosine hydroxylase (TH) in the substantia nigra (SNc) and striatum was performed to assess the reliability of the model. The exercise group was given treadmill exercise intervention for 4 weeks (11 m/min, 30 min/day, 5 days/week) 1 week after the operation. The open field test (OFT) was performed to assess the locomotor activity of the rats; the Western blot technique was used to detect SNc TH and striatal mGluR2/3 protein expressions; real-time polymerase chain reaction (RT-PCR) was applied to detect striatal mGluR2 and mGluR3 mRNA expressions; the microdialysis—high-performance liquid chromatography (HPLC) method was adopted to detect the concentration of extracellular Glu in striatal neurons.Results: Compared with the control group, the number of rotations of each model group at the first week was significantly increased (P < 0.01); compared with the PD group, the number of rotations of the PD + exercise group at the third week and the fifth week was significantly decreased (P < 0.05, P < 0.01). Compared with the control group, the total movement distance, the total movement time, and the mean velocity of each model group at the first week were significantly reduced (P < 0.05); compared with the PD group, the total movement distance, the total movement time, and the mean velocity of the PD + exercise group at the third week and the fifth week were significantly increased (P < 0.01). Compared with the control group, the count of immunopositive cells and protein expression of SNc TH, and the content of immunopositive fiber terminals in the striatal TH of each model group significantly declined (P < 0.01). Compared with the PD group, the striatal mGluR2/3 protein expression of the PD + exercise group significantly rose (P < 0.01). Compared with the control group, the concentration of extracellular Glu in striatal neurons of each model group at the first week significantly grew (P < 0.05); compared with the PD group, the concentration of extracellular Glu in striatal neurons of the PD + exercise group at the third week and the fifth week was significantly decreased (P < 0.01); compare...

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Tricetin protects against 6-OHDA-induced neurotoxicity in Parkinson's disease model by activating Nrf2/HO-1 signaling pathway and preventing mitochondria-dependent apoptosis pathway

Ren

Yuan

Wang

et al. 2019

Toxicology and Applied Pharmacology

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The oscillatory boundary conditions of different frequency bands in Parkinson’s disease

Cited by 3 publications

References 92 publications

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels: An Emerging Role in Neurodegenerative Diseases

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels: An Emerging Role in Neurodegenerative Diseases

Study on Effect of Striatal mGluR2/3 in Alleviating Motor Dysfunction in Rat PD Model Treated by Exercise Therapy

Tricetin protects against 6-OHDA-induced neurotoxicity in Parkinson's disease model by activating Nrf2/HO-1 signaling pathway and preventing mitochondria-dependent apoptosis pathway

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