2020
DOI: 10.1016/j.bbi.2020.07.035
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Subthalamic nucleus deep brain stimulation suppresses neuroinflammation by Fractalkine pathway in Parkinson’s disease rat model

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Cited by 33 publications
(24 citation statements)
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“…In patients with poor neurological outcomes, decreased levels of plasma CX 3 CL1 persisted up to 180 days after stroke injury compared with patients with better outcomes. In keeping with these findings, brain tissue from human patients and rats with subarachnoid hemorrhage had lower expression of CX 3 CL1 and CX 3 CR1 as well as enhanced microglial activation and neuroinflammation (119).…”
Section: Role Of CX 3 Cl1-cx 3 Cr1 In Vascular Inflammationsupporting
confidence: 72%
“…In patients with poor neurological outcomes, decreased levels of plasma CX 3 CL1 persisted up to 180 days after stroke injury compared with patients with better outcomes. In keeping with these findings, brain tissue from human patients and rats with subarachnoid hemorrhage had lower expression of CX 3 CL1 and CX 3 CR1 as well as enhanced microglial activation and neuroinflammation (119).…”
Section: Role Of CX 3 Cl1-cx 3 Cr1 In Vascular Inflammationsupporting
confidence: 72%
“…Moreover, Chen et al showed that electrical stimulation of anterior thalamic nuclei in the field of epilepsy downregulated inflammatory processes in the hippocampus, leading to a reduction of neuronal loss and neurogenesis in a rat model (Chen et al, 2017). Similar results were obtained in a Parkinson disease (PD) rat model, in which subthalamic nucleus-DBS-suppressed neuroinflammation and led to an increased survival of dopaminergic neurons in the substantia nigra (Chen et al, 2020). In addition, Dandekar et al showed a significant downregulation of the inflammatory mediators IL-5 and IL-18 in the hippocampus and of IL-6 in the nucleus accumbens after seven days of DBS of the medial forebrain bundle in a depression model (Dandekar et al, 2019).…”
Section: Introductionmentioning
confidence: 73%
“…Interestingly, invasive electrical stimulation of other brain regions also attenuates neuroinflammation: high-frequency deep brain stimulation (DBS) (130 Hz) of the anterior thalamic nucleus resulted in a decrease of TNF-α and IL-1β in a rat model of epilepsy [21]. Similarly, DBS of the subthalamic nucleus revealed a reduced level of IL-1β in the substantia nigra of a rat model of Parkinson's disease [20].…”
Section: Discussionmentioning
confidence: 99%
“…In stimulated rats, ChAT + CD4 + -cells were significantly more abundant in the lesioned brain hemisphere compared to sham animals (ChAT + CD4 + -cells stim vs. sham: 0.15 [IQR 0.13-0.21] vs. 0.07 [IQR 0.02-0.07], ChAT + CD4 + -cells/cells of ROI, * p < 0.05, n = 4/group; Figure 2B,C). The receptor polypeptide α7nAchR, responding to the neurotransmitter acetylcholine, is expressed in many regions of the central and peripheral nervous system but also on non-neuronal cells including astrocytes and microglia [20][21][22]. Activation of α7nAchR via receptor agonists results in anti-inflammatory effects such as a decrease in the synthesis of cytokines and chemokines [23,24].…”
Section: Mlr-hfs Is Associated With An Increased Number Of Chat Expressing Cells But Does Not Change the Amount Of α7nachr-positive Cellsmentioning
confidence: 99%