Downregulated spinal IRF8 and BDNF in NAC are involved in neuropathic pain-induced depression relief via pulsed radiofrequency on dorsal root ganglion in rat SNI model

Xiangyu, Fang; Xu, Xueru; Lin, Xingwu; Liu, Rongguo

doi:10.1016/j.brainresbull.2019.01.008

Cited by 19 publications

(18 citation statements)

References 35 publications

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“…As previously described, glial cells are very important for the maintenance of the inflammatory response within the nervous system. Interferon regulatory factor 8 (IRF8) deficiency prevents the activation of microglia ( Liu et al, 2018 ), and the mechanisms by which IRF8 deficiency improves pain sensitivity and depressive-like behavior are very similar to those of pulsed radiofrequency, which decreases IRF8 in the spinal cord and BDNF in the NAc, demonstrating that non-pharmacological treatments also play an important role in microglial activation and the VTA-NAc reward pathway ( Fang et al, 2019 ). High-mobility group box-1 (HMBG1) is secreted and activates immune cells via Toll-like receptor 4 (TLR4), inducing the production of cytokines and chemokines ( Andersson and Tracey, 2011 ; Agalave and Svensson, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Neuroinflammation, Pain and Depression: An Overview of the Main Findings

et al. 2020

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Chronic pain is a serious public health problem with a strong affective-motivational component that makes it difficult to treat. Most patients with chronic pain suffer from severe depression; hence, both conditions coexist and exacerbate one another. Brain inflammatory mediators are critical for maintaining depression-pain syndrome and could be substrates for it. The goal of our paper was to review clinical and preclinical findings to identify the neuroinflammatory profile associated with the cooccurrence of pain and depression. In addition, we aimed to explore the regulatory effect of neuronal reorganization on the inflammatory response in pain and depression. We conducted a quantitative review supplemented by manual screening. Our results revealed inflammatory signatures in different preclinical models and clinical articles regarding depression-pain syndrome. We also identified that improvements in depressive symptoms and amelioration of pain can be modulated through direct targeting of inflammatory mediators, such as cytokines and molecular inhibitors of the inflammatory cascade. Additionally, therapeutic targets that improve and regulate the synaptic environment and its neurotransmitters may act as anti-inflammatory compounds, reducing local damage-associated molecular patterns and inhibiting the activation of immune and glial cells. Taken together, our data will help to better elucidate the neuroinflammatory profile in pain and depression and may help to identify pharmacological targets for effective management of depression-pain syndrome.

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Section: Discussionmentioning

confidence: 99%

Neuroinflammation, Pain and Depression: An Overview of the Main Findings

et al. 2020

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“…Despite all these protocol variations, the majority of reported studies could asses a presence of anhedonia from one week (Fang, Zhan, et al, 2019; Goffer et al, 2013; Martinez‐Navarro et al, 2019; Wu et al, 2018; Xu et al, 2017; Zhu et al, 2017) to 10–11 weeks (Fang, Xu, Lin, & Liu, 2019; Fu et al, 2018; Thompson et al, 2018; Wu et al, 2014) after neuropathic pain induction (see also Figures 5 and 6 and Table 1). However, this time window depends on the considered model.…”

Section: Evaluating Anxiety‐like and Depression‐like Behaviours In Anmentioning

confidence: 99%

How to study anxiety and depression in rodent models of chronic pain?

Kremer

Becker

Barrot

et al. 2020

Eur J of Neuroscience

104

100

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“…It was found that IRF8 expression was significantly upregulated from day 1, peaked on day 3, and the enhancement of IRF8 lasted for several weeks following peripheral nerve injury [7]. Furthermore, the increased spinal IRF8 expression is closely linked to the activation of microglia in neuropathic pain [7,32,33]. ese results indicated that both IRF8 in the spinal cord and its triggering microglial activation contributed to neuropathic pain development.…”

Section: Discussionmentioning

confidence: 90%

“…It was found that SNL can markedly promote the elevation of CX3CR1 in the spinal microglia [35]. Conversely, intrathecal injection of an antibody against CX3CR1 in the spinal cord distinctly blocked mechanical allodynia induced by SNL [33]. Additionally, in CX3CR1 knockout mice, the spinal microglial activation was attenuated, the mechanical allodynia was not developed, and the thermal hypersensitivity was delayed after SNI [36].…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Treatment Suppresses Transcription Factor IRF8 in Spinal Cord of Rats with Spared Nerve Injury

Wang

Xue

Xia

et al. 2020

Pain Research and Management

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Objective. Neuropathic pain with complex mechanisms has become a major public health problem that greatly impacts patients’ quality of life. Therefore, novel and more effective strategies against neuropathic pain need further investigation. Electroacupuncture (EA) has an ameliorating effect on neuropathic pain following spared nerve injury (SNI), but the underlying mechanism remains to be fully clarified. Interferon regulatory factor 8 (IRF8), a critical transcription factor, was reported to be involved in the modulation of neuropathic pain. Here, we focused on exploring whether 2 Hz EA stimulation exerts an inhibitory action on spinal IRF8 in SNI rats. Methods. In this study, SNI rats were treated with 2 Hz EA once every other day for 21 days. Paw withdrawal threshold (PWT) was applied to determine the analgesic effect of 2 Hz EA on SNI rats. The spinal IRF8 and CX3CRl expressions were detected with qRT-PCR and western blot, and immunofluorescence staining was used to evaluate colocation of IRF8 or CX3CRl with microglial activation marker CD11b in the spinal cord. Results. It was found that SNI induced significant elevation of spinal IRF8 and CX3CRl mRNA and protein expression. Additionally, immunofluorescence results showed that SNI elicited the coexpression of IRF8 with CD11b, as well as CX3CRl with CD11b in the spinal cord. Meanwhile, 2 Hz EA treatment of SNI rats not only reduced IRF8 and CX3CRl mRNA and protein expression, but also reversed the coexpression of IRF8 or CX3CRl with CD11b in the spinal cord, along with an attenuation of SNI-evoked mechanical hypersensitivity. Conclusion. This experiment highlighted that 2 Hz EA can inhibit IRF8 expression and microglial activation in the spinal cord of SNI rats. Hence, targeting IRF8 may be a promising therapeutic strategy for 2 Hz EA treatment of neuropathic pain.

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Downregulated spinal IRF8 and BDNF in NAC are involved in neuropathic pain-induced depression relief via pulsed radiofrequency on dorsal root ganglion in rat SNI model

Cited by 19 publications

References 35 publications

Neuroinflammation, Pain and Depression: An Overview of the Main Findings

Neuroinflammation, Pain and Depression: An Overview of the Main Findings

How to study anxiety and depression in rodent models of chronic pain?

Electroacupuncture Treatment Suppresses Transcription Factor IRF8 in Spinal Cord of Rats with Spared Nerve Injury

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