A neural circuit for comorbid depressive symptoms in chronic pain

Zhou, Wenjie; Jin, Yan; Qian, Meng; Zhu, Xia; Bai, Tongjian; Tian, Yanghua; Mao, Yu; Wang, Likui; Xie, Wen; Zhong, Hui; Zhang, Na; Luo, Min‐Hua; Tao, Wenjuan; Wang, Haitao; Li, Jie; Li, Juan; Qiu, Bensheng; Zhou, Jiang‐Ning; Li, Xiang-Yao; Han, Xu; Wang, Kai; Zhang, Xiaochu; Liu, Yong; Richter‐Levin, Gal; Xu, Lin; Zhang, Zhi

doi:10.1038/s41593-019-0468-2

Cited by 224 publications

(205 citation statements)

References 53 publications

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“…There is just as much evidence that the SNI model of neuropathic pain is associated with the development of anxiety-like behavior in mice. In particular, anxiety-like behavior has been observed in the elevated plus-maze and open fields tests at day 14 [37,46], day 23 [47], day 28 [48] and weeks 4-6 [49,50] after injury. Anxiety-like behavior was also observed in the black box emergency test on day 12 [35], in the marble-burying test, which also measures compulsive behavior [51] at day 30 [36,37], in the light-dark box on day 30 [36] and in the hole board test in weeks 4-6 [49].…”

Section: Behavioral Symptoms Associated With the Spared Nerve Injurymentioning

confidence: 99%

Behavioral, Biochemical and Electrophysiological Changes in Spared Nerve Injury Model of Neuropathic Pain

Guida¹,

Gregorio

Palazzo³

et al. 2020

IJMS

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Neuropathic pain is a pathological condition induced by a lesion or disease affecting the somatosensory system, with symptoms like allodynia and hyperalgesia. It has a multifaceted pathogenesis as it implicates several molecular signaling pathways involving peripheral and central nervous systems. Affective and cognitive dysfunctions have been reported as comorbidities of neuropathic pain states, supporting the notion that pain and mood disorders share some common pathogenetic mechanisms. The understanding of these pathophysiological mechanisms requires the development of animal models mimicking, as far as possible, clinical neuropathic pain symptoms. Among them, the Spared Nerve Injury (SNI) model has been largely characterized in terms of behavioral and functional alterations. This model is associated with changes in neuronal firing activity at spinal and supraspinal levels, and induces late neuropsychiatric disorders (such as anxious-like and depressive-like behaviors, and cognitive impairments) comparable to an advanced phase of neuropathy. The goal of this review is to summarize current findings in preclinical research, employing the SNI model as a tool for identifying pathophysiological mechanisms of neuropathic pain and testing pharmacological agent.

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Section: Behavioral Symptoms Associated With the Spared Nerve Injurymentioning

confidence: 99%

Behavioral, Biochemical and Electrophysiological Changes in Spared Nerve Injury Model of Neuropathic Pain

Guida¹,

Gregorio

Palazzo³

et al. 2020

IJMS

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“…e mobile phase component was 19.1968 g of NaH 2 PO 4 and 400 mL of methyl alcohol, pH � 3.48, in 2 L. A total of 20 μL of each sample was mixed with 5 μL of OPA (25 mg OPA, 250 μL methyl alcohol, 250 μL 1 mol/L Na 2 SO 3 , and 4.5 mL boric acid) for 3 min, and the compounds were separated on a 1 mm × 50 mm column (ALF-105, ANTEC). An online analysis system (ANTEC Leyden), which consisted of a DECADE II electrochemical detector and VT-3 electrochemical flow cells, was used for detection [27]. e data were analysed using Clarity software (ANTEC, Netherlands) based on standard samples.…”

Section: In Vivo Microdialysis Combined With Hplc Test Ofmentioning

confidence: 99%

Acupuncture at Gastric Back‐Shu and Front‐Mu Acupoints Enhances Gastric Motility via the Inhibition of the Glutamatergic System in the Hippocampus

Wang

Liu

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Acupuncture strongly alleviates gastrointestinal symptoms and especially promotes gastrointestinal motility. However, the mechanism underlying these processes is poorly understood. is study was designed to examine the effect of electroacupuncture (EA) at gastric back-shu (BL21) and front-mu (RN12) acupoints on gastric motility in functional dyspepsia (FD) rats and to investigate the mechanisms of its effects on the glutamatergic system in the hippocampus. We found that EA at RN12 or BL21 enhanced gastric motility in FD rats, whereas EA at the combination of RN12 and BL21 showed an additional effect. Microdialysis combined with HPLC showed that EA reduced the glutamate content in the hippocampus, and the NMDAR-NO-cGMP signalling pathway was downregulated, as determined by Western blot assays, in FD rats. In addition, we found that decreased gastric motility was significantly restored by the hippocampal infusion of an NMDAR, nNOS, or sGC antagonist. Interestingly, EA had no further effects on gastric motility in the presence of these antagonists in FD rats. Taken together, these results suggest that the hippocampal glutamatergic system is involved in the regulation of gastric motility by EA at RN12 and BL21.

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“…Chronic pain (defined in humans as the pain of more than three months) describes pain such as neuropathic pain, low-back pain, osteoarthritis, traumatic injury and postoperative pain, among others. Interestingly, chronic pain may induce anxiety and depression in rodents and humans (Wang et al, 2019;Zhou et al, 2019). In addition, chronic pain leads to cognitive impairment (Zhou et al, 2016;Shiers et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Metformin: A Prospective Alternative for the Treatment of Chronic Pain

et al. 2020

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Metformin (biguanide) is a drug widely used for the treatment of type 2 diabetes. This drug has been used for 60 years as a highly effective antihyperglycemic agent. The search for the mechanism of action of metformin has produced an enormous amount of research to explain its effects on gluconeogenesis, protein metabolism, fatty acid oxidation, oxidative stress, glucose uptake, autophagy and pain, among others. It was only up the end of the 1990s and beginning of this century that some of its mechanisms were revealed. Metformin induces its beneficial effects in diabetes through the activation of a master switch kinase named AMP-activated protein kinase (AMPK). Two upstream kinases account for the physiological activation of AMPK: liver kinase B1 and calcium/ calmodulin-dependent protein kinase kinase 2. Once activated, AMPK inhibits the mechanistic target of rapamycin complex 1 (mTORC1), which in turn avoids the phosphorylation of p70 ribosomal protein S6 kinase 1 and phosphatidylinositol 3kinase/protein kinase B signaling pathways and reduces cap-dependent translation initiation. Since metformin is a disease-modifying drug in type 2 diabetes, which reduces the mTORC1 signaling to induce its effects on neuronal plasticity, it was proposed that these mechanisms could also explain the antinociceptive effect of this drug in several models of chronic pain. These studies have highlighted the efficacy of this drug in chronic pain, such as that from neuropathy, insulin resistance, diabetic neuropathy, and fibromyalgia-type pain. Mounting evidence indicates that chronic pain may induce anxiety, depression and cognitive impairment in rodents and humans. Interestingly, metformin is able to reverse some of these consequences of pathological pain in rodents. The purpose of this review was to analyze the current evidence about the effects of metformin in chronic pain and three of its comorbidities (anxiety, depression and cognitive impairment).

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A neural circuit for comorbid depressive symptoms in chronic pain

Cited by 224 publications

References 53 publications

Behavioral, Biochemical and Electrophysiological Changes in Spared Nerve Injury Model of Neuropathic Pain

Behavioral, Biochemical and Electrophysiological Changes in Spared Nerve Injury Model of Neuropathic Pain

Acupuncture at Gastric Back‐Shu and Front‐Mu Acupoints Enhances Gastric Motility via the Inhibition of the Glutamatergic System in the Hippocampus

Metformin: A Prospective Alternative for the Treatment of Chronic Pain

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