The molecular neurobiology of chronic pain–induced depression

Humo, Muris; Han, Lu; Yalçın, İpek

doi:10.1007/s00441-019-03003-z

Cited by 100 publications

(102 citation statements)

References 194 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The imaging studies on human found that many brain areas involved in pain and depression were overlaped, such as primary and secondary somatosensory cortex, anterior cingular cortex, hippocumpus and so on (Doan, Manders, & Wang, ; Green et al, ; Ushinsky, Reinhardt, Simmons, & Strigo, ; Zeng et al, ). Animal studies, based on NeP induced depression model, revealed that some common neuroplasticity changes were shared between pain and depression in central nerve system and the underlying mechanism included monoamine neurotransmitters, inflammatory factors and glutamate and its receptors (Doan et al, ; Humo, Lu, & Yalcin, ; Sheng, Liu, Wang, Cui, & Zhang, ). Since chronic pain, especially NeP, shares common neuro‐mechanism with depression, depression may affect or facilitate the feeling of pain in patients with NeP and increases the risk of pain, which may lead to decreased QoL (Velly & Mohit, ).…”

Section: Discussionmentioning

confidence: 99%

Depression as a mediator of quality of life in patients with neuropathic pain: A cross‐sectional study

Liu

2019

Journal of Advanced Nursing

View full text Add to dashboard Cite

Aims To explore whether pain intensity has an indirect effect on quality of life through mediation of depression in patients with neuropathic pain (NeP). Design An observational, questionnaire‐based, cross‐sectional study. Methods A convenience sample of patients suffering from NeP were enrolled from June 2015 ‐ May 2016. Three questionnaires were used to collect data of pain intensity, Quality of life and depression. Andrew Hayes' PROCESS macro modelling tool for the SPSS software, based on the mediation Bootstrap confidence interval method, was used to analyse the mediation effect. Results Both pain intensity and depression correlated negatively with the quality of life of patients. The indirect effect of pain intensity on the quality of life through depression was negative. Conclusions Increased pain intensity and depression were associated with a decreased quality of life in patients suffering from NeP and pain intensity had an indirect effect on the quality of life of patients through depression. Impact A low quality of life and depression are commonly seen in patients with NeP. However, little is known about the relationship between pain, quality of life and depression. Both pain intensity and depression had some negative effect on quality of life in patients with NeP. Pain intensity had an indirect effect on quality of life through a mediation effect of depression in patients with NeP. When caring for patients with NeP, nurses should assess depression routinely and try to alleviate it.

show abstract

Section: Discussionmentioning

confidence: 99%

Depression as a mediator of quality of life in patients with neuropathic pain: A cross‐sectional study

Liu

2019

Journal of Advanced Nursing

View full text Add to dashboard Cite

show abstract

“…It is certainly not easy to understand the reason for this inconsistency. The time factor is certainly critical [53,54] since measuring anxio-depressive behavior at very early or late time can produce misleading outcomes. Other factors (and a combination thereof) that can generate variability in behavioral responses are the species, the strain, the night-day cycle in which the animals are tested, and the tests used.…”

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

View full text Add to dashboard Cite

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.

show abstract

“…Chronic pain is the first determinant of mood disorders. 1 Comorbidities of anxiety show its significant contribution to pain. 2,3 However, most patients with chronic pain are often administered at specialty pain clinics with opioids as the most effective treatment, but they are commonly already suffering from evident mood disorders.…”

Section: Introductionmentioning

confidence: 99%

Anxiolytic effects of polydatin through the blockade of neuroinflammation in a chronic pain mouse model

et al. 2020

View full text Add to dashboard Cite

Background: Chronic pain is frequently comorbid with anxiety disorder, thereby complicating its treatment. Polydatin, a component from the root of Polygonum cuspidatum, has shown neuroprotection in the central nervous system. However, its effects on pain and anxiety processing have been rarely investigated. In this study, mice were injected with complete Freund's adjuvant (CFA) at the hindpaw to induce pain-and anxiety-like behaviors. Results: Treatment with polydatin (25 mg/kg) alleviated the anxiety-like behaviors but not pain perception in these mice. Polydatin treatment reversed the upregulation of N-methyl-D-aspartic acid receptors and GluA1-containing a-amino-3hydroxy-5-methyl-4-isoxazole-propionic acid receptors in the amygdala of CFA-injected mice. Additionally, this treatment reduced the levels of proinflammatory cytokines, namely, tumor necrosis factor-alpha and interleukin-1b, in the amygdala. Furthermore, activated nuclear factor kappa-B signaling was blocked in the amygdala from CFA-injected mice. By using docking technology, we found potential structural binding between polydatin and IjB kinase beta. Conclusion: This study indicates the anxiolytic effects of polydatin by suppressing inflammatory cytokines in the amygdala.

show abstract

The molecular neurobiology of chronic pain–induced depression

Cited by 100 publications

References 194 publications

Depression as a mediator of quality of life in patients with neuropathic pain: A cross‐sectional study

Depression as a mediator of quality of life in patients with neuropathic pain: A cross‐sectional study

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

Anxiolytic effects of polydatin through the blockade of neuroinflammation in a chronic pain mouse model

Contact Info

Product

Resources

About