Depression comorbid with hyperalgesia: Different roles of neuroinflammation induced by chronic stress and hypercortisolism

Zhao, Jingjie; Gao, Xuesong; Wang, Anna; Wang, Yongzhi; Du, Yi; Li, Li; Li, Mingzhen; Li, Chong; Jin, Xiaorong; Zhao, Mei

doi:10.1016/j.jad.2019.05.065

Cited by 28 publications

(16 citation statements)

References 30 publications

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“…Focusing on neuroinflammation, Arora and Chopra (2013) observed increases in TNF-α and IL-1β in the hippocampus and PFC after chronic administration of reserpine. In another study, chronic unpredictable mild stress and chronic corticosterone treatment induced an increase in TNF-α, IL-1β, and IL-6 in different brain structures, as well as in the hippocampus and PFC ( Zhao et al, 2019 ). In combined models of pain and depression, increases in the cytokines IL-1β and IL-6 in the amygdala have also been noted ( Burke et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

“…Considering the role of Nrf2 in activating antioxidative mechanisms (Zhang et al, 2013), these mice show greater depressive-like behavior than wild-type mice (López-Granero et al, 2017). Interestingly, increases in TNF-α, IL-1β, IL-6 and caspase-1 are found in the serum of animals submitted to chronic stress paradigms that induce depressive behavior (Zhao et al, 2019). Stress models have been used to study the etiological and developmental components of depression and to screen antidepressant drugs (Nollet et al, 2013).…”

Section: Target Structures Involved In Pain and Depressionmentioning

confidence: 99%

“…TNF receptor (TNFR) knockout mice are protected against CCI-induced pain; however, inflammation in the hippocampus and depressive-like behavior remain (Fischer et al, 2019). Inflammation of the limbic system also occurs in chronic stress models with increased proinflammatory cytokines in the PFC, hippocampus, raphe nuclei and pituitary (Zhao et al, 2019). Additionally, the olfactory bulbectomy-induced depression model exhibited increased CD11b (macrophage/microglia marker), GFAP (Glial fibrillary acidic protein, astrocyte marker) and IL-1β levels in the amygdala, but the spinal nerve ligation-induced neuropathic pain alone or combined with olfactory bulbectomy does not change the expression of these cytokines (Burke et al, 2013), demonstrating that although pain and depression have several similarities, they may also involve different pathways.…”

Section: Target Structures Involved In Pain and Depressionmentioning

confidence: 99%

“…Additionally, the olfactory bulbectomy-induced depression model exhibited increased CD11b (macrophage/microglia marker), GFAP (Glial fibrillary acidic protein, astrocyte marker) and IL-1β levels in the amygdala, but the spinal nerve ligation-induced neuropathic pain alone or combined with olfactory bulbectomy does not change the expression of these cytokines (Burke et al, 2013), demonstrating that although pain and depression have several similarities, they may also involve different pathways. Inflammation of the structures of the limbic system often correlates with increased serum ACTH and corticosterone levels (Zhao et al, 2019). Increased expression of these hormones is often used as a biomarker for the activation of the HPA axis, which is strongly related to stress (Abrahams et al, 2012;Stephens and Wand, 2012).…”

Section: Target Structures Involved In Pain and Depressionmentioning

confidence: 99%

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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%

Section: Target Structures Involved In Pain and Depressionmentioning

confidence: 99%

Section: Target Structures Involved In Pain and Depressionmentioning

confidence: 99%

Section: Target Structures Involved In Pain and Depressionmentioning

confidence: 99%

See 2 more Smart Citations

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

et al. 2020

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“…On the other hand, the perception of cold and warmth has been shown to be unaltered in patients with MD [15]. Further, inflammatory pathways and the hypothalamic-pituitary-adrenal (HPA) axis have been identified to play a role in the interaction between pain and depression [16,17].…”

Section: Introductionmentioning

confidence: 99%

Differential neural processing of unpleasant sensory stimulation in patients with major depression

Malejko

Brown

Plener

et al. 2020

Eur Arch Psychiatry Clin Neurosci

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An altered processing of negative salient stimuli has been suggested to play a central role in the pathophysiology of major depression (MD). Besides negative affective and social stimuli, physical pain as a subtype of negative sensory stimulation has been investigated in this context. However, the few neuroimaging studies on unpleasant sensory stimulation or pain processing in MD report heterogeneous findings. Here, we investigated 47 young females, 22 with MD and 25 healthy controls (HC) using fMRI (3.0 T). Four levels of increasingly unpleasant electrical stimulation were applied. Ratings of stimulus intensity were assessed by a visual analogue scale. fMRI-data were analyzed using a 2 × 4 ANOVA. Behavioral results revealed no group differences regarding accuracy of unpleasant stimulation level ratings and sensitivity to stimulation. Regarding neural activation related to increasing levels of unpleasant stimulation, we observed increasing activation of brain regions related to the pain and salient stimulus processing corresponding to increasingly unpleasant stimulation in controls. This modulation was significantly smaller in MD compared to controls, particularly in the dorsal anterior cingulate cortex, the somatosensory cortex, and the posterior insula. Overall, brain regions associated with the processing of unpleasant sensory stimulation, but also associated with the salience network, were highly reactive but less modulated in female patients with MD. These results support and extent findings on altered processing of salience and of negative sensory stimuli even of a non-painful quality in female patients with MD.

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