Persistent Pain Produces Stress-like Alterations in Hippocampal Neurogenesis and Gene Expression

Đurić, Vanja; McCarson, Kenneth E.

doi:10.1016/j.jpain.2006.01.458

Cited by 148 publications

(125 citation statements)

References 61 publications

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“…One of the major insights that emerge from these studies is that both NK-1 receptor and BDNF mRNA levels are significantly attenuated by acute (formalin injection) or chronic pain (CFA injection), in accordance with the results initiated by acute or chronic restraint stress. These findings in the hippocampus are in sharp contrast to those uncovered in the spinal cord [25,186] , potentially reflecting varied roles of these neuromodulators in the de- but not acute pain (a single formalin injection), significantly reduced the neurogenesis in the DG area of the HF, measured by bromedeoxyuridine staining [196] , similar to previous observations from various stress models [192,197] . This paininduced decrease in hippocampal cell proliferation was recently confirmed by another immunoblotting study, comparing the apoptotic effects of chronic inflammatory pain and immobilization stress in rats [198] .…”

Section: Egr1 Expression the Zinc Finger Transcription Factorsupporting

confidence: 84%

“…Implicit within these observations is the hypothesis that chronic pain may regulate the expression of NK-1 receptor and BDNF in the hippocampus in a manner similar to that exerted by stress. To address this issue, McCarson's lab has conducted lots of work by using multiple approaches, such as solution hybridization-nuclease protection assays [24,25,195] , and in-situ hybridization [196] . One of the major insights that emerge from these studies is that both NK-1 receptor and BDNF mRNA levels are significantly attenuated by acute (formalin injection) or chronic pain (CFA injection), in accordance with the results initiated by acute or chronic restraint stress.…”

Section: Egr1 Expression the Zinc Finger Transcription Factormentioning

confidence: 99%

“…It has been generally believed that pain is characterized as a complex experience, dependent not only on the regulation of nociceptive sensory systems, but also on the activation of mechanisms that control mood-affect and emotioncognition in higher brain centers [1,2,25,72,195,196,221] . The emergence of imaging approaches such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) allows functional mapping of the intact brain and measurement of the responses in multiple areas simultaneously, thus bringing the study of pain into a deep level [13] .…”

Section: Functional Imaging Studiesmentioning

confidence: 99%

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Roles of the hippocampal formation in pain information processing

2009

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Abstract:Pain is a complex experience consisting of sensory-discriminative, affective-motivational, and cognitive-evaluative dimensions. Now it has been gradually known that noxious information is processed by a widely-distributed, hierarchicallyinterconnected neural network, referred to as neuromatrix, in the brain. Thus, identifying the multiple neural networks subserving these functional aspects and harnessing this knowledge to manipulate the pain response in new and beneficial ways are challenging tasks. Albeit with elaborate research efforts on the cortical responses to painful stimuli or clinical pain, involvement of the hippocampal formation (HF) in pain is still a matter of controversy. Here, we integrate previous animal and human studies from the viewpoint of HF and pain, sequentially representing anatomical, behavioral, electrophysiological, molecular/ biochemical and functional imaging evidence supporting the role of HF in pain processing. At last, we further expound on the relationship between pain and memory and present some unresolved issues.

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Section: Egr1 Expression the Zinc Finger Transcription Factorsupporting

confidence: 84%

Section: Egr1 Expression the Zinc Finger Transcription Factormentioning

confidence: 99%

Section: Functional Imaging Studiesmentioning

confidence: 99%

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Roles of the hippocampal formation in pain information processing

2009

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“…Indeed, an overlap exists in components of the pain neuromatrix and brain regions involved in cognitive processing (e.g., anterior cingulate cortex, insular cortex, periaqueductal gray) (14). Together with the demonstrated changes in neuroplasticity [e.g., gray matter volume reduction (15)(16)(17)] and dysregultated neurochemistry [e.g., decreased levels of brain-derived neurotrophic factor (18), increased levels of gamma-aminobutric acid (19), increased levels of pro-inflammatory cytokines (20)], these pain-induced changes in resource utilization may (in part) explain (pain-related) cognitive impairment in chronic pain patients.…”

Section: Participants and Assessmentsmentioning

confidence: 99%

Associations between cognitive performance and pain in chronic fatigue syndrome: comorbidity with fibromyalgia does matter

et al. 2015

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Background: In addition to the frequently reported pain complaints, performance-based cognitive capabilities in patients with chronic fatigue syndrome (CFS) with and without comorbid fibromyalgia (FM) are significantly worse than those of healthy controls. In various chronic pain populations, cognitive impairments are known to be related to pain severity. However, to the best of our knowledge, the association between cognitive performance and experimental pain measurements has never been examined in CFS patients.Objectives: This study aimed to examine the association between cognitive performance and self-reported as well as experimental pain measurements in CFS patients with and without FM.Study Design: Observational study.Setting: The present study took place at the Vrije Universiteit Brussel and the University of Antwerp.Methods: Forty-eight (18 CFS-only and 30 CFS+FM) patients and 30 healthy controls were studied. Participants first completed 3 performance-based cognitive tests designed to assess selective and sustained attention, cognitive inhibition, and working memory capacity. Seven days later, experimental pain measurements (pressure pain thresholds [PPT], temporal summation [TS], and conditioned pain modulation [CPM]) took place and participants were asked to fill out 3 questionnaires to assess self-reported pain, fatigue, and depressive symptoms.Results: In the CFS+FM group, the capacity of pain inhibition was significantly associated with cognitive inhibition. Self-reported pain was significantly associated with simple reaction time in CFS-only patients. The CFS+FM but not the CFS-only group showed a significantly lower PPT and enhanced TS compared with controls. Limitations:The cross-sectional nature of this study does not allow for inferences of causation. Conclusions:The results underline disease heterogeneity in CFS by indicating that a measure of endogenous pain inhibition might be a significant predictor of cognitive functioning in CFS patients with FM, while self-reported pain appears more appropriate to predict cognitive functioning in CFS patients without FM.

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“…Repeated exposure to low-dose formaldehyde increased basal corticosterone levels and produced stresslike alterations in hippocampal neurogenesis in rats 43) . In the present study, significant elevation of serum cortisol levels was observed at the 5th formalin application when the magnitude of skin reactions to formalin was most prominent.…”

Section: Discussionmentioning

confidence: 94%

Effect of Chronic Topical Exposure to Low‐Dose Noxious Chemicals and Stress on Skin Sensitivity in Mice

Nakano

2007

Journal of Occupational Health

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Effect of Chronic Topical Exposure toLow-Dose Noxious Chemicals and Stress on Skin Sensitivity in Mice: Yumiko NAKANO. Department of Environmental Health, Osaka Prefectural Institute of Public Health-It has been suggested that the recent increase in inflammatory diseases is related to an increase in environmental chemicals and psychiatric stress. To investigate the effect of chronic topical exposure to chemicals and isolation stress, low-dose formalin (a mild contact sensitizer and an irritant), 2,4,6-trinitrochlorobenzene (TNCB; a potent contact sensitizer) and sodium lauryl sulphate (SLS; an irritant) were applied to mouse ears at 7-d intervals under nostress or stress conditions. Skin reactions (ear swelling) elicited by formalin and TNCB increased time dependently. At the chronic stage, a significant skin reaction peaking at 1 h after application was elicited on the formalin-treated sites, while a shift from a delayed-type hypersensitivity to an immediate-type response was observed on the TNCB-treated sites. At the formalin-treated sites, genes related to neurogenic inflammation, i.e., bradykinin (BK) B2 receptor, IL-6, and membrane metallo endopeptidase (NEP) mRNA were upregulated. In the TNCB-treated sites, marked upregulation of IFN-γ, IL-1β, IL-4, and IL-6 mRNA was observed in addition to B2 receptor mRNA. Pretreatment with HOE140, the B2 receptor antagonist suppressed these skin reactions. Increased skin sensitivity to an unrelated chemical, ethanol, and thermal stimuli were elicited in formalin and TNCBtreated mice. Cortisol levels in formalin-treated mice and IgE levels in TNCB-treated mice were elevated respectively. Stress markedly amplified the skin reactions and gene expression related to neurogenic inflammation. SLS did not induce any changes. It was concluded that chronic topical exposure to low-dose noxious chemicals and stress could easily induce skin sensitivity relating to the BK-B2 pathway and nociceptive sensitization reflecting neural sensitization. (J Occup Health 2007; 49: 431-442)

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Persistent Pain Produces Stress-like Alterations in Hippocampal Neurogenesis and Gene Expression

Cited by 148 publications

References 61 publications

Roles of the hippocampal formation in pain information processing

Roles of the hippocampal formation in pain information processing

Associations between cognitive performance and pain in chronic fatigue syndrome: comorbidity with fibromyalgia does matter

Effect of Chronic Topical Exposure to Low‐Dose Noxious Chemicals and Stress on Skin Sensitivity in Mice

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