2013
DOI: 10.1124/pr.113.008144
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Neuroinflammation and Comorbidity of Pain and Depression

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Cited by 372 publications
(332 citation statements)
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References 183 publications
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“…Although it is unclear how cytokines may initiate or influence the pathogenesis of depressive disorders, one hypothesis postulates that proinflammatory cytokines stimulate indoleamine 2,3-dioxygenase (IDO) in glial cells to convert tryptophan to kynurenine which is transformed into the neurotoxic quinolinic acid inside the brain (Müller and Schwarz, 2007;Walker et al, 2014). Quinolinic acid binds to N-methyl-D-aspartate receptors while also depleting tryptophan leading to a decrease in overall serotonin levels and an increase in glutamatergic activity commonly associated with depression (Sublette et al, 2011).…”
Section: The Inflammatory Process and Hypothesis In Mddmentioning
confidence: 99%
“…Although it is unclear how cytokines may initiate or influence the pathogenesis of depressive disorders, one hypothesis postulates that proinflammatory cytokines stimulate indoleamine 2,3-dioxygenase (IDO) in glial cells to convert tryptophan to kynurenine which is transformed into the neurotoxic quinolinic acid inside the brain (Müller and Schwarz, 2007;Walker et al, 2014). Quinolinic acid binds to N-methyl-D-aspartate receptors while also depleting tryptophan leading to a decrease in overall serotonin levels and an increase in glutamatergic activity commonly associated with depression (Sublette et al, 2011).…”
Section: The Inflammatory Process and Hypothesis In Mddmentioning
confidence: 99%
“…Some investigators have looked for biological mechanisms that might explain the link between low mood and musculoskeletal pain, including the possible role of neurotransmitters [33] and cytokine receptors [34]. However, there is still no established neuro-chemical explanation for the association.…”
Section: Association With Musculoskeletal Illnessmentioning
confidence: 99%
“…However, recent findings from longitudinal studies suggest that among individuals who are initially free from musculoskeletal pain, those with low mood are more likely subsequently to develop pain and associated disability (Table 1). In addition, there is some evidence from experimental studies that induction of negative mood reduces pain tolerance and leads to higher levels of self-reported pain severity [32].Some investigators have looked for biological mechanisms that might explain the link between low mood and musculoskeletal pain, including the possible role of neurotransmitters [33] and cytokine receptors [34]. However, there is still no established neuro-chemical explanation for the association.…”
mentioning
confidence: 99%
“…Обычно этот тип воспаления не сопровождается харак-терными для острого воспаления симптомами и не ощу-щается индивидуумом. Активация глиальных клеток и нейровоспаление все чаще рассматриваются как одна из основных причин хронической боли в спине и многих сопровождающих ее синдромов, включая депрессию, усталость, бессонницу [11,12]. Активация глиальных кле-ток приводит к пролонгированному патологическому процессу в центральной нервной системе (ЦНС), который включает нейровоспаление, дисфункцию глиальных кле-ток, стимуляцию гипоталамо-гипофизарного комплекса.…”
Section: центральные механизмы формирования хронической боли в спинеunclassified