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Journal ArticleDOI

Importance of glial activation in neuropathic pain

TLDR
Since it is known that the opioid-induced glial activation opposes opioid analgesia, some glial inhibitors are proposed as potential useful ko-analgesic agents for opioid treatment of neuropathic pain.
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This article is published in European Journal of Pharmacology.The article was published on 2013-09-15. It has received 360 citations till now. The article focuses on the topics: Chronic pain & Neuropathic pain.

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Journal ArticleDOI

Neuropathic pain: mechanisms and their clinical implications

TL;DR: Because of the considerable overlap between neuropathic and nociceptive pain in terms of mechanisms and treatment modalities, it might be more constructive to view these entities as different points on the same continuum.
Journal ArticleDOI

Diabetic neuropathic pain: Physiopathology and treatment.

TL;DR: A better understanding of the mechanisms underlying diabetic neuropathic pain will contribute to the search of new therapies, but also to the improvement of the guidelines to optimize pain control with the drugs currently available.
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Opioid-induced hyperalgesia: Cellular and molecular mechanisms.

TL;DR: The molecular actors identified include the Toll-like receptor 4 and the anti-opioid systems as well as some other excitatory molecules, receptors, channels, chemokines, pro-inflammatory cytokines or lipids, which contribute to OIH.
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Salivary markers of inflammation in response to acute stress.

TL;DR: A review of published studies that have examined salivary markers of inflammation following exposure to an acute laboratory stressor suggests that specific targets may be valid and highlights specific areas of need for future research.
Journal ArticleDOI

Biological hypotheses and biomarkers of bipolar disorder.

TL;DR: Current biological hypotheses of BD are summarized, including related pathophysiological processes and key biomarkers, which have been associated with changes in genetics, systems of neurotransmitter and neurotrophic factors, neuroinflammation, autoimmunity, cytokines, stress axis activity, chronobiology, oxidative stress, and mitochondrial dysfunctions.
References
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Microglia: a sensor for pathological events in the CNS

TL;DR: An understanding of intercellular signalling pathways for microglia proliferation and activation could form a rational basis for targeted intervention on glial reactions to injuries in the CNS.
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Immunosuppression by Glucocorticoids: Inhibition of NF-κB Activity Through Induction of IκB Synthesis

TL;DR: It is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B activation in mice and cultured cells, mediated by induction of the IκBα inhibitory protein, which traps activated NF-κB in inactive cytoplasmic complexes.
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Neuropathic pain: aetiology, symptoms, mechanisms, and management

TL;DR: This work highlights current theories about peripheral neuropathic pain and shows that progress in management is contingent on targeting treatment not at the aetiological factors or the symptoms but at the mechanisms that operate to produce the symptoms.
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Role of Transcriptional Activation of IκBα in Mediation of Immunosuppression by Glucocorticoids

TL;DR: It is shown that the synthetic glucocorticoid dexamethasone induces the transcription of the IκBα gene, which results in an increased rate of Iκbα protein synthesis, which is predicted to markedly decrease cytokine secretion and thus effectively block the activation of the immune system.
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Immune function of microglia

TL;DR: The signals regulatingmicroglia innate immune functions, the role of microglia in antigen presentation, and their possible involvement in the development of CNS immunopathology are focused on.
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