| The role of glia and the immune system in the development and maintenance of neuropathic pain. | |
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MedLine Citation:
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PMID: 20384965 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Neuropathic pain refers to a variety of chronic pain conditions with differing underlying pathophysiologic mechanisms and origins. Recent studies indicate a communication between the immune system and the nervous system. A common underlying mechanism of neuropathic pain is the presence of inflammation at the site of the damaged or affected nerve(s). This inflammatory response initiates a cascade of events resulting in the concentration and activation of innate immune cells at the site of tissue injury. The release of immunoactive substances such as cytokines, neurotrophic factors, and chemokines initiate local actions and can result in a more generalized immune response. The resultant neuroinflammatory environment can cause activation of glial cells located in the spinal cord and the brain, which appear to play a prominent role in nociception. Glial cells, also known as neuroglia, are nonconducting cells that modulate neurotransmission at the synaptic level. Glial cells can be subdivided into two primary categories: microglia and macroglia, which include astrocytes and oligodendrocytes. Astrocytes and microglia are known to play a role in the development, spread, and potentiation of neuropathic pain. Following peripheral nociceptive activation via nerve injury, microglia become activated and release pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6, thereby initiating the pain process. Microglia propagate the neuroinflammation by recruiting other microglia and eventually activating nearby astrocytes, which prolongs the inflammatory state and leads to a chronic neuropathic pain condition. Our review focuses on the role of glia and the immune system in the development and maintenance of neuropathic pain. |
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Authors:
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Ricardo Vallejo; Dana M Tilley; Laura Vogel; Ramsin Benyamin |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2010-04-05 |
Journal Detail:
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Title: Pain practice : the official journal of World Institute of Pain Volume: 10 ISSN: 1533-2500 ISO Abbreviation: Pain Pract Publication Date: 2010 May-Jun |
Date Detail:
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Created Date: 2010-06-15 Completed Date: 2010-09-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101130835 Medline TA: Pain Pract Country: United States |
Other Details:
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Languages: eng Pagination: 167-84 Citation Subset: IM |
Affiliation:
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Millennium Pain Center, Bloomington, Illinois 61701, USA. vallejo@millenniumpaincenter.com |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cytokines / metabolism Humans Immune System / physiopathology* Inflammation / etiology, pathology Nerve Growth Factors / metabolism Neuralgia / immunology*, pathology* Neuroglia / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Nerve Growth Factors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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