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Loss of glycinergic and GABAergic inhibition in chronic pain-contributions of inflammation and microglia


Zeilhofer, H U (2008). Loss of glycinergic and GABAergic inhibition in chronic pain-contributions of inflammation and microglia. International Immunopharmacology, 8(2):182-187.

Abstract

Tissue trauma, inflammation and neuropathy can under unfortunate condition progress into chronic pain syndromes. It is meanwhile generally accepted that chronic pain, i.e. pain, which persists beyond the resolution of tissue traumata and inflammation, is due to plastic changes in the neuronal processing of sensory stimuli in the CNS. A loss of synaptic inhibition (i.e. dis-inhibition) in the spinal cord dorsal horn has been increasingly recognized as an important process in the development and maintenance of chronic pain of both inflammatory and neuropathic origin. Although inflammation and neuropathy involve distinct mechanisms of synaptic dis-inhibition, the production of inflammatory mediators and/or the activation of immune cells, two events that have once been thought to be normally excluded from the CNS, appear to be critical for both conditions.

Tissue trauma, inflammation and neuropathy can under unfortunate condition progress into chronic pain syndromes. It is meanwhile generally accepted that chronic pain, i.e. pain, which persists beyond the resolution of tissue traumata and inflammation, is due to plastic changes in the neuronal processing of sensory stimuli in the CNS. A loss of synaptic inhibition (i.e. dis-inhibition) in the spinal cord dorsal horn has been increasingly recognized as an important process in the development and maintenance of chronic pain of both inflammatory and neuropathic origin. Although inflammation and neuropathy involve distinct mechanisms of synaptic dis-inhibition, the production of inflammatory mediators and/or the activation of immune cells, two events that have once been thought to be normally excluded from the CNS, appear to be critical for both conditions.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Pharmacology and Toxicology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:February 2008
Deposited On:27 Oct 2008 14:22
Last Modified:05 Apr 2016 12:31
Publisher:Elsevier
ISSN:1567-5769
Publisher DOI:10.1016/j.intimp.2007.07.009
PubMed ID:18182224
Permanent URL: http://doi.org/10.5167/uzh-4689

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