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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-4699

Zeilhofer, H U (2005). The glycinergic control of spinal pain processing. Cellular and Molecular Life Sciences, 62(18):2027-2035.

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Abstract

Alterations in synaptic transmission within the spinal cord dorsal horn play a key role in the development of pathological pain. While N-methyl-D-aspartate (NMDA) receptors and activity-dependent synaptic plasticity have been the focus of research for many years, recent evidence attributes very specific functions to inhibitory glycinergic and gamma-aminobutyric acid (GABA)-ergic neurotransmission in the generation of inflammatory and neuropathic pain. The central component of inflammatory pain originates from a disinhibition of dorsal horn neurons, which are relieved from glycinergic neurotransmission by the inflammatory mediator prostaglandin E2 (PGE2). PGE2 activates prostaglandin E receptors of the EP2 subtype and leads to a protein kinase A-dependent phosphorylation and inhibition of glycine receptors containing the alpha3 subunit (GlyRalpha3). This GlyRalpha3 is distinctly expressed in the superficial dorsal horn, where nociceptive afferents terminate. Other but probably very similar disinhibitory mechanisms may well contribute to abnormal pain occurring after peripheral nerve injury.

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Pharmacology and Toxicology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:September 2005
Deposited On:26 Mar 2009 14:01
Last Modified:01 Jan 2013 21:18
Publisher:Springer
ISSN:1420-682X
Publisher DOI:10.1007/s00018-005-5107-3
PubMed ID:15968463
Citations:Google Scholar™
Scopus®. Citation Count: 109

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