Quick Search:

uzh logo
Browse by:

Zurich Open Repository and Archive

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.

[img] PDF - Registered users only
View at publisher


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.


108 citations in Web of Science®
122 citations in Scopus®
Google Scholar™



3 downloads since deposited on 26 Mar 2009
0 downloads since 12 months

Detailed statistics

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
Date:September 2005
Deposited On:26 Mar 2009 14:01
Last Modified:05 Apr 2016 12:31
Publisher DOI:10.1007/s00018-005-5107-3
PubMed ID:15968463

Users (please log in): suggest update or correction for this item

Repository Staff Only: item control page