Abstract |
The ephrin family of receptors (Eph) and their ephrin ligands are involved in pain associated hyperalgesia, but the underlying mechanisms involved have not been fully elucidated. The EphB6 receptor is a distinctive member of the EphB subclass in that its kinase domain contains several alterations in the conserved amino acids and thus lacks catalytic activity. We sought to identify a role for EphB6 in inflammatory pain, with the murine dextran sulfate sodium (DSS) colitis model of inflammatory bowel disease (IBD). Colitis, induced with the administration of 4% (wt./vol.) DSS in the drinking water, significantly decreased EphB6 protein expression levels in neurons of the lower thoracic superficial layers of spinal dorsal horns, the location of neurons that receive the majority of nociceptive information from the colon, via the primary afferents. A shift towards increased EphB/ephrinB forward signaling, mediated by EphB6 down-regulation in neurons of the dorsal horn, may play a role in inflammatory pain caused by IBD.
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Authors | Dale E King |
Journal | Neuroscience letters
(Neurosci Lett)
Vol. 559
Pg. 105-10
(Jan 24 2014)
ISSN: 1872-7972 [Electronic] Ireland |
PMID | 24309292
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2013 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- Receptor, EphB6
- Dextran Sulfate
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Topics |
- Acute Disease
- Animals
- Colitis
(chemically induced, metabolism, pathology)
- Dextran Sulfate
(toxicity)
- Disease Models, Animal
- Down-Regulation
(physiology)
- Male
- Mice
- Mice, Inbred C57BL
- Posterior Horn Cells
(drug effects, metabolism, pathology)
- Receptor, EphB6
(biosynthesis)
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