Abstract | BACKGROUND:
EphB receptors and their ephrin-B ligands play an important role in nervous system development, as well as synapse formation and plasticity in the adult brain. Recent studies show that intrathecal treatment with EphB-receptor activator ephrinB2-Fc induced thermal hyperalgesia and mechanical allodynia in rat, indicating that ephrin-B2 in small dorsal root ganglia (DRG) neurons and EphB receptors in the spinal cord modulate pain processing. To examine the role of ephrin-B2 in peripheral pain pathways, we deleted ephrin-B2 in Nav1.8+ nociceptive sensory neurons with the Cre-loxP system. Sensory neuron numbers and terminals were examined using neuronal makers. Pain behavior in acute, inflammatory and neuropathic pain models was assessed in the ephrin-B2 conditional knockout (CKO) mice. We also investigated the c-Fos expression and NMDA receptor NR2B phosphorylation in ephrin-B2 CKO mice and littermate controls. RESULTS: CONCLUSIONS: Presynaptic ephrin-B2 expression thus plays an important role in regulating inflammatory pain through the regulation of synaptic plasticity in the dorsal horn and is also involved in the pathogenesis of some types of neuropathic pain.
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Authors | Jing Zhao, Guanglu Yuan, Cruz M Cendan, Mohammed A Nassar, Malin C Lagerström, Klas Kullander, Isabella Gavazzi, John N Wood |
Journal | Molecular pain
(Mol Pain)
Vol. 6
Pg. 77
(Nov 08 2010)
ISSN: 1744-8069 [Electronic] United States |
PMID | 21059214
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Activating Transcription Factor 3
- Ephrin-B2
- Glial Fibrillary Acidic Protein
- NAV1.8 Voltage-Gated Sodium Channel
- NR2B NMDA receptor
- Proto-Oncogene Proteins c-fos
- Receptors, N-Methyl-D-Aspartate
- Scn10a protein, mouse
- Scn10a protein, rat
- Sodium Channels
- Cre recombinase
- Integrases
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Topics |
- Activating Transcription Factor 3
(metabolism)
- Acute Disease
- Animals
- Behavior, Animal
- Cell Survival
- Disease Models, Animal
- Ephrin-B2
(metabolism)
- Exons
(genetics)
- Ganglia, Spinal
(metabolism, pathology)
- Gene Deletion
- Glial Fibrillary Acidic Protein
(metabolism)
- Inflammation
(complications, metabolism, pathology)
- Integrases
(metabolism)
- Mice
- Microglia
(metabolism, pathology)
- NAV1.8 Voltage-Gated Sodium Channel
- Neuralgia
(complications, metabolism, pathology)
- Neurons, Afferent
(metabolism, pathology)
- Nociceptors
(metabolism, pathology)
- Phosphorylation
- Proto-Oncogene Proteins c-fos
(metabolism)
- Receptors, N-Methyl-D-Aspartate
(metabolism)
- Sodium Channels
(metabolism)
- Spinal Cord
(metabolism, pathology)
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