EphrinB–EphB signaling regulates spinal pain processing via PKCγ

• Published in: Neuroscience Vol. 307; pp. 64 - 72
• Main Authors: Zhou, X.-L, Zhang, C.-J, Wang, Y, Wang, M, Sun, L.-H, Yu, L.-N, Cao, J.-L, Yan, M
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 29.10.2015
• Subjects: Analysis of Variance; Animals; Bone Neoplasms - complications; central sensitization; Disease Models, Animal; Eph; ephrin; Ephrin-B2 - chemistry; Ephrin-B2 - metabolism; Ephrin-B2 - toxicity; Formaldehyde - toxicity; hyperalgesia; Hyperalgesia - physiopathology; Injections, Spinal; Male; Mice; Mice, Inbred C57BL; Neuralgia - chemically induced; Neuralgia - etiology; Neuralgia - metabolism; Neurology; protein kinase C; Protein Kinase C - genetics; Protein Kinase C - metabolism; Receptors, Eph Family - metabolism; Receptors, Eph Family - toxicity; RNA, Small Interfering - pharmacology; Signal Transduction - drug effects; Signal Transduction - physiology; Time Factors; protein kinase C-γ; intrathecally; central sensitization; paw withdrawal threshold; analysis of variance; ANOVA; ethylenediaminetetraacetic acid; protein kinase C; small interfering RNAs; tibia bone cavity tumor cell implantation; PWL; CCI; chronic constriction injury; siRNA; EDTA; paw withdrawal latency; PWT; N-methyl- d-aspartate receptor; i.t; PKCγ; ephrin; EGTA; NMDAR; TCI; hyperalgesia; ethylene glycol tetraacetic acid; Eph
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2015.08.048

Highlights • EphrinB2-Fc caused PKCγ activation. • Knockdown of PKCγ prevented pain induced by ephrinB2-Fc. • EphB2-Fc reduced PKCγ activation in pain models.