Browsing by Author "Sommer, Claudia"
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Item Open Access 5-Hydroxyindolacetic Acid (5-HIAA), a Main Metabolite of Serotonin, is Responsible for Complete Freund's Adjuvant-Induced Thermal Hyperalgesia in Mice(Molecular Pain, 2011-08-05) Chen, Yong; Palm, Florian; Lesch, Klaus-Peter; Gerlach, Manfred; Moessner, Rainald; Sommer, ClaudiaItem Open Access Activation of the nociceptin opioid system in rat sensory neurons produces antinociceptive effects in inflammatory pain: Involvement of inflammatory mediators(Journal of Neuroscience Research, 2007-05-15) Chen, Yong; Sommer, ClaudiaItem Open Access Activation of TRPV1 Contributes to Morphine Tolerance: Involvement of the Mitogen-Activated Protein Kinase Signaling Pathway(Journal of Neuroscience, 2008-05-28) Chen, Yong; Geis, Christian; Sommer, ClaudiaItem Open Access Differences in inflammatory pain in nNOS-, iNOS- and eNOS-deficient mice(European Journal of Pain, 2007-10) Boettger, Michael Karl; Üceyler, Nurcan; Zelenka, Marek; Schmitt, Angelika; Reif, Andreas; Chen, Yong; Sommer, ClaudiaItem Open Access Nociceptin and its receptor in rat dorsal root ganglion neurons in neuropathic and inflammatory pain models: implications on pain processing(Journal of the Peripheral Nervous System, 2006-09) Chen, Yong; Sommer, ClaudiaItem Open Access Reduced thermal hyperalgesia and enhanced peripheral nerve injury after hind paw inflammation in mice lacking the serotonin-transporter(European Journal of Pain, 2008-08) Palm, Florian; Mössner, Rainald; Chen, Yong; He, Lan; Gerlach, Manfred; Bischofs, Stefan; Riederer, Peter; Lesch, Klaus‐Peter; Sommer, ClaudiaItem Open Access The role of mitogen-activated protein kinase (MAPK) in morphine tolerance and dependence.(Mol Neurobiol, 2009-10) Chen, Yong; Sommer, ClaudiaDespite the existence of a large body of information on the subject, the mechanisms of morphine tolerance and dependence are not yet fully understood. There is substantial evidence indicating that mitogen-activated protein kinase (MAPK), a family including extracellular signal-regulated protein kinase, p38 MAPK, and c-Jun N-terminal kinase, can be activated by chronic morphine treatment in the central and peripheral nervous systems and that application of a MAPK inhibitor reduces morphine tolerance and dependence. While the exact mechanism is not completely understood, recent evidence suggests that the activation of MAPK induced by long-term morphine exposure may participate in tolerance and dependence by regulating the downstream targets, such as calcitonin gene-related peptide, substance P, nitric oxide, transient receptor potential vanilloid 1, and proinflammatory cytokines. In this review, we focus on the current understanding of the role of MAPK signaling pathways in morphine tolerance and dependence.