Artigo Acesso aberto Revisado por pares

Modulation of Neuropathic Pain by Endocannabionid Signalling

2009; Frontiers Media; Volume: 3; Linguagem: Inglês

10.3389/conf.neuro.01.2009.04.039

ISSN

1662-5137

Autores

Rafael Malach,

Tópico(s)

Botulinum Toxin and Related Neurological Disorders

Resumo

Event Abstract Back to Event Modulation of Neuropathic Pain by Endocannabionid Signalling Ildikó Rácz1*, Xavier Nadal2, Judith Alferink1, 3, Josep E. Banos2, Jennifer Rehnelt1, Miquel Martín2, Alfonso G. Adan4, Elena Sanguino5, Jorge Manzanares5, Andreas Zimmer1 and Rafael Malach2 1 Institute of Molecular Psychiatry, Germany 2 Universitat Pompeu Fabra, Parc de Recerca Biomèdica de Barcelona, Spain 3 Department of Psychiatry, University of Bonn, Germany 4 Instituto Nacional de Investigación y Tecnología Agraria, Departamento de Reproducción Animal y Conservación de Recursos Zoogenéticos, Spain 5 Universidad Miguel Hernández-CSIC, Spain Neuropathic pain develops as a consequence of peripheral nerve injury. Because it is difficult to treat there is a great medical need for novel pharmacotherapies. Recent studies suggest that CB2 selective ligands seem to be effective in animal models of neuropathic pain. In this study, we have investigated CB2 mediated mechanisms in the modulation of neuropathic pain. We used genetically modified mice lacking or overexpressing cannabinoid CB2 receptors to evaluate the contribution of these receptors in the development of neuropathic pain. We performed partial sciatic nerve ligation followed by nocicepive, histological and expression profiling studies. INF- and CB2 receptor double knockout mice, as well as irradiated wild type mice receiving bone marrow transplantation from CB2 knockout animals were used to address the role of inflammatory responses. CB2 knockout animals subjected to a partial nerve injury developed mechanical allodynia and thermal hyperalgesia to a similar extend as wild type control animals on the ipsilateral side of the nerve injury. However, they also displayed increased pain sensitivity on the contralateral side. Transgenic mice overexpressing CB2 receptors had attenuated neuropathic pain responses. Expression profiling studies revealed an enhanced INF- response in the absence of CB2 receptors. Analysis of double knockout animals confirmed that the enhanced INF- response caused the expansion of the hyperalgesic area in the absence of CB2 receptors. These results suggest that CB2 mediated mechanisms contribute to the local containment of the hyperalgesic response after peripheral nerve injury. CB2 receptors thus represent an interesting therapeutic target for the treatment of neuropathic pain. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Pathophysiology and neurology - non-degenerative disorders Citation: Rácz I, Nadal X, Alferink J, Banos JE, Rehnelt J, Martín M, Adan AG, Sanguino E, Manzanares J, Zimmer A and Malach R (2009). Modulation of Neuropathic Pain by Endocannabionid Signalling. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.039 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 27 Feb 2009; Published Online: 27 Feb 2009. * Correspondence: Ildikó Rácz, Institute of Molecular Psychiatry, Bonn, Germany, iracz@uni-bonn.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ildikó Rácz Xavier Nadal Judith Alferink Josep E Banos Jennifer Rehnelt Miquel Martín Alfonso G Adan Elena Sanguino Jorge Manzanares Andreas Zimmer Rafael Malach Google Ildikó Rácz Xavier Nadal Judith Alferink Josep E Banos Jennifer Rehnelt Miquel Martín Alfonso G Adan Elena Sanguino Jorge Manzanares Andreas Zimmer Rafael Malach Google Scholar Ildikó Rácz Xavier Nadal Judith Alferink Josep E Banos Jennifer Rehnelt Miquel Martín Alfonso G Adan Elena Sanguino Jorge Manzanares Andreas Zimmer Rafael Malach PubMed Ildikó Rácz Xavier Nadal Judith Alferink Josep E Banos Jennifer Rehnelt Miquel Martín Alfonso G Adan Elena Sanguino Jorge Manzanares Andreas Zimmer Rafael Malach Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

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