Metabotropic GABA-B receptors in the PNS: role in nociception and myelination

Abstract

Event Abstract Back to Event Metabotropic GABA-B receptors in the PNS: role in nociception and myelination Valerio Magnaghi1*, M. Ballabio1, B. Bettler2, A. Faroni1 and P. Procacci3 1 University of Milan, Department of Endocrinology, Italy 2 University of Basel, Department of Biomedicine, Switzerland 3 University of Milan, Department of Human Morphology, Italy Metabotropic GABA-B receptors are present in the CNS where they play important roles in the modulation of nociceptive transmission and pain. Many preclinical studies reported that the GABA-B specific agonist baclofen is antinociceptive in different models of acute and chronic pain. The study of GABA-B1 knockout mice further supports the contribution of GABA-B receptors to central nociceptive processing. These mice are hyperalgesic, showing a reduced latency to thermal and mechanical stimuli. A tonic GABA-B receptor activation therefore appears to contribute to the establishment of the nociceptive threshold. Interestingly, GABA-B receptors are expressed in the peripheral nervous system (PNS), mainly in the Schwann cells where they control cell proliferation and myelination. Emerging evidence obtained in GABA-B1 knockout mice indicates that these mice exhibit gait alterations and reduced allodynic sensitivity too. Furthermore, GABA-B1-deficient mice show morphological and molecular changes in peripheral nerves, including an increase in the number of small myelinated fibers, as well as in small neurons of the lumbar dorsal root ganglia. These fibers are supposed to be A_ nociceptive fibers. Consequently, it has been suggested that GABA-B receptors are implicated in the PNS myelination process. The possibility that PNS alterations contribute to the sensory phenotypes observed in GABAB1- deficient mice has been also hypothesized. The study in conditional mice that specifically lack the GABA-B1 receptor in the Schwann cells or in motoneurons will aim to clarify the role of GABA-B receptors in peripheral pain sensitivity. Conference: 3rd Mediterranean Conference of Neuroscience , Alexandria, Egypt, 13 Dec - 16 Dec, 2009. Presentation Type: Oral Presentation Topic: Symposium 04 – Dis-inhibition processes in pain sensitization Citation: Magnaghi V, Ballabio M, Bettler B, Faroni A and Procacci P (2009). Metabotropic GABA-B receptors in the PNS: role in nociception and myelination. Front. Neurosci. Conference Abstract: 3rd Mediterranean Conference of Neuroscience . doi: 10.3389/conf.neuro.01.2009.16.019 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: 19 Nov 2009; Published Online: 19 Nov 2009. * Correspondence: Valerio Magnaghi, University of Milan, Department of Endocrinology, Milan, Italy, valerio.magnaghi@unimi.it 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 Valerio Magnaghi M. Ballabio B. Bettler A. Faroni P. Procacci Google Valerio Magnaghi M. Ballabio B. Bettler A. Faroni P. Procacci Google Scholar Valerio Magnaghi M. Ballabio B. Bettler A. Faroni P. Procacci PubMed Valerio Magnaghi M. Ballabio B. Bettler A. Faroni P. Procacci 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.