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Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain

Recent studies have shown that cannabidiol (CBD) could have a great therapeutic potential for treating disorders such as chronic pain and anxiety. In the target article, the authors propose that CBD modulates serotonergic transmission and reverses allodynia and anxiety-like behaviour in a rat model...

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Detalles Bibliográficos
Autor principal: Schott, Marion
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6882574/
https://www.ncbi.nlm.nih.gov/pubmed/32766463
http://dx.doi.org/10.1097/PR9.0000000000000774
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author Schott, Marion
author_facet Schott, Marion
author_sort Schott, Marion
collection PubMed
description Recent studies have shown that cannabidiol (CBD) could have a great therapeutic potential for treating disorders such as chronic pain and anxiety. In the target article, the authors propose that CBD modulates serotonergic transmission and reverses allodynia and anxiety-like behaviour in a rat model of neuropathic pain. Furthermore, this study shows an antinociceptive effect mediated by TRPV(1) and partially by 5-HT(1A) receptors, as well as an anxiolytic effect mediated by 5-HT(1A) receptors. Commentary on: De Gregorio D, McLaughlin RJ, Posa L, Ochoa-Sanchez R, Enns J, Lopez-Canul M, Aboud M, Maione S, Comai S, and Gobbi G. Cannabidiol modulates serotonergic transmission and reverses both allodynia and anxiety-like behavior in a model of neuropathic pain. PAIN 2019;160:36–150.
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spelling pubmed-68825742020-08-05 Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain Schott, Marion Pain Rep Journal Club Recent studies have shown that cannabidiol (CBD) could have a great therapeutic potential for treating disorders such as chronic pain and anxiety. In the target article, the authors propose that CBD modulates serotonergic transmission and reverses allodynia and anxiety-like behaviour in a rat model of neuropathic pain. Furthermore, this study shows an antinociceptive effect mediated by TRPV(1) and partially by 5-HT(1A) receptors, as well as an anxiolytic effect mediated by 5-HT(1A) receptors. Commentary on: De Gregorio D, McLaughlin RJ, Posa L, Ochoa-Sanchez R, Enns J, Lopez-Canul M, Aboud M, Maione S, Comai S, and Gobbi G. Cannabidiol modulates serotonergic transmission and reverses both allodynia and anxiety-like behavior in a model of neuropathic pain. PAIN 2019;160:36–150. Wolters Kluwer 2019-08-13 /pmc/articles/PMC6882574/ /pubmed/32766463 http://dx.doi.org/10.1097/PR9.0000000000000774 Text en Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The International Association for the Study of Pain. This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY) (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Journal Club
Schott, Marion
Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain
title Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain
title_full Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain
title_fullStr Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain
title_full_unstemmed Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain
title_short Insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain
title_sort insights on cannabidiol's antiallodynic and anxiolytic mechanisms of action in a model of neuropathic pain
topic Journal Club
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6882574/
https://www.ncbi.nlm.nih.gov/pubmed/32766463
http://dx.doi.org/10.1097/PR9.0000000000000774
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