Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/73301
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Title

Excitotoxicity in a chronic model of multiple sclerosis: Neuroprotective effects of cannabinoids through CB1 and CB2 receptor activation

AuthorsDocagne, Fabian CSIC ORCID; Muñetón-Gómez, Vilma; Clemente, Diego; Ali, C.; Loría, Frida CSIC ORCID; Correa, Fernando Gabriel CSIC; Hernangómez-Herrero, Miriam CSIC; Mestre, Leyre CSIC ORCID ; Vivien, Denis; Guaza, Carmen CSIC ORCID
KeywordsMultiple sclerosis
TMEV
Axonal damage
Excitotoxicity
Cannabinoids
Issue DateApr-2007
PublisherAcademic Press
CitationMolecular and Cellular Neurosciences 34(4): 551-561 (2007)
AbstractInflammation, autoimmune response, demyelination and axonal damage are thought to participate in the pathogenesis of multiple sclerosis (MS). Understanding whether axonal damage causes or originates from demyelination is a crucial issue. Excitotoxic processes may be responsible for white matter and axonal damage. Experimental and clinical studies indicate that cannabinoids could prove efficient in the treatment of MS. Using a chronic model of MS in mice, we show here that clinical signs and axonal damage in the spinal cord were reduced by the AMPA antagonist, NBQX. Amelioration of symptomatology by the synthetic cannabinoid HU210 was also accompanied by a reduction of axonal damage in this model. Moreover, HU210 reduced AMPA-induced excitotoxicity both in vivo and in vitro through the obligatory activation of both CB1 and CB2 cannabinoid receptors. Together, these data underline the implication of excitotoxic processes in demyelinating pathologies such as MS and the potential therapeutic properties of cannabinoids. © 2006 Elsevier Inc. All rights reserved.
Publisher version (URL)http://doi.org/10.1016/j.mcn.2006.12.005
URIhttp://hdl.handle.net/10261/73301
DOI10.1016/j.mcn.2006.12.005
Identifiersdoi: 10.1016/j.mcn.2006.12.005
issn: 1044-7431
Appears in Collections:(IC) Artículos

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