Endocannabinoids control spasticity in a multiple sclerosis model.
Spasticity is a complicating sign in multiple sclerosis that also develops in a model of chronic relapsing experimental autoimmune encephalomyelitis (CREAE) in mice. In areas associated with nerve damage, increased levels of the endocannabinoids, anandamide (arachidonoylethanolamide, AEA) and 2-arac...
| Main Authors: | , , , , , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
2001
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| _version_ | 1797072139036131328 |
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| author | Baker, D Pryce, G Croxford, J Brown, P Pertwee, R Makriyannis, A Khanolkar, A Layward, L Fezza, F Bisogno, T Di Marzo, V |
| author_facet | Baker, D Pryce, G Croxford, J Brown, P Pertwee, R Makriyannis, A Khanolkar, A Layward, L Fezza, F Bisogno, T Di Marzo, V |
| author_sort | Baker, D |
| collection | OXFORD |
| description | Spasticity is a complicating sign in multiple sclerosis that also develops in a model of chronic relapsing experimental autoimmune encephalomyelitis (CREAE) in mice. In areas associated with nerve damage, increased levels of the endocannabinoids, anandamide (arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG), and of the AEA congener, palmitoylethanolamide (PEA), were detected here, whereas comparable levels of these compounds were found in normal and non-spastic CREAE mice. While exogenously administered endocannabinoids and PEA ameliorate spasticity, selective inhibitors of endocannabinoid re-uptake and hydrolysis-probably through the enhancement of endogenous levels of AEA, and, possibly, 2-arachidonoyl glycerol-significantly ameliorated spasticity to an extent comparable with that observed previously with potent cannabinoid receptor agonists. These studies provide definitive evidence for the tonic control of spasticity by the endocannabinoid system and open new horizons to therapy of multiple sclerosis, and other neuromuscular diseases, based on agents modulating endocannabinoid levels and action, which exhibit little psychotropic activity. |
| first_indexed | 2024-03-06T23:03:22Z |
| format | Journal article |
| id | oxford-uuid:62f1bc98-3ac4-4ac9-a2c6-8254a2e9bb49 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T23:03:22Z |
| publishDate | 2001 |
| record_format | dspace |
| spelling | oxford-uuid:62f1bc98-3ac4-4ac9-a2c6-8254a2e9bb492022-03-26T18:09:35ZEndocannabinoids control spasticity in a multiple sclerosis model.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:62f1bc98-3ac4-4ac9-a2c6-8254a2e9bb49EnglishSymplectic Elements at Oxford2001Baker, DPryce, GCroxford, JBrown, PPertwee, RMakriyannis, AKhanolkar, ALayward, LFezza, FBisogno, TDi Marzo, VSpasticity is a complicating sign in multiple sclerosis that also develops in a model of chronic relapsing experimental autoimmune encephalomyelitis (CREAE) in mice. In areas associated with nerve damage, increased levels of the endocannabinoids, anandamide (arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG), and of the AEA congener, palmitoylethanolamide (PEA), were detected here, whereas comparable levels of these compounds were found in normal and non-spastic CREAE mice. While exogenously administered endocannabinoids and PEA ameliorate spasticity, selective inhibitors of endocannabinoid re-uptake and hydrolysis-probably through the enhancement of endogenous levels of AEA, and, possibly, 2-arachidonoyl glycerol-significantly ameliorated spasticity to an extent comparable with that observed previously with potent cannabinoid receptor agonists. These studies provide definitive evidence for the tonic control of spasticity by the endocannabinoid system and open new horizons to therapy of multiple sclerosis, and other neuromuscular diseases, based on agents modulating endocannabinoid levels and action, which exhibit little psychotropic activity. |
| spellingShingle | Baker, D Pryce, G Croxford, J Brown, P Pertwee, R Makriyannis, A Khanolkar, A Layward, L Fezza, F Bisogno, T Di Marzo, V Endocannabinoids control spasticity in a multiple sclerosis model. |
| title | Endocannabinoids control spasticity in a multiple sclerosis model. |
| title_full | Endocannabinoids control spasticity in a multiple sclerosis model. |
| title_fullStr | Endocannabinoids control spasticity in a multiple sclerosis model. |
| title_full_unstemmed | Endocannabinoids control spasticity in a multiple sclerosis model. |
| title_short | Endocannabinoids control spasticity in a multiple sclerosis model. |
| title_sort | endocannabinoids control spasticity in a multiple sclerosis model |
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