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Through the activation of cannabinoid CB\n                    <jats:sub>1<\/jats:sub>\n                    receptors (CB\n                    <jats:sub>1<\/jats:sub>\n                    R) expressed by neurons and oligodendrocyte lineage cells, endocannabinoid signaling restricts neurodegeneration and promotes remyelination in preclinical MS models. However, despite accumulating evidence that supports cell-specific roles for CB\n                    <jats:sub>1<\/jats:sub>\n                    R in brain physiology and pathology, the implications of astrocyte CB\n                    <jats:sub>1<\/jats:sub>\n                    R signaling in MS initiation and progression remain uncertain. Using complementary in vivo disease models, here we investigated the effects of targeted genetic deletion of astrocyte CB\n                    <jats:sub>1<\/jats:sub>\n                    R on the expression of MS-like pathology in mice. Interestingly, astrocyte-specific deletion of CB\n                    <jats:sub>1<\/jats:sub>\n                    R reduced demyelinating neuropathology, attenuated astrocyte reactivity and improved clinical deficits during the time-course of experimental autoimmune encephalomyelitis (EAE). Mice with astrocyte CB\n                    <jats:sub>1<\/jats:sub>\n                    R inactivation displayed unaltered oligodendrocyte populations both in EAE plaques and in lysolecithin-induced remyelinating spinal cord lesions, likely excluding that CB\n                    <jats:sub>1<\/jats:sub>\n                    R expressed by astroglial cells modulate myelin repair processes. Conversely, inactivation of CB\n                    <jats:sub>1<\/jats:sub>\n                    R in astrocytes restricted humoral and leukocyte parenchymal infiltration and reduced the expression of vascular effectors in EAE lesions. Finally, loss of blood-brain barrier (BBB) function induced by cortical microinjection of VEGF-A was less severe in astrocyte CB\n                    <jats:sub>1<\/jats:sub>\n                    R null mice. These results show that astrocyte CB\n                    <jats:sub>1<\/jats:sub>\n                    R signaling constitutes a significant pro-inflammatory mechanism in experimental MS and bring to light a deleterious role for endocannabinoid-mediated modulation of astroglial cells with potential implications in the etiopathology and therapy of neuroinflammatory disorders.\n                  <\/jats:p>","DOI":"10.1186\/s12974-026-03708-3","type":"journal-article","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T03:24:37Z","timestamp":1769657077000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Astrocyte CB1 receptors drive blood-brain barrier disruption in central nervous system inflammatory disease"],"prefix":"10.1186","volume":"23","author":[{"given":"Teresa","family":"Colomer","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana","family":"Bernal-Chico","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ester","family":"S\u00e1nchez-Mart\u00edn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alvaro","family":"Moreno-Garc\u00eda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andr\u00e9s Mateo","family":"Baraibar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aitziber","family":"Uribe-Irusta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ander","family":"Iriarte-Sarria","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra","family":"Beriain","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Urszula","family":"Skupio","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charlotte","family":"Gatuingt-Chasseriaud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Delphine","family":"Gonzales","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guillaume","family":"Laplagne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rom\u00e1n","family":"Serrat","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabel Pidal-Ladr\u00f3n","family":"de Guevara","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos","family":"Matute","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diego","family":"Clemente","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vanja","family":"Tepavcevic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ignacio","family":"Fern\u00e1ndez-Moncada","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Candice","family":"Chapouly","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giovanni","family":"Marsicano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susana","family":"Mato","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,1,29]]},"reference":[{"issue":"2","key":"3708_CR1","doi-asserted-by":"crossref","first-page":"169","DOI":"10.1056\/NEJMra1401483","volume":"378","author":"DS Reich","year":"2018","unstructured":"Reich DS, Lucchinetti CF, Calabresi PA. 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