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Changes in Cannabinoid Receptors, Aquaporin 4 and Vimentin Expression after Traumatic Brain Injury in Adolescent Male Mice. Association with Edema and Neurological Deficit

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López Rodríguez, Ana Belén y Acaz Fonseca, Estefanía y Viveros, María Paz y García Segura, Luis Miguel (2015) Changes in Cannabinoid Receptors, Aquaporin 4 and Vimentin Expression after Traumatic Brain Injury in Adolescent Male Mice. Association with Edema and Neurological Deficit. PLoS ONE, 10 (6). pp. 1-17. ISSN ESSN: 1932-6203

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URL Oficial: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0128782



Resumen

Traumatic brain injury (TBI) incidence rises during adolescence because during this critical neurodevelopmental period some risky behaviors increase. The purpose of this study was to assess the contribution of cannabinoid receptors (CB1 and CB2), blood brain barrier proteins (AQP4) and astrogliosis markers (vimentin) to neurological deficit and brain edema formation in a TBI weight drop model in adolescent male mice. These molecules were selected since they are known to change shortly after lesion. Here we extended their study in three different timepoints after TBI, including short (24h), early mid-term (72h) and late midterm (two weeks). Our results showed that TBI induced an increase in brain edema up to 72 h after lesion that was directly associated with neurological deficit. Neurological deficit appeared 24 h after TBI and was completely recovered two weeks after trauma. CB1 receptor expression decreased after TBI and was negatively correlated with edema formation and behavioral impairments. CB2 receptor increased after injury and was associated with high neurological deficit whereas no correlation with edema was found. AQP4 increased after TBI and was positively correlated with edema and neurological impairments as occurred with vimentin expression in the same manner. The results suggest that CB1 and CB2 differ in the mechanisms to resolve TBI and also that some of their neuroprotective effects related to the control of reactive astrogliosis may be due to the regulation of AQP4 expression on the end-feet of astrocytes.


Tipo de documento:Artículo
Palabras clave:Edema; Traumatic brain injury; Vimentin; Cytoskeletal proteins; Brain damage; Astrocytes; Analysis of variance; Behavior
Materias:Ciencias Biomédicas > Biología > Fisiología animal
Ciencias Biomédicas > Biología > Neurociencias
Código ID:42504
Depositado:04 May 2017 08:47
Última Modificación:08 May 2017 08:52

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