Further evidence for the neuroplastic role of cannabinoids: a study in organotypic hippocampal slice cultures

Endocannabinoid receptors CB1R and CB2R are present in the CNS and modulate synaptic activity. By using an in vitro model, two concentrations of CB1R agonist ACEA at 0.5 and 5 μM doses and CB1R antagonist AM251 at 1 and 10 μM doses were administered in organotypic slice cultures of mouse hippocampus...

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Detalles Bibliográficos
Autores: Caltana, Laura Romina, Heimrich, Bernd, Brusco, Herminia Alicia
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2015
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/17782
Acceso en línea:http://hdl.handle.net/11336/17782
Access Level:acceso abierto
Palabra clave:Cannabinoids
Neuron
Neurotoxicity
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Descripción
Sumario:Endocannabinoid receptors CB1R and CB2R are present in the CNS and modulate synaptic activity. By using an in vitro model, two concentrations of CB1R agonist ACEA at 0.5 and 5 μM doses and CB1R antagonist AM251 at 1 and 10 μM doses were administered in organotypic slice cultures of mouse hippocampus, and their effects on neurons and glial cells were analyzed at different time points. Exposure to low concentrations of ACEA (0.5 μM) did not seem to affect tissue organization, neuronal morphology, or glial response. In contrast, at a higher concentration of ACEA, many neurons in the dentate gyrus exhibited strong caspase-3 immunoreactivity. After treatment with AM251, we observed an increase in caspase-3 immunoreactivity and a downregulation of CB1R expression. Results show that long-term hippocampal slice cultures respond to both CB1R activation and inactivation by changing neuronal protein expression patterns. In the present study, we demonstrate that CB1R agonist ACEA promotes alterations in the neuronal cytoskeleton as well as changes in CB1R expression in organotypic hippocampal slice cultures, and that CB1R antagonist AM251 promotes neuronal death and astroglial reaction.