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Spontaneous Cannabinoid Receptor 2 (CB(2)) Expression in the Cochlea of Adult Albino Rat and Its Up-Regulation after Cisplatin Treatment

We provide evidence for the presence of cannabinoid CB(2) receptors in some cellular types of the cochlea of the adult albino rat. Cannabinoids and their receptors are increasingly being studied because of their high potential for clinical use. As a hyperspecialized portion of the peripheral nervous...

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Detalles Bibliográficos
Autores principales: Martín-Saldaña, Sergio, Trinidad, Almudena, Ramil, Elvira, Sánchez-López, Antonio J., Coronado, Maria José, Martínez-Martínez, Esther, García, José Miguel, García-Berrocal, José Ramón, Ramírez-Camacho, Rafael
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5001640/
https://www.ncbi.nlm.nih.gov/pubmed/27564061
http://dx.doi.org/10.1371/journal.pone.0161954
Descripción
Sumario:We provide evidence for the presence of cannabinoid CB(2) receptors in some cellular types of the cochlea of the adult albino rat. Cannabinoids and their receptors are increasingly being studied because of their high potential for clinical use. As a hyperspecialized portion of the peripheral nervous system, study of the expression and function of cannabinoid receptors in the hearing organ is of high interest. Stria vascularis and inner hair cells express CB(2) receptor, as well as neurites and cell bodies of the spiral ganglion. Cellular types such as supporting cells and outer hair cells, in which the expression of other types of functional receptors has been reported, do not significantly express CB(2) receptors in this study. An up-regulation of CB(2) gene expression was detected after an ototoxic event such as cisplatin treatment, probably due to pro-inflammatory events triggered by the drug. That fact suggests promising potential of CB(2) receptor as a therapeutic target for new treatments to palliate cisplatin-induced hearing loss and other ototoxic events which triggers inflammatory pathways.