par Cutando, Laura;Puighermanal, Emma;Castell, Laia;Tarot, Pauline;Bertaso, Federica;Bonnavion, Patricia 
;de Kerchove d'Exaerde, Alban ;Isingrini, Elsa;Galante, Micaela;Dallerac, Glenn;Pascoli, Vincent;Lüscher, Christian;Giros, Bruno B.G.;Valjent, Emmanuel
Référence Addiction biology
Publication Publié, 2020-01-01
;de Kerchove d'Exaerde, Alban ;Isingrini, Elsa;Galante, Micaela;Dallerac, Glenn;Pascoli, Vincent;Lüscher, Christian;Giros, Bruno B.G.;Valjent, EmmanuelRéférence Addiction biology
Publication Publié, 2020-01-01
Article révisé par les pairs
| Résumé : | Prescription stimulants, such as d-amphetamine or methylphenidate are used to treat suffering from attention-deficit hyperactivity disorder (ADHD). They potently release dopamine (DA) and norepinephrine (NE) and cause phosphorylation of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluA1 in the striatum. Whether other brain regions are also affected remains elusive. Here, we demonstrate that d-amphetamine and methylphenidate increase phosphorylation at Ser845 (pS845-GluA1) in the membrane fraction of mouse cerebellum homogenate. We identify Bergmann glial cells as the source of pS845-GluA1 and demonstrate a requirement for intact NE release. Consequently, d-amphetamine-induced pS845-GluA1 was prevented by β1-adenoreceptor antagonist, whereas the blockade of DA D1 receptor had no effect. Together, these results indicate that NE regulates GluA1 phosphorylation in Bergmann glial cells in response to prescription stimulants. |
