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dc.rights.licenseopenen_US
hal.structure.identifierDe Montfort University [Leicester, United Kingdom] [DMU]
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorDI MICELI, Mathieu
hal.structure.identifierDe Montfort University [Leicester, United Kingdom] [DMU]
dc.contributor.authorOMOLOYE, Adesina
hal.structure.identifierDe Montfort University [Leicester, United Kingdom] [DMU]
dc.contributor.authorGRONIER, Benjamin
dc.date.accessioned2022-12-12T10:42:21Z
dc.date.available2022-12-12T10:42:21Z
dc.date.issued2022-01-10
dc.identifier.issn0278-5846en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/170556
dc.description.abstractEnMethylphenidate (MPH) is a drug routinely used for patients with attention deficit and hyperactivity disorder (ADHD). Concerns arise about psychostimulant use, with dramatic increases in prescriptions. Besides, antipsychotic drugs are often administered in combination with MPH. In this study, we examine the consequences of MPH exposure in combination with dopamine D2 receptor antagonism (eticlopride) on midbrain dopaminergic neurons in anaesthetised rodents, using in vivo extracellular single-cell electrophysiology. As expected, we show that methylphenidate (2 mg/kg, i.v.) decreases the firing and bursting activities of ventral tegmental area (VTA) dopamine neurons, an effect that is reversed with eticlopride (0.2 mg/kg, i.v.). However, using such a paradigm, we observed higher firing and bursting activities than under baseline conditions. Furthermore, we demonstrate that such an effect is dependent on dual alpha-1 and dopamine D1 receptors, as well as glutamatergic transmission, through glutamate N-Methyl-D-aspartate (NMDA) receptor activation. Chronic MPH treatment during adolescence greatly dampens MPH-induced excitatory effects measured at adulthood. To conclude, we demonstrated here that a combination of methylphenidate and a dopamine D2 receptor antagonist produced long-lasting consequences on midbrain dopamine neurons, via glutamatergic-dependent mechanisms. © 2021
dc.language.isoENen_US
dc.subject.enMethylphenidate
dc.subject.enAntipsychotics
dc.subject.enDopamine
dc.subject.enGlutamatergic neurotransmission
dc.title.enCharacterisation of methylphenidate-induced excitation in midbrain dopamine neurons, an electrophysiological study in the rat brain
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.pnpbp.2021.110406en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed34339759en_US
bordeaux.journalProgress in Neuro-Psychopharmacology and Biological Psychiatryen_US
bordeaux.volume112en_US
bordeaux.hal.laboratoriesNutriNeurO (Laboratoire de Nutrition et Neurobiologie Intégrée) - UMR 1286en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINRAEen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03894405
hal.version1
hal.date.transferred2022-12-12T10:42:23Z
hal.exporttrue
dc.rights.ccPas de Licence CCen_US
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