Modeling chronic brain exposure to amphetamines using primary rat neuronal cortical cultures

• Published in: Neuroscience 2014-09, Vol.277, p.417-434
• Main Authors: Nogueira, T.B, da Costa Araújo, S, Carvalho, F, Pereira, F.C, Fernandes, E, Bastos, M.L, Costa, V.M, Capela, J.P
• Format: Article
• Language: English
• Subjects: Adrenergic Uptake Inhibitors - pharmacology; Amphetamine - pharmacology; amphetamines; Animals; Astrocytes - drug effects; Astrocytes - pathology; Astrocytes - physiology; Caspase 3 - metabolism; Cell Count; Cell Culture Techniques; Cell Death - drug effects; Cell Death - physiology; Cells, Cultured; Cerebral Cortex - drug effects; Cerebral Cortex - pathology; Cerebral Cortex - physiopathology; chronic exposure; cortical neurons; Dose-Response Relationship, Drug; ecstasy; Excitatory Amino Acid Antagonists - pharmacology; Glutathione - metabolism; long-term neuronal cultures; Mitochondria - drug effects; Mitochondria - physiology; N-Methyl-3,4-methylenedioxyamphetamine - pharmacology; Neurology; Neurons - drug effects; Neurons - pathology; Neurons - physiology; neurotoxicity; Rats, Wistar; Receptors, Glutamate - metabolism; Time Factors
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2014.07.009

Highlights • Chronic exposure of primary rat cortical cultures to amphetamines up to 28 DIV. • The percentage of neurons and astroglia was altered by amphetamine exposure. • Amphetamine concentrations of 10 μM or lower are not neurotoxic up to 28 DIV. • Amphetamine (AMPH) not MDMA (“ecstasy”) decreased intraneuronal glutathione levels. • Long-term exposure to either AMPH or MDMA did not increase senescent neurons.