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Memory impairment and hippocampus specific protein oxidation induced by ethanol intake and 3, 4‐Methylenedioxymethamphetamine (MDMA) in mice

Clara Ros‐simó, Maria Moscoso‐castro, Jéssica Ruiz‐medina, Joaquim Ros, Olga Valverde

Journal of Neurochemistry March 25, 2013 DOI: 10.1111/jnc.12247 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Adolescent CD1 mice
Interventions Ethanol MDMA
Duration 72 hours after treatment
Topics MDMA
Keywords Hippocampus Oxidative stress Radial arm maze Prefrontal cortex Neurotransmitter Pharmacology Ethanol
Citations 35
Key findings MDMA treatment caused oxidative damage to specific hippocampal proteins and impaired long-term declarative memory, whereas ethanol alone did not affect memory acquisition.

Abstract

Abstract Ethanol and 3, 4‐Methylenedioxymethamphetamine ( MDMA ) are popular recreational drugs widely abused by adolescents that may induce neurotoxic processes associated with behavioural alterations. Adolescent CD 1 mice were subjected to ethanol intake using the drinking in the dark ( DID ) procedure, acute MDMA or a combination. Considering that both drugs of abuse cause oxidative stress in the brain, protein oxidative damage in different brain areas was analysed 72 h after treatment using a proteomic approach. Damage to specific proteins in treated animals was significant in the hippocampus but not in the prefrontal cortex. The damaged hippocampus proteins were then identified by mass spectrometry, revealing their involvement in energy metabolism, structural function, axonal outgrowth and stability, and neurotransmitter release. Mice treated with MDMA displayed higher oxidative damage than ethanol‐treated mice. To determine whether this oxidative damage was affecting hippocampus activity, declarative memory was evaluated at 72 h after treatment using the object recognition assay and the radial arm maze. Although acquisition in the radial arm maze was not impaired by ethanol intake, MDMA treatment impaired long‐term memory in both tests. Therefore, oxidative damage to specific proteins observed under MDMA treatment affects important cellular function on the hippocampus that may contribute to declarative memory deficits.

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