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Jéssica Ruiz‐medina

Pompeu Fabra University

2 papers in the library · 68 citations · publishing 2011-2013

Papers

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

Journal of Neurochemistry March 25, 2013 Clara Ros‐simó, Maria Moscoso‐castro, Jéssica Ruiz‐medina et al. 35 citations

Ethanol and MDMA, two widely abused recreational drugs, cause oxidative stress in the brain. In adolescent CD1 mice, acute MDMA treatment, alone or combined with ethanol, produced significant protein oxidative damage specifically in the hippocampus, but not in the prefrontal cortex, 72 hours after treatment. The damaged proteins are involved in energy metabolism, structural function, axonal outgrowth and stability, and neurotransmitter release. MDMA-treated mice showed greater oxidative damage than ethanol-only mice. While ethanol did not impair radial arm maze acquisition, MDMA impaired long-term declarative memory in both the object recognition assay and the radial arm maze, suggesting that MDMA-induced oxidative damage to hippocampal proteins contributes to memory deficits.

The A2a adenosine receptor modulates the reinforcement efficacy and neurotoxicity of MDMA

Journal of Psychopharmacology January 24, 2011 Jéssica Ruiz‐medina, Catherine Ledent, Olga Carretón et al. 33 citations

Adenosine A2a receptors are crucial for the rewarding and neuroinflammatory effects of MDMA. In mice lacking these receptors, MDMA failed to support self-administration, indicating a complete loss of its reinforcing properties. Additionally, the neurotoxic regimen of MDMA caused increased glial activation in the striatum of normal mice, but this inflammatory response was attenuated in mice without A2a receptors. Acute effects on body temperature, locomotion, and anxiety were similar in both genotypes. This work identifies the A2a adenosine receptor as a key mediator of MDMA's addictive potential and neurotoxicity.