PLoS ONE
February 10, 2010
Clara Touriño, Andreas Zimmer, Olga Valverde
55 citations
The main psychoactive compound in cannabis, THC, can protect against brain damage caused by MDMA (ecstasy) in mice, primarily by preventing the dangerous rise in body temperature that MDMA induces. MDMA caused hyperthermia, glial activation, and loss of dopamine terminals in the striatum, especially at a warm ambient temperature of 26 degrees Celsius. THC prevented MDMA-induced hyperthermia and glial activation at both room and warm temperatures, and reversed dopamine terminal loss at the warm temperature. These protective effects were blocked by the CB1 receptor antagonist AM251 and in CB1 knockout mice, but only partially blocked by CB2 receptor antagonism or knockout, indicating that THC's neuroprotection is primarily mediated by CB1 receptor activation reducing hyperthermia, with CB2 receptors contributing to reduced neuroinflammation.
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.
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.