In rats, MDMA (ecstasy) impairs both short-term and long-term visuospatial memory while increasing long-term potentiation (LTP) in the prefrontal cortex. Its brominated analog, 2Br-4,5-MDMA, preserves long-term visuospatial memory and slightly accelerates short-term memory compared to controls, yet also increases LTP similarly to MDMA. These findings suggest that aromatic bromination of the MDMA molecule, which eliminates typical entactogenic-like effects, also modifies effects on higher cognitive functions like visuospatial learning. The cognitive changes do not appear linked to the increase in prefrontal cortex LTP.
MDMA (Ecstasy) suppressed helping behavior in adult male rats at doses of 5 mg/kg and 10 mg/kg, fully eliminating the behavior, while lower doses (1 mg/kg and 0.5 mg/kg) caused partial inhibition only after the rats switched roles. The lowest dose (0.25 mg/kg) had no effect. Electrophysiological recordings showed that MDMA reinforced long-term depression in the nucleus accumbens core and increased long-term potentiation in the anterior cingulate cortex, with the latter depending on serotonin and oxytocin. These neuroplastic effects align with mechanisms thought to promote prosocial behavior, yet the drug disrupted helping behavior, suggesting MDMA may impair neural processes essential for executing helping actions without reducing the willingness to help.