MDMA (ecstasy) produces a unique set of behavioral effects in rats that distinguishes it from both stimulants and hallucinogens. In a series of behavioral tests, the effects of MDMA at various doses were compared with those of methamphetamine (a stimulant) and DOI (a hallucinogen). The behavioral profiles allowed researchers to differentiate MDMA from these other drugs. Additionally, four structural analogues of MDMA were tested, but none exactly replicated MDMA's profile, some resembling the stimulant or hallucinogen instead. This highlights MDMA's distinct pharmacological identity as an entactogen.
A computational model of associative learning, the double error dynamic asymptote model, can help explain how spurious associations arise in schizophrenia. The model simulates mediated conditioning, mediated extinction, and a novel prediction of mediated enhancement of latent inhibition. Manipulating a parameter that controls memory retrieval and the decay of nonperceptual representations produces effects similar to those caused by ketamine on associative memories and mediated learning. The model offers a plausible error-correction mechanism that may account for associative deficits observed in animal models of schizophrenia.
A new chemical, t-BOC-3,4-MDMA, is a modified form of MDMA that can evade detection in the illicit drug market and can be converted into the controlled substance MDMA. In mice, a 5 mg/kg dose of t-BOC-3,4-MDMA significantly altered place preference, indicating rewarding effects, and at 0.5 mg/kg/infusion it induced drug-taking behavior in self-administration tests. Microdialysis in rats showed that the chemical increased dopamine levels in the striatum. These findings suggest that t-BOC-3,4-MDMA has potential for misuse.