Two retrospective comparisons of ecstasy users and non-users (Morgan et al. 2002; Reneman et al. 2002), one examination of ecstasy user demographics (Strote et al. 2002), one review paper (Teter 2001), and seven in-vitro and non-human animal studies (Bankson and Cunningham 2002; Fone et al. 2002; Mechan et al. 2002; Whitworth et al. 2002; Winsaur et al. 2002; Young et al. 2002) were located during this time period.

Memory versus Psychological Problems
Current and former ecstasy users were found in one retrospective study (Morgan et al. 2002) to have impaired verbal recall and increased behavioral impulsivity when compared with polydrug using or non-drug using controls. However, number of self-reported psychological problems was more strongly associated with use of other drugs, such as cannabis, LSD or amphetamines, and not ecstasy use.

Imaging: Ecstasy and Amphetamine Users
An imaging study comparing ecstasy users who either did or did not report intentional use of amphetamines with non-user controls found ecstasy + amphetamine users had lower radioligand (Beta-CIT) binding ratios in presumably dopaminergic brain areas than those using ecstasy alone. The ecstasy-alone users had higher Beta-CIT binding than controls (Reneman et al 2002). These study findings do not support a link between ecstasy use and reduced dopamine function or parkinsonism.

Demographics
The demographic study (Strote et al. 2002) found that undergraduate ecstasy use (increased from 1997 to 2000) was associated with marijuana and other drug use.

Rats: Hyperthermia, Hyperactivity, Drug Discrimination
The pharmacology behind MDMA-induced hyperthermia in rats was examined in one study (Mechan et al. 2002). Another study investigated the pharmacology of MDMA-induced hyperactivity in rats (Bankson and Cunningham 2002). Stimulation of dopamine D1 receptors, presumably via MDMA-induced dopamine release, is implicated in the production of elevation in rat body temperature. The study authors propose that the ability of ketanserin to block MDMA-induced elevation in human body temperature (Liechti et al. 2000) result from adrenergic effects rather than through 5-HT2A antagonism. A series of experiments examining hyperactivity in rats after MDMA suggest that were it not for the activation of 5HT2C receptors (via serotonin release and perhaps also direct action), MDMA would apparently produce even more hyperactivity through dopamine-related pathways (Bankson and Cunningham 2002). In a drug discrimination study, MDMA partially substituted for the novel compound 5,6,7,8-tetrahydro-1,3-dioxolo[4,5-g]isoquinoline (TDIQ), a possible sign that the MDMA stimulus may be produced in part from 5HT1A or noradrenergic activity (Young and Glennon 2002).

Long Term Effects in Squirrel Monkeys
A neurotoxic regimen of MDMA failed to alter the effects of the serotonergic drugs mCPP and fenfluramine on a repeated acquisition task in squirrel monkeys (Winsaur et al. 2002). Given that 5-HT is greatly reduced in MDMA-treated monkeys, study findings raise questions as to whether MDMA neurotoxicity is specific to neurons not involved on task performance.

Rats: Behavioral Change Unrelated to Neurotoxicity
A demonstrably non-neurotoxic MDMA regimen in young rats reduced number of social interactions and enhanced cocaine-induced place preference (Fone et al. 2002), suggesting that changes in behavior cannot be used as indications of selective serotonergic neurotoxicity. At the same time, these findings suggest that even non-neurotoxic doses of MDMA could potentially change behavior.

Developmental Effects
An in vitro examination of embryonic rat brain slices found that MDMA, cocaine and fluoxetine may all influence the development of glutamatergic cells, which "borrow" serotonin as they develop (Whitworth et al. 2002).