In humans, MDMA (3,4-methylenedioxy-N-methylamphetamine) is taken inside presynaptic serotonergic neurons via serotonin transporters (SERT). MDMA uptake simultaneously reverses SERT mediated serotonin transport and causes SERTs to pump serotonin into the synaptic cleft. This, in part, causes the intoxicating effects of MDMA. Normally SERTs would reuptake serotonin from the cleft. Brackets [x] signify "concentration of x".
"In humans, the relative selectivity [of MDMA] for monoamine modulation is NE &gt; 5-HT &gt; DA. During monoamine uptake into the neuronal cytoplasm, Na+, Cl and one molecule of the neurotransmitter are transported via the membranal transporter protein in a single step, followed by a second step in which K+ is transported out of the neuron via the transporter protein. Artificially increasing the extracellular K+ concentration can reverse this transport process by transporting Na+, Cl and neurotransmitter out of the cell, while transporting K+ into the cell. MDMA can take the place of K+ in this process by acting as a substrate that is transported into the neuron in exchange for Na+, Cl and neurotransmitter. MDMA thus directly stimulates efflux of cytoplasmic monoamines by reversing the action of biogenic monoamine transporters." Citation from:

Oeri E: Beyond ecstasy: alternative entactogens to 3,4-methylenedioxymethamphetamine with potential applications in psychotherapy. Journal of Psychopharmacology. 2020. PMID 32909493. doi:10.1177/0269881120920420.
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