Psychedelia.dk

Det har de mig bekendt heller ikke...MDMA virker frigivende på serotonin imens SSRI'er jo hæmmer genoptagelsen. Hvilket også ligger i navnet: Selective Serotonin Reuptake Inhibitor = Selektiv Serotonin Genoptagelses Hæmmer.

Ashoka: er det før eller efter MDMA det er godt og spise det der? altså hvornår hjælper det bedst?

Some studies suggest that possible MDMA-induced neurotoxicity to the serotonin system can be largely prevented by taking a double dose of fluoxetine (Prozac) or another SSRI shortly after starting to "come down". Post-E Prozac in particular mitigates the oxidative stress and consequent risk of serotonergic axon damage caused by reactive products of dopamine deamination. The long-acting SSRI Prozac/fluoxetine, and its even longer-acting metabolite norfluoxetine, apparently prevents the uptake of dopamine (and any toxic metabolite(s)?) into the serotonergic nerve terminals by binding to the serotonin reuptake transporter with higher affinity than MDMA or serotonin. Unfortunately, although liquid refreshment is now freely available at most MDMA-propelled raves, most chill-out rooms don't offer Prozac. Two days and more after taking MDMA, heavy recreational users are typically more irritable, subdued, unsociable and subtly less empathetic than before their weekend binge: the "Terrible Tuesday's" syndrome of midweek blues. So with cruel irony, two or three days after communing on Ecstasy and declaring their undying love, couples are more likely to have rows and split up. Other heavy regular MDMA users, even those who aren't self-medicating for a pre-existing malaise, may experience depression, anxiety, emotional burnout, rejection-sensitivity, fatigue, insomnia, aching limbs, subtle cognitive deficits, immune system dysfunction, body temperature dysregulation, and a sense of derealisation or depersonalisation for several weeks or months afterwards. This litany of woe sounds a high price to pay even for the peak experience of a lifetime.

Administered at low doses, selegiline is neuroprotective against possible damage to the serotonergic fine axon terminals caused by overconsumption of the popular drug MDMA (Ecstasy). Several competing theories exist that purport to explain MDMA-induced neurotoxicity. One theory blames the deamination by MAO-B of excessive dopamine taken up by the membrane-bound transporter into the depleted serotonin terminals. This abnormal uptake follows MDMA-induced reversal of the serotonin reuptake pump. In the absence of MAO-B inhibition, deamination by MAO-B of excess dopamine taken up into the serotonergic axon terminals is liable to generate a glut of toxic free radicals. These highly reactive compounds cause membrane lipid peroxidation and consequent fine terminal degeneration. Selegiline prevents such serotonergic damage, in theory at any rate.
On the other hand, co-administering unselective selegiline dosages or unselective irreversible MAOIs like tranylcypromine (Parnate) or phenelzine (Nardil) with MDMA is potentially lethal.