Not sure if OP will see this as the threads a few months old, but...
ALCAR is a good choice for reducing neurotoxicity. But if it's causing you comedown problems, L-Deprenyl (selegiline) might be a better choice. You might want to give it a shot. I don't roll anymore, but I took it before and after my last couple of rolls, and had very easy comedowns both times. Overall, though, you're doing the right thing. NO ONE with an ounce of sense and an internet connection should ever take MDMA without a well-researched pre and post load regimen.
So on selegilinie / L-Deprenyl, and comedowns:
Conventional rave wisdom has it that comedowns and tuesday blues happen because all your serotonin has been used up. People think they can rescue themselves by taking 5-HTP. But that doesn't work, and the reason it doesn't is because MDMA depletes Tryptophan hydroxylase (TPH), the enzyme that makes Serotonin. No enzyme, no serotonin, no matter how much 5-HTP you hook down.
Luckily, we have L-Deprenyl, which, when taken before a roll, not only can reduce peroxide formation and other routes oxidative stress in the brain, but also rescues your TPH, so you can continue manufacturing the blessed serotonin. It's not sold in the states, as far as I can tell, but pretty easy to find through a google search.
The Study -->
The monoamine oxidase-B inhibitor L-deprenyl protects against 3,4-methylenedioxymethamphetamine-induced lipid peroxidation and long-term serotonergic deficits.
Sprague JE, Nichols DE.
Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana, USA.
Abstract
3,4-Methylenedioxymethamphetamine (MDMA)-induced serotonergic neurotoxicity was assessed in the striatum, hippocampus and frontal cortex of rats by using [3H]paroxetine binding to label serotonin (5-HT) uptake sites and 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels as markers of serotonergic function. NMDA (40 mg/kg) induced a significant decrease in both [3H]paroxetine binding Bmax and 5-HT and 5-HIAA levels 7 days after treatment. The monoamine oxidase-B inhibitor L-deprenyl (2 mg/kg) administered 30 min before MDMA blocked these decreases. MDMA (40 mg/kg) also maximally increased the formation of thiobarbituric acid reactive substances (an indicator of lipid peroxidation) 12 hr after treatment in all three brain regions studied. This increase in malondialdehyde formation was also blocked by pretreatment with L-deprenyl. Tryptophan hydroxylase (TPH) activity was also significantly reduced 18 hr after MDMA. L-Deprenyl reversed this decrease in TPH activity. Another experiment confirmed that a significant fraction of [3H]dopamine uptake into hippocampal synaptosomes was blocked by 500 nM fluoxetine, a selective 5-HT uptake inhibitor. These data suggest that the deamination by monoamine oxidase-B of excessive dopamine within the 5-HT terminal generates hydrogen peroxide that may lead to membrane lipid peroxidation, and perhaps other oxidative insults, resulting in selective 5-HT terminal degeneration subsequent to MDMA treatment.
PMID: 7538579 [PubMed - indexed for MEDLINE]
