Det har svjv. længe været kendt for at substituere 100% for MDMA i mus - lad mig lige se om jeg kan finde artiklen. Det er en MDA-analog, som Nichols og hans hold fandt non-neurotoksiske i deres datidige forsøg.
Teknisk set menes MDAT at være en SERA/SRA (Serotonin Releasing Agent) - men så ved man heller ikke så meget mere.
Jeg vil anbefale dig at læse på Bluelight (advanced drug discussion) hvis du har i sinde at tage dette stof. Det skulle (efter hvad jeg har hørt - tag det lige med et ton salt, og læs op så du er sikker) være lidt ala MDAI, hvis det siger dig noget.
For mig virker MDAI som en slags stimulansfri MDMA, uden de voldsomme "skubbende" kræfter, der virkelig gør dig blæst. Alene er det ret sumpet, og ret udefinérbart - og har i visse tilfælde endda så stor effekt på følelserne, at det kan få en til at lukke op og græde igennem.
Jeg tror personligt at MDAI blandet med et empatogen, der har lidt flere stimulerende egenskaber end MDMA - såsom Methylon, kunne være rigtig lækkert. Sikkerheden skal selvølgelig tages alvorligt, og at blande to så ukendte stoffer (virkningsmæssigt set) bør gøres med forsigt og omhu
take care derude!
Edit:
Bingo!
Nonneurotoxic tetralin and indan analogues of 3,4-(methylenedioxy)amphetamine (MDA).
AbstractFour cyclic analogues of the psychoactive phenethylamine derivative 3,4-(methylenedioxy)amphetamine were studied. These congeners, 5,6- and 4,5-(methylenedioxy)-2-aminoindan (3a and 4a, respectively), and 6,7- and 5,6-(methylenedioxy)-2-aminotetralin (3b and 4b, respectively) were tested for stimulus generalization in the two-lever drug-discrimination paradigm. Two groups of rats were trained to discriminate either LSD tartrate (0.08 mg/kg) from saline, or (+/-)-MDMA.HCl (1.75 mg/kg) from saline. In addition, a 2-aminoindan (5a) and 2-aminotetralin (5b) congener of the hallucinogenic amphetamine 1-(2,5-dimethoxy-4- methylphenyl)-2-aminopropane (DOM) were also evaluated. None of the methylenedioxy compounds substituted in LSD-trained rats, while both 3a and 3b fully substituted in MDMA-trained rats. Compounds 4a and 4b did not substitute in MDMA-trained rats. Compounds 5a and 5b did not substitute in MDMA-trained rats, although 5a substituted in LSD-trained rats, but with relatively low potency compared to its open-chain counterpart. In view of the now well-established serotonin neurotoxicity of 3,4-(methylenedioxy)amphetamine and its N-methyl homologue 1, 3a and 3b were evaluated and compared to 1 for similar toxic effects following a single acute dose of 40 mg/kg sc. Sacrifice at 1 week showed that neither 3a nor 3b depressed rat cortical or hippocampal 5-HT or 5-HIAA levels nor were the number of binding sites (Bmax) depressed for [3H]paroxetine. By contrast, and in agreement with other reports, 1 significantly depressed all three indices of neurotoxicity. These results indicate that 3a and 3b have acute behavioral pharmacology similar to 1 but that they lack similar serotonin neurotoxicity.
http://www.ncbi.nlm.nih.gov/pubmed/1967651
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