• Psychedelic Drugs Welcome Guest
    View threads about
    Posting RulesBluelight Rules
    PD's Best Threads Index
    Social ThreadSupport Bluelight
    Psychedelic Beginner's FAQ

The Big & Dandy MDAI Thread

Status
Not open for further replies.
Stopping SSRIs without tapering is associated with brain zaps. No one knows exactly why brain zaps occur, but with both them and MDAI discontinuation is associated with brain zaps. Perhaps it's either low serotonin levels or simply a sudden drop off in the amount of serotonin in the synapse that leads to them starting. But when we're talking about infrequent use by a person who gets brain zaps of either MDAI alone in high doses or MDAI in standard doses with a DARI or releaser it's difficult to say which is going to cause more damage on average. I do get brain zaps after using aMT for two days in a row, so for me personally I'm going to go with the devil I know and use MDAI with a DARI or releaser if I want strong euphoria.
 
must admit I've been on and off various SSRI's over the last 5 years or so and never really experienced brain zaps as such, at least not the sort of noticable ones some report of.

this forum is fucking ace.
 
I've never really had brain zaps myself other than one time I stopped cold turkey from a long spell on a high dose of paroxetine (Seroxat). That was just pure hell in every way but also coincided with sudden cessation of a gram a day IV heroin habit and was brought down to insane levels of crapness by eating a whole pack of Nytol (diphenhydramine) trying desperately to knock myself out for a while but having no idea about it's delirient properties. That really was almost as much fun as it sounds :|

But other than that never had brain zaps despite extremely heavy MDMA (and other stuff) abuse and lengthy periods on SSRIs. I did feel several shades of pure shite for a few days when I went much over 500mg of MDAI - either alone or in combo - in a session though. Less appears to be more really - chasing your own tail to try to make it something it isn't. Great as an ingredient in various combos though and also nice on its own or with alcohol and the like too if you take it on its own terms :)

High (or IV) doses will get you a bit of the MDMA mellow magic but comes with a heftier price tag than MDMA itself does with heavy use for me. YMMV, of course.
 
ebola? said:
Well, as a caveat, we can't really narrow down the negative after-effects of MDMA to depletion of serotonin alone. However, MDAI has a few advantages over MDMA, which make the former a bit less likely to cause negative after-effects:
1. There is no concurrent release of dopamine, meaning that there will be reduced oxidative stress (at DA and 5ht neurons).
2. Due to its cylcization, MDAI doesn't form the same toxic metabolites that MDMA does.
3. MDAI doesn't inhibit tryptophan hydroxylase as MDMA does.

However, MDAI is not magic; if used in doses a few times the active 150 mg or a few days in a row, you very likely will experience negative after-effects.

ebola
Click to expand...

So you think the infamous tuesday blues thing is not only a serotonin shortage but the neuronal damage/stress is involved?
Didn't know about MDMA inhibiting tryptophan hydroxylase, is it known after how long the inhibition is reversed?
Another thing I was wondering is: is MDMA also a SRI other than a releaser?
 
Yes, MDMA is a reuptake inhibitor (though it's much stronger as a releaser); It's very rare for a releaser to not also act as a reuptake inhibitor.
 
Well, it's Monday and the 1g of MDAI I got on Thursday morning was gone by Saturday night. The first few bombs were good but the effect diminished with redosing, so there does seem to be a fairly fast tolerance build-up. Now, I feel a pleasant sort of afterglow, like the day after smoking a lot of weed - I feel inclined to smile and be nice to people. :) The other afer-effect is that I feel sexually quite sensitised - ready for a good shag or two! :)

There's a bit of a, well not a headache, more a vague fuzziness in the brain, sort of a hangover but it's not strong and there's no actual physical pain. My eyes feel a bit tired, focussing requires a bit of effort sometimes.

Apart from that, no worries! Overall, I'd say it's not a bad drug - not earth-shakingly fantastic in its effects but nice enough. I'll give it a rest for now because I think the after-effects may get heavier I kept on dosing but I'd have no concerns about doing it again.
 
I've just been doing some experiments with a batch of mdai that I bought recently as I am convinced that there is a lot of variation between batches and I also think the bioavailability is very low, which can account for some less than impressive experiences. This is my third batch of mdai, the first (tan) seemed to work fine, the second (white) was not mdai and this one looks OK and tests OK but I am not getting the hit I used to from the first.

As I have never been able to get mdai to completely dissolve in water and have usually ended up taking it as a suspension, this time I thought I would see what it would take to completely dissolve it. I tried neat lemon juice and that left plenty of residue, even after a good old fashioned cooking on a spoon. I tried 96% ethanol which was as effective as pure water, ie not at all. With a mixture of lemon juice and ethanol and water, heated, I eventually got the liquid to turn a slight yellow colour, indicating that something had dissolved, but there was an awful lot of residue.

So I separated off the powder residue, which was still tan coloured, from the liquid and ran a Marquis test on both. The residue reacted the same way as the original powder, turning a deep red. The solution went orange to yellow. I know that Shambles gets his samples to dissolve by cooking but has anyone else tried disssolving before swallowing?
 
TheAzo said:
Yes, MDMA is a reuptake inhibitor (though it's much stronger as a releaser); It's very rare for a releaser to not also act as a reuptake inhibitor.
Click to expand...

Isn't MDAI just a releaser and not a SRI? This would make some sense to me.

I also have to update on my preious (2w ago) experiment with insufflated crystalized tan MDAI: I tried again yesterday night, 40mg insufflated exactly as the last time. Got absolutely zero effects! But I got a theory ongoing and need more experiments to ind out.
 
cmon simpltons

^^^ basicly when these drugs bind to the SERT and DAT, which is the transport proteins, and pretty much responsible for the effects they reverse the flow of chemicals, so that instead of flowing extracellular into intracellular they flow intracellular to extracellular. They literally take the neurotransmitters from inside the cell and flood the synaptic cleft where ya want them to be so they can act on the lovely receptors giving there effects. Everyone plz take a second and think about it, if a drug puts a transporter in reverse how is it ganne reuptake into the cell. Basicly drugs with mechanisms of action like this make the transporters so they cannot reuptake; however sense they release neurotransmitters lets call them releasers ok plz? Does anyone get the picture, or is it just me? Someone will correct me if I am wrong as this is BL, but odds are I will get more people posting random text.
 
Last edited:
Everyone plz take a second and think about it, if a drug puts a transporter in reverse how is it ganne reuptake into the cell.
Click to expand...

Well, it could alternately be that the timing of synaptic release allows some passive diffusion back into the cell. However, binding affinities demonstrate that most every releaser is also a reuptake inhibitor.

ebola
 
ill edit my post as i reread what you said i think i understand what your trying to say
 
Last edited:
Well I think it's pretty obvious that while reversing SERT a drug also inhibits the reuptake. What I was thinkin tho is: is possible that some drugs reverse SERT and release 5-ht, and then after say few hours the SERT go back to working as normal reuptaking some of the 5-ht that's been released, while other drugs keep blocking the SERT even after it's back working normally? Basically is it possible that SRI effects can either coincide with the release action or last a good deal longer depending on the drug?
 
Can I restate with WHILE the chemical is bound to the transporter protein it will be a releasing agent and hense also inhibit the reuptake. What timing there?
Click to expand...

When a ligand binds to a receptor, it may be conceptualized as constantly forming and breaking hydrogen bonds with the active site on said receptor (this is a bit of an abstraction, as these bonds are subject to quantum-level dynamics). Thus, a releaser of remarkably low binding affinity in contrast with its efficacy could theoretically fail to significantly inhibit reuptake.

All of this is idle speculation: it turns out that releasers of significant efficacy all bind with sufficient affinity to act as reuptake inhibitors.

ebola
 
what stimulant would be better to take with mdai - buphedrone or ethcathinone? i know that mdpv should be the least neurotixic but i am not very comfortable with using it... thks.
 
Whats going on!

Pretty crappy isnt it. Since the ban of cathinones I find myself having to rifle through what is supplied on steet corners to prepare myself for a good rave. God knows whats gone through my body. At least with what was a 'legal high' you knew what you were getting and if you didn't like it you could get a refund! Try that on a street corner. After observing this thread for months, it looks like we are left with is decent people having to rifle through crappy legal highs just to prepare themselves for their annual good night rave. I work too hard for this shit! Maybe im just an old time raver still searching for that time I was at the leeds Love parade when I took my first pill with a can of red bull on an empty stomach! But hey mabe we have Fury?? Just hope something develops before I go Global Gathering!x
 
Someplace saying they now have white MDAI, which is supposedly stronger.

Anyone want to comment on how appearance relates to strength?

The stuff I had before was tan and I needed 250mg for a worthwhile hit, when supposedly 125mg should do it.
 
I bought white crystalline 'mdai' and it was not mdai. It tested completely differently with Marquis.
 
Silverfox said:
I bought white crystalline 'mdai' and it was not mdai. It tested completely differently with Marquis.
Click to expand...

There's a vendor selling mephedrone as MDAI.
Table 1

WSa Label Comment
1 NRG-1 - Butylone + MDPV
2 NRG-1 - Flephedrone (4-fluoromethcathinone)
3 NRG-1 - Flephedrone + MDPV
3 NRG-2 - 4-Methyl-N-ethylcathinone
4 NRG-1 - Flephedrone + MDPV
5 NRG-1 - Caffeine + traces of mephedrone
6 NRG-1 - Naphyrone
7 NRG-1 - Butylone + MDPV
8 MDAI - Inorganic composition
9 NRG-1 - Mephedrone
10 NRG-1 - Inorganic composition
10 NRG-2 - Mephedrone + benzocaine
11 NRG-1 - Mephedrone
11 NRG-2 - Mephedrone
11 DMC - Caffeine + lidocaine
11 MDAI - Mephedrone
12 NRG-2 - 4-Methyl-N-ethylcathinone
Click to expand...
 
I tried 75 mg of the brown MDAI orally a little while back and it was a pleasant experience. I didn't feel at all sick afterwards - in fact I didn't notice when it wore off as I fell asleep. Combined with a small dose of butylone (50mg) and buphedrone (10 mg) which blended nicely. I may be impure but I don't know that it's worth cleaning up unless you plan to smoke it of IV.
 
Status
Not open for further replies.
Top