• N&PD Moderators: Skorpio | thegreenhand

Natural NMDA antagonists

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^ tried what, high dose harmaline...can you be more exact in what you did?

is there any real danger to MAO inhibition as long as one is aware to avoid the substances that can in conjucntion cause the problems such as tyramine...????
 
^Maybe a peak in oxidative stress when all the accumulated dopamine is targetted by MAO-B?
 
^ How is that going to happen? If you're using a selective MAO-A inhibitor, MAO-B will still be taking care of dopamine per usual.

If you're using an MAO-B inhibitor, you still don't accumulate mass amounts of dopamine because MAO-A is still around to destroy it.

If you're using a nonselective inhibitor, I don't think DA just keeps accumulating, either. It's not as if high dose selegiline users develop hyperkinesia. You still have other methods of metabolizing it, so it should raise levels but not beyond a certain point.

But even if it would, since MAO-B levels take quite a while to accumulate to natural levels, they'll be slowly removing any build up while they regenerate, so it's not like there'll be a sudden spike in dopamine metabolism. IIRC, the half life for MAO-B regeneration is something like 14 days.

As long as you're abstaining from everything you need to abstain from, something like selegiline should only do positive things for you. I think I've been on it for 2 weeks now, and I love it.

Hammilton
 
^Indeed, I was speaking of nonselective inhibitors and forgot that Harmaline isn't one.

I know you wouldn't keep upping your dopamine levels on a nonselective MAOi, but when your dopamine levels are returning to normal after nonselective inhibitors, that should result in (slightly) elevated levels of oxidative stress, shouldn't it?
 
^ How is that going to happen? If you're using a selective MAO-A inhibitor, MAO-B will still be taking care of dopamine per usual.

If you're using an MAO-B inhibitor, you still don't accumulate mass amounts of dopamine because MAO-A is still around to destroy it.

Catechol-O-methyltransferase enzymes break dopamine down too.

Apparently, there are a number of inhibitors of these enzymes in foods and herbs and stuff.
 
^ tried what, high dose harmaline...can you be more exact in what you did?

is there any real danger to MAO inhibition as long as one is aware to avoid the substances that can in conjunction cause the problems such as tyramine...????

Harmine inhibits MAO-A but not B.

Be aware there's a harmine-containing plant called Banisteriopsis caapi
aka "yage" or "ayahuasca" (mostly used to make DMT orally active) as well as "passionflower" (refers to quite a few plants whos species name begin with "passiflora").

Syrian rue (Peganum harmala) is the concoction I used, bought from a place called Eye Of Horus (one of those places that serve the wicca/goth community but also had a shitload of drug paraphernalia like bongs and pipes as well as stuff like Syrian rue and salvia(!)[which I wasted $25 on not realizing the good stuff is really in the extracts, not so much the dried leaf version]). There's got to be a few Western Pennsylvania bluelighters that remember this store...it was open until 2000 when Pittsburgh and PA state police shut it down due to newly reinforced anti-paraphernalia laws. I also remember one time buying what I thought was "crystallized betel nuts" due to a misleading sign on the crystal-containing bottle...turned out the crystal was flesh-eating lime and I had to literally run to a ER to stop the burning in my mouth. I was rather lucky I didn't try to swallow the crap. I had to tell the ER I was drunk when they asked why I had lime in my mouth...they couldn't stop laughing at me even as I was in serious pain. My mouth fully recovered in a few weeks - the viscera in it easily regenerates thankfully.

I only really did it once in college in a probably inappropriate situation (I was living in dorms and already in trouble regarding substance abuse of "odd" chemicals like DXM and salvia). I ate this stuff whole...disgusting. The gravity increase occured when I was out at a computer lab reading various trip reports to see how fast it would kick in...I literally spent half of the walk back crawling when there was no one around. I'm sure if there had been anyone really paying attention in security I would've ended up in a hospital bed with charcoal being shoved down my throat. After I got to my room, the 8-bit "pixelated" hallucinations began...they were light sensitive as I could only see them in the dark (not just when I closed my eyelids). After about 6-8 hours all of the effects were gone, gravity and all.

This chemical has a somewhat heavy bodyload (you'll definitely be cooling your heels the next day). As far as restrictions there aren't too many...you could probably even get away with a little tyrosine-containing food if it weren't for the fact you'll probably have no appetite. Remember to drink water on the stuff, I guess.

I have no idea if syrian rue would make DMT orally soluble (i.e. by eating a plant or powder containing DMT instead of smoking or injecting it). I couldn't see why not if the harmine is the same as B. caapi. I personally wouldn't do this mixture first without seeing how the harmine affects you by itself, though. I don't think I could handle both DMT and harmine together...I definitely would be having some panic attacks.
 
^ How is that going to happen? If you're using a selective MAO-A inhibitor, MAO-B will still be taking care of dopamine per usual.

If you're using an MAO-B inhibitor, you still don't accumulate mass amounts of dopamine because MAO-A is still around to destroy it.

If you're using a nonselective inhibitor, I don't think DA just keeps accumulating, either. It's not as if high dose selegiline users develop hyperkinesia. You still have other methods of metabolizing it, so it should raise levels but not beyond a certain point.

But even if it would, since MAO-B levels take quite a while to accumulate to natural levels, they'll be slowly removing any build up while they regenerate, so it's not like there'll be a sudden spike in dopamine metabolism. IIRC, the half life for MAO-B regeneration is something like 14 days.

As long as you're abstaining from everything you need to abstain from, something like selegiline should only do positive things for you. I think I've been on it for 2 weeks now, and I love it.

Hammilton

I thought about getting on that drug because of the mostly positive stories I hear from responsible users, but what stopped me in the past was the two to four week "detox" I would have to do from all psychiatric drugs, which back then my depression wouldn't have allowed. Now that I don't take any psychiatric drug regularly (mostly because of all the "poopouts" and side effects) I found another excuse not to take selegiline...mainly the fact I'd probably have to give up all recreational use of all drugs in general...I like my DXM and prescription speed (among other things) too much unfortunately.
 
^ why and why

and MAOB-I does not engender this

and again even a non-selective MAO-I has no dangers if one is not on any conflicting meds and watches their diet accordingly so why does everyone make it sound like it is inherently and implicitly dangerous as it does not have to be in many circumstances...if one wants to give warning to the obvious of scenarios where it can be, more power to ya, but this is not universally so

also people seem to have this unfounded fear of combining certain things and again that such is implicitly and inherently dangerous, but actually if these 'dangerous' combos (such as those people scream will cause SE syndrome) are metered to reflect the interaction they can not only not be dangerous, but have greater benefit and effect in many cases

OK, i guess this thread is way off course :\

anyway, to date it appears there are no naturally derived NMDA antagonists that are truly recreational...though i still want to explore psychotridine a bit more...and while it is a mixed ope/NMDA-antag Hodgkinsine as well, which will be soon enough ;)
 
Lux, psychotridine makes me wonder, isn't that fairly closely related structurally to metabolites of physostigmine analog of some sort? a polymeric form of such a metabolite, I forget which analog, that is neurotoxic?
 
as what i think is an interesting point if we look at the classical drugs for most all of the main types of psychoactives we have we have indeed natural counterparts or a natural substance is the standard, but what would one deem as the closest natural couterpart to K if any warrant to even be considered such as to being substantially close enough:

Stimulants: Cocaine (DARI); possible naturally occurring amphetamine and meth (standard) as in the Texas study and of course ephedrine, cathinone, and their analogues amongst others

Opioids: Morphine (standard)

CB agonists: THC (standard)

Depressants: Many GABAergics of varying nature such as Kava, Mulungu as well as others, many unexplored to date but known to have potential and there is speculation if not proof of naturally occuring known benzodiazepines including diazepam which is one standard

Varying Psychedelics: Mescaline (PEA) , DMT (tryptamine), ...etc

Dissociatives:
None are quite K so to speak, but thoughts on which are most similar:
K-like: Salvinorin used sub-L, ...Muscimol ???... noscapine??? ...Ibogaine

also interesting for discussion maybe some combos that would further potentiate those that have some K-like aspects to get closer to K itself
 
Muscimol is not a dissociative. It's a sedative with some odd effects on visionn. Ibogaine shares as much with serotonergic psychedelics as with the NMDA antagonists.

I haven't gotten noscapine yet, unfortunately.
 
indeed i was thinking only Salv A as even close and that is a reach perhaps though some seem to liken certain modes of its use with a K-like experience, but was throwing them out there...
 
What about Glaucine? Until it is revealed what causes the supposedly psychoactive effects of this naturally occuring anti-tussive... NMDA antagonism, at least partially may be the answer.
 
I thought glaucine was a sigma antagonist?

I think you mean agonist.

Hammilton, if you've been following my post about DHEA as a sigma 1 agonist:
http://www.bluelight.ru/vb/showthread.php?t=422869

...you'd see my confusion. I have yet to find reports of hallucinogenic activity in purely sigma agonists like DHEA, Opipramol, Pentoxyverine, or Noscapine. (Please note that some of these are sigma subtype selective. Also, Opipramol has some 5ht2a antagonism which might counter hallucinogenic activity.) Glaucine, according to several accounts, produces colorful visuals.

I have become a little obsessed with purely sigma ligands because of past DXM experiences, and I wish I could learn more. I very much look forward to the possible bioassay you plan with Noscapine... if I understood correctly.
 
Well, don't hold your breath I'm afraid I'm really not actively pursuing it. I understand it's used in Israel to treat prostate cancer (or another cancer?), and being studied for that purpose in a lot of other studies, IIRC.

Nocapine, Hydrastine/Hydrastinine, azaprocin, psychotridine, herkinorin, and gaboxadol are a few of the things I really want to try but haven't yet. Oooh, that dichloromethylphenidate analogue, methyl cyclopentyl(3,4-dichlorophenyl)acetate. That's a super interesting drug even if it's less potent. At least I will be scratching Gaboxadol off my list soon.
 
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Oooh, that dichloromethylphenidate analogue, methyl cyclopentyl(3,4-dichlorophenyl)acetate.
Here's a pic of this compound, for anyone that's curious.
i1l4q0.png

Cool, a non-alkaloid stimulant!

My current dream list of exotic chemicals includes Histamine 3 antagonists like Thioperamide, sigma agonists like Opipramol, and the PDE4 inhibitor Rolipram. I'm more interested in "nootropic" type stuff rather than recreational.
 
i think if one mainlined a good amount of DHEA it may have some psychoactive effect, but otherwise ain;t happening
 
^ I just took 25mg's orally w/resveratrol. Theirs definately an increase in vitality and well-being, mostly with routine supplementation. Don't forget it also breaks down into steroid hormones like testosterone and estrogens. Some DHEA supplement's put the potent anti-oxidant resveratrol into them as well, mostly as a prohormone. According to Patrick Arnold, it significantly increases natural testosterone production from being both a selective estrogen receptor modulator and an aromatase inhibitor.
 
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