• N&PD Moderators: Skorpio | thegreenhand

NMDA antagonists for tolerance, a collection of the evidence and anecdotal reports

MeDieViL

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Yes every dose; and i really mean abscence seizures like my girlfriend sees me shouting making repetive movements and other seizure related things.

Minocycline or ginseng prevented this from occuring tough.

Apoligizies; indeed stims related posts i usually dont post much when sober:d ill try to remember to edit my posts.
 
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MeDieViL

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That anecdote comes from a person that was previously addicted; you are correct that just a few doses a day likely wont produce much tolerance.
(apologies forgot the edit function again)

"You can ride that coaster every day until you no longer find pleasure in it"
I do not consider this possible as recreational drugs directly induce pleasure; thus if they keep working pleasure will allways be found.

True ibogaine works on a shitload of differend pathways; there are so many involved in tolerance; nmda is just one of many.
 
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thikal

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Anecdote of a personal friend says that DXM allowed GBL to stay working well; its possible DXM is more effective for GBL perhaps give that a trial run and eventually amisulpiride. Id be curious for your results.

DXM at 60mg gave me a great mood lift when I tried it for tolerance when I abused GBL. I don't know if it is due to his serotonine reuptake inhibitor proprieties or/and to his NDMA antagonist proprieties (certainly boths). But i'm asmathic so it's not ideal for me, just took 1 week 2x60mg a day DXM. DXM or memantine on me keep the dose really low, but I clearly don't have the almost empathogenic/stimulant proprieties than I had at the beggining, and It can be explain that my GHB receptors are fucked and aren't "healed" by memantine and other NDMA antagonist. Iboga may have an other action on GHB receptors tolerance.

If I can find some amilsupride I will try it really slow and post my results. But this pharm have a shitload of side-effects and I don't know if it's really worth it. I read a little bit about this in the vidal, and I plan to take it at the low dosage (50-100mg/day) to avoid the antipsychotic part, but I'm not sure if the action I seek on GHB receptors take place at this dosage.

When tolerant to gbl it feels more sedating and far less euphoric this would indicate the problem is in the GHB receptor; G does indeed downregulate the ghb receptor wich amisulpiride upregulates again altough im sure GABAB downregulates as well.

I think GHB receptors take longer to reset because I don't have a physical tolerance yet (1,7mL and I'm sleeping like in the beggining), but don't have the euphoric part. Can you explain to me why amislpiride can upregulate GHB receptor and be an agonist GHB receptor in the same time? That's really interesting hehe!

Anecdotally its know the racetams potentiate several drugs (personally i experience massive mpa potentiation of mpa) however the racetams likely accelerate the formation of new tolerance (eg look up ethanol aniracetam) however one anecdote suggests that the combo of a racetam and a nmda antagonist offers the best of both worlds.

I tried piracetam with GBL, and without (more than a few months each) and didn't manage to find a real difference! Maybe I should try a more potent racetam, but my finances are low (that's an other problem hehe). A few months ago you weren't able to say if racetam stop the good effect on tolerance of NMDA antagonist, now you have evidences that there is no problems mixing them? I may be interested to read this anecdote because I was thinking on this question too!

From what I have heard, GHB/GBL is pretty reliable in terms of producing effects, pleasurable or otherwise, unless dosed very frequently.(seeing as it's an endogenous n/t and all). 1-3x a day is probably nothing to worry about. I guess it varies between people.

You are totally right. I took GBL during 1 year three time a day most days in the week and didn't have a big tolerance or big issues, and after a shitload (for me) of MDMA in 3 days and the depression that followed, I started to take it around the clock and shit followed^^

Thanks to share you're knowledge sekio and Medivil it's really appreciated!
 
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/navarone/

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*cough* just buy homotaurine *cough*
Pretty sure the whole deal with acamprosate's N-acetyl group was to make it patentable seeing as homotaurine is found in several seaweeds.

Acetylation of the compound you mentioned probably prevents homotaurine from becoming a zwitterion and thus increasing direct bioavailability by not needing an amino acid transporter to cross the BBB (a la gabapentin style).

Also on PubMed I have found only 5 papers when searching "Homotaurine NMDA" and they all inevitably refer to N-Acetyl-Homotaurine and it's NMDA antagonistic potential. One of these studies also suggests that acamprosate has antagonistic activity at the metabotropic glutamate receptors.
 
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