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Matrine

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Soul137

Bluelighter
Joined
May 23, 2012
Messages
112
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I recently came across a strange website selling this compound, a notably long Kappa-Opioid agonist.
In an effort to collect the truest oddities of the hallucinogenic world, I did some research and found out almost exactly 0 about this drug. There are a few archived threads here on BL but I wanted to bring a new one to life to see if any information has been gathered since freaking 2008.

I can't even get accurate dosing information on it. No half-life; nothing. So, do any of you know anything? Have any of you intrepid souls tried this alien compound?
 
Salvia is also a kappa opioid agonist and I take it that this is what gives it the unique dysphoric and dissociative effects it has. However menthol is also a kappa opioid receptor agonist and it definitely does not have the same effects. Unless I am mistaken. Is it being sold along other psychoactive chemicals? I too am curious as to what effects it has.
 
Mostly the site sells enzymes and proteins and binding inhibitors, not recreational drugs, but they do have Dizocilpine and Scopolamine hidden among the (literally) hundreds of other things they sell.

Salvia is a k-opioid agonist; so is Ibogaine. I wouldn't call Salvia dysphoric, just insane. The thing about Matrine is that it also hits µ-opioid receptors, so it might balance out it's own negative vibes. Wonder what the fuck that would do to addictive properties. "My body wants more but my head is too full of fuck." Lol.
 
I'm really curious about kappa opioids, because of their dissociative effects - I absolutely love dissociatives. Maybe the subjective dysphoria has to do with the lack of dopaminergic activity what most dissociatives - at least those used recreationally - do have. But well if kappa agonism counters mu then it's no surprise as it would mean to work against endorphins, again the opposite of NMDA antagonism. Strange.
 
Most dissociatives don't hit dopamine. I don't know what you're saying.
 
Most dissociatives don't hit dopamine.
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a lot of them do, either as D2 receptor direct agonists or as dopamine reuptake inhibitors (notably PCP, ketamine, diphenidine is supected to be a DRI too)
 
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I've heard of PCP doing that (and experienced it's stimulant style rush while on it) but Ketamine? That seems hard to believe. CHECK: just looked it up. I see that you're correct; but then why does that not come across in the effects, or at least never seems to have for me? Or am I missing something about Dopamine's actions in the body and brain?
 
sekio said:
a lot of them do, either as D2 receptor direct agonists or as dopamine reuptake inhibitors (notably PCP, ketamine, diphenidine is supected to be a DRI too)
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Philip Seaman reported that ketamine and PCP bind to D2 but no other labs have ever been able to replicate his findings. I think in this case his findings should be viewed with skepticism. He reported the same thing for several of the mGlu2/3 agonists developed by Lilly and no one has been able to replicate those findings either.

http://www.ncbi.nlm.nih.gov/pubmed/19755662
http://www.ncbi.nlm.nih.gov/pubmed/20506301
 
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Going by experience alone I'd say that Memantine feels mildly more dopaminergic than many other dissociatives. The only one I've ever felt a truly dopaminergic push with though is PCP.
 
Definitely don't let possible D2 agonism hold you back from trying Memantine. It's a wonderful substance IMO.
 
Dopaminergic activity doesn't have to be pushy as in stimulants ... that of memantine is pretty unnoticeable acutely but it's equally strong as it's NMDA antagonism and contributes to the overall effects (anxiolysis etc).

Pure agonists can even be sedating, those used for Parkinson's have this side effect listed. And they aren't 'ab'used like e.g. amphetamine. But they work to lift mood etc. Just that there's the potential for prolonged withdrawal what makes most people avoid them, think the NMDA activity of memantine prevents that.

MXE has been shown to bind to D2 too.
 
Cotcha Yankinov said:
How is such a possible mistake made? One of my biggest reasons for not trialing memantine was because I didn't want to use a dopaminergic.
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I wouldn't really call it a mistake -- that is how science works. Papers get published all the time that turn out to be wrong or can't be replicated. That's why you have to critically evaluate papers when you read them and look for replication.

Cotcha Yankinov said:
There is even this study suggesting that the D2 agonism is involved in the LTD effects https://www.researchgate.net/public...ynaptic_responses_toward_long-term_depression

But couldn't this LTD be explained without involving a possible direct agonism of D2?
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LTD is known to be dependent on D2. So if memantine enhances LTD then it would not be surprising to find that the effect could be blocked by a D2 antagonist. That doesn't necessarily mean, however, that memantine binds directly to D2.
 
dopamimetic said:
think the NMDA activity of memantine prevents that.
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Sidenote: in my trials with it, Memantine was remarkably good at reducing tolerance to other classes of drugs, specifically my regulars, weed and benzos.

But Matrine is the drug at hand. Is there any (even shoddy) speculation as to what this drug would come out as in effects, dissociative/psychedelic like Salvia? Or will the µ-opioid alter that entirely? The only other thread I could find everybody basically just said It's probably miserable, which Salvia was not IMO, so why everyone was so quick to just eww at it I don't know.
 
dopamimetic said:
Just that there's the potential for prolonged withdrawal what makes most people avoid them, think the NMDA activity of memantine prevents that.
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I really wonder what the effect of long term NMDA antagonism is, someone warned that the NMDA projections to the suprachiasmatic nucleus (circadian rhythms center) were very important and thought there might be concern there with long term NMDA antagonism. Then again isn't memantine supposed to (for the most part) leave alone normal neurotransmission and only block NMDArs that have already fired (more pathological over-firing NMDArs?) because it can't bind with the Mg block in place?

I think my main concern would be some sort of pathological weakening of learning circuits with long term NMDA antagonism.
 
Soul137 said:
Sidenote: in my trials with it, Memantine was remarkably good at reducing tolerance to other classes of drugs, specifically my regulars, weed and benzos.

But Matrine is the drug at hand. Is there any (even shoddy) speculation as to what this drug would come out as in effects, dissociative/psychedelic like Salvia? Or will the µ-opioid alter that entirely? The only other thread I could find everybody basically just said It's probably miserable, which Salvia was not IMO, so why everyone was so quick to just eww at it I don't know.
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Some members of the benzomorphan class have a similar profile. See, for example, pentazocine. It has opioid effects but can also cause hallucinations, especially at high doses.
 
Interesting. Does this mean though that in pursuing hallucinogenic doses might be dangerous in terms of CNS depression of the µ-opioid agonism?

With pentazocine that would seem true, since it's more on the µ side. But Matrine is more on kappa side (I gather). Well for that matter, what is safety like with k-opioids. I've never heard of death by Salvia or Ibogaine, but that's understandable, even if they did have a narrow therapeutic index.
 
Soul137 said:
Interesting. Does this mean though that in pursuing hallucinogenic doses might be dangerous in terms of CNS depression of the µ-opioid agonism?

With pentazocine that would seem true, since it's more on the µ side. But Matrine is more on kappa side (I gather). Well for that matter, what is safety like with k-opioids. I've never heard of death by Salvia or Ibogaine, but that's understandable, even if they did have a narrow therapeutic index.
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It depends on how strongly matrine can activate the mu receptor. But in general, yes, if matrine is a mu agonist then it can potentially produce some degree of respiratory depression.

Kappa agonists don't produce respiratory depression. Ibogaine does far more than just activate kappa; it has caused several deaths due to arrhythmia
 
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