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Opioids Psychotria colorata dosing?

uncouplingreversed

Bluelighter
Joined
Mar 18, 2018
Messages
61
I've been waiting months try this and I finally got some on it's way. Has anyone used this? It's supposed to be strong for euphoria and mood. I used to take kratom but it's banned in my state so I tried akuamma but that didn't really work very well. Tried tianeptine and it felt too drug like. Anyone have any information on dosing there's very little out there I could find.
 
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Well being in the same family doesn't really mean much in terms of botany. It's in the family rubiaceae along with kratom. But coffee is also in the family rubiaceae and coffee is nothing like kratom in terms of effects.

If it were in the same genus that would be something. But in botany being in the family doesn't really imply that much similarity.

If we were talking a species in the same genus (e.g the genus mitragyna) then I would be more interested to see if it had similar effects.

Psychotria is the genus of Psychotria viridis, which is the dmt containing component in ayahuasca. So if I were to guess I would say it is probably more likely to contain dmt or something similar rathere than being like kratom
 
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Well being in the same family doesn't really mean much in terms of botany. It's in the family rubiaceae along with kratom. But coffee is also in the family rubiaceae and coffee is nothing like kratom in terms of effects.

If it were in the same genus that would be something. But in botany being in the family doesn't really imply that much similarity.

If we were talking a species in the same genus (e.g the genus mitragyna) then I would be more interested to see if it had similar effects.

Psychotria is the genus of Psychotria viridis, which is the dmt containing component in ayahuasca. So if I were to guess I would say it is probably more likely to contain dmt or something similar rathere than being like kratom

Here's what I read about it. Says it's been used for pain by Amazonians in Brazil and acts on the opioid system. But no DMT. I like the part about the NMDA antagonist in theory this would reduce any tolerance or addiction compared to other opioids and further help with nerve pain. But none of the research says anything about dosing.

'Psychotria colorata is a species of plant in the Rubiaceae family. It has been documented in an ethnobotanical context among the Ka'apor people of Maranhão, Brazil by Dr. William Balée, the Tulane University anthropologist and historical ecologist:[1]
"Fishhooks (pinar) and line (pina-ham) are obtained through trade. The bait is usually worms, but two species of plants serve an intermediate role. Fruits of the rubiaceous forest herb Psychotria colorata and seeds of Ricinus communis, a treelet of dooryard gardens, are used for baiting hooks and catching small fish: characins called pirapisi. Fishermen cut chunks of the characins as bait for hooking larger, more desirable fish" (Balée 1994: 61).

"It is said that a boy should rub leaves of tapesi'i (Cephalia sp. 1) or leaves of Psychotria colorata(tapi'ika'a), both of which are in the madder family, between his hands so that upon maturity he will be able to fashion well the manioc press (tapesi), an exclusive task of men" (Balée 1994: 107).

Extracts from the leaves, flowers, fruits and root of Psychotria colorata are traditionally used as an analgesic by Amazonian cabaclos native peoples. This analgesic effect has been studied in animals and shown to be reversible by naloxone, suggesting a mu opioid receptor mediated effect.[2][3] Subsequent research has identified several active alkaloids in the plant,[4][5] the most important of which are hodgkinsine, which acts as both a mu-opioid agonist and NMDA antagonist,[6] and psychotridine which is an NMDA antagonist with little or no mu-opioid affinity.[7]


Neurochem Res. 1996 Jan;21(1):97-102.
Effects of Psychotria colorata alkaloids in brain opioid system.

An ethnopharmacological survey showed that home remedies prepared with flowers and fruits of Psychotria colorata are used by Amazonian peasants as pain killers. Psychopharmacological in vivo evaluation of alkaloids obtained from leaves and flowers of this species showed a marked dose-dependent naloxone-reversible analgesic activity, therefore suggesting an opioid-like pharmacological profile. This paper reports an inhibitory effect of P. colorata flower alkaloids on [3H]naloxone binding in rat striata as well as a decrease in adenylate cyclase basal activity. The alkaloids did not affect [3H] GMP-PNP binding. These findings provide a neurochemical basis for the opioid-like activity previously detected in vivo and point to Psychotria alkaloids as a potential source of new bioactive opiate derivatives."
 
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Hodgkinsine does appear to be opioidergic. The structure is odd, kind of ibogainesque.

No clue as to how this is dosed, but ive always bee curious about it. My guess is that it is not particularly pleasant but who knows...
 
Hodgkinsine does appear to be opioidergic. The structure is odd, kind of ibogainesque.

No clue as to how this is dosed, but ive always bee curious about it. My guess is that it is not particularly pleasant but who knows...

Really? Indoles really get around don't they. It's one of the 6 known according to this source.

"an alkaloid extract of Psychotria colorata flowers led to the isolation of six alkaloids, identified by UV, 1D and 2D NMR, and MS as (-)-calycanthine, isocalycanthine, (+)-chimonanthine, hodgkinsine, quadrigemine C, and a new alkaloid (1), whose structure was deduced by X-ray analysis to be (8-8a),(8'-8'a)-tetradehydroisocalycanthine 3a(R), 3'a(R). "

Calycanthine seems to work on GABA and the gabapentinoid receptors. isocalycanthine I have no idea maybe similar. chimonanthine no idea. Oh wait " (+)-chimonanthine (12) and calycosidine resemble the analgesic profile found for hodgkinsine. "
2 more indoles.

I'm guessing leafy. I'm surprised there's not more research on this it's a whole class of new indoles. I feel like I should meet an amazonian who's been on this for years first before trying it but there's no reports of any side effects I could find.
 
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My guess is that it would be a partial MOR agonist and be pretty dirty feeling over all. Very interesting though, please report back.

I suppose where'd you start is with an allergy test, then chew a leaf and see how it goes from there.

The structure of psychotridine is even weirder which is in both p. cholorata and p. forsteriana

14248
 
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My guess is that it would be a partial MOR agonist and be pretty dirty feeling over all. Very interesting though, please report back.

I suppose where'd you start is with an allergy test, then chew a leaf and see how it goes from there.

The structure of psychotridine is even weirder which is in both p. cholorata and p. forsteriana

View attachment 14248

I don't see anything on how selective it is for MOR but it was near equal strength to morphine in an animal study. Maybe someday they can do a receptor test on it.
 
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Really? Indoles really get around don't they. It's one of the 6 known according to this source.

"an alkaloid extract of Psychotria colorata flowers led to the isolation of six alkaloids, identified by UV, 1D and 2D NMR, and MS as (-)-calycanthine, isocalycanthine, (+)-chimonanthine, hodgkinsine, quadrigemine C, and a new alkaloid (1), whose structure was deduced by X-ray analysis to be (8-8a),(8'-8'a)-tetradehydroisocalycanthine 3a(R), 3'a(R). "

Calycanthine seems to work on GABA and the gabapentinoid receptors. isocalycanthine I have no idea maybe similar. chimonanthine no idea. Oh wait " (+)-chimonanthine (12) and calycosidine resemble the analgesic profile found for hodgkinsine. "
2 more indoles.

I'm guessing leafy. I'm surprised there's not more research on this it's a whole class of new indoles. I feel like I should meet an amazonian who's been on this for years first before trying it but there's no reports of any side effects I could find.
Hmm it does sound very interesting. Now I want to try it haha, let us know once you get it
 
My guess is that it would be a partial MOR agonist and be pretty dirty feeling over all. Very interesting though, please report back.

I suppose where'd you start is with an allergy test, then chew a leaf and see how it goes from there.

The structure of psychotridine is even weirder which is in both p. cholorata and p. forsteriana

View attachment 14248

Looks like it's somewhat related to Eseroline

400px-Eseroline_skeletal.svg.png
400px-Hodgkinsine.png
 
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Hmm it does sound very interesting. Now I want to try it haha, let us know once you get it

I'm tempted to lab test some of it. I'm curious how much of the Hodgkinsine is in it this may give me a better idea of dosing since there is some animal studies I can roughly estimate a human dose off that. For sure.
 
Interesting ive never heard of eseroline (apparently a metabolite of the toxic ACE inhibitor physostigmine, a constituent of the calabar bean). If you get your doses right perhaps you could take atropine with the calabar and hope to take advantage of opioidergic metabolite eseroline...

Although this could be tricky business since, apparently, "the antagonism between physostigmine and atropine is not perfect...in such cases there comes a time when, if the action of the two drugs is summated, death results sooner than from either alone. Thus atropine will save life if three and a half times the fatal dose of physostigmine has been taken, but will hasten the end if four or more times the fatal dose has been ingested."

Still i have a sense hodgkinsine would feel pretty dirty given that NMDA antagonism. One danger could be if it had a ibogaine like half-life, putting you in for a long haul psychotomimetic experience (though i don't think that is the case). It could also be a hERG inhibitor like ibogaine and possess some cardiotoxicity. I'd probably chew it however. I looked into obtaining p. colorata once but the african source seemed pretty questionable...
 
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Interesting ive never heard of eseroline (apparently a metabolite of the toxic ACE inhibitor physostigmine, a constituent of the calabar bean). If you get your doses right perhaps you could take atropine with the calabar and hope to take advantage of opioidergic metabolite eseroline...

Although this could be tricky business since, apparently, "the antagonism between physostigmine and atropine is not perfect...in such cases there comes a time when, if the action of the two drugs is summated, death results sooner than from either alone. Thus atropine will save life if three and a half times the fatal dose of physostigmine has been taken, but will hasten the end if four or more times the fatal dose has been ingested."

Still i have a sense hodgkinsine would feel pretty dirty given that NMDA antagonism. One danger could be if it had a ibogaine like half-life, putting you in for a long haul psychotomimetic experience (though i don't think that is the case). I looked into obtaining p. colorata once but the african source seemed pretty questionable...

I can only go based off the animal studies and human traditional use of the plant which contains many alkaloids acting synergically. If the amazonians have used it for centuries for common pain conditions, given to teens, and no mention of psychedelic effects I'm not too worried for a short trial.

You seen to be guessing it's effects solely based on what chemicals it is related to namely ibogaine. Many chemicals are related to it and other indoles. Vinpocetine is a common one and has no concerning effects and feels nothing like ibogaine. While it blocks glutamate instead of NMDA it acts on AMPA.

I take theanine, magnesium, huperzine a because of the neuroprotective effects they offer in part via NMDA blocking. I've never felt sick from them.

Did you do a lab test that came back with something concerning? I lab test every ethno I take mostly for metals and micros so I know there's no common impurities...
 
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It could also be a hERG inhibitor like ibogaine and possess some cardiotoxicity.

Can you cite anything showing this link?

The only paper I found on toxicity was this one.

August 2011 Toxicology Letters. Subchronic and reproductive toxicity of Psychotria colorata in male rats

"Twenty adult male Wistar rats (60 days old) were randomly allotted into two groups. The rats in the control group were given pellets of commercial diet and experimental rats consumed diet containing 5% of dried and ground P. colorata, during 60 days.

Neither mortality nor clinical signs of toxicity were observed."

I would offhand compare it to kratom relatively safe by itself in doses historically used but when taking isolates in high doses of
mitragynine or 7-Hydroxymitragynine more severe side effects were seen...
 
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You seen to be guessing it's effects solely based on what chemicals it is related to namely ibogaine. Many chemicals are related to it and other indoles. Vinpocetine is a common one and has no concerning effects and feels nothing like ibogaine. While it blocks glutamate instead of NMDA it acts on AMPA.

I take theanine, magnesium, huperzine a because of the neuroprotective effects they offer in part via NMDA blocking. I've never felt sick from them.

You are right, I am making alot of assumptions based on its vague structural similarity to ibogaine and the knowledge that it has affinity for opioid receptors with NMDA blocking properties. In reality, it probably is nothing like ibogaine. Who knows though -- when I was looking into it years ago I found very little information on it, and zero reports of its subjective effects (it seems as though you're more well armed information-wise, perhaps information is more accessible now).

Also one quick note: l-theanine is an NMDA-agonist.

And as far as hodgkinsine being a hERG inhibitor, that was purely speculative on my part. If I had a sample of the plant I'm sure I would conduct some trials with it (with probably fewer precautions than you're taking).

Still, my guess is that it isn't particularly reinforcing, or the secret would have gotten out by now. I could be totally wrong.
 
You are right, I am making alot of assumptions based on its vague structural similarity to ibogaine and the knowledge that it has affinity for opioid receptors with NMDA blocking properties. In reality, it probably is nothing like ibogaine. Who knows though -- when I was looking into it years ago I found very little information on it, and zero reports of its subjective effects (it seems as though you're more well armed information-wise, perhaps information is more accessible now).

Also one quick note: l-theanine is an NMDA-agonist.

And as far as hodgkinsine being a hERG inhibitor, that was purely speculative on my part. If I had a sample of the plant I'm sure I would conduct some trials with it (with probably fewer precautions than you're taking).

Still, my guess is that it isn't particularly reinforcing, or the secret would have gotten out by now. I could be totally wrong.

I'm trying to go off all the available info you're right there's not alot out there but there's some research.

I would have to disagree regarding theanine.


"These results indicate that the inhibition of the NMDA subtype of glutamate receptors and its related pathways is the crucial point of the neuroprotective effect of l-theanine in the cell model. "

It's saying theanine's neuroprotective effect is solely due to it's ability to inhibit NMDA thus reducing excessive glutamate levels in the brain.

"Local treatment with L-theanine at reperfusion prevents glutamate receptor agonist-mediated brain injury. "

Here it literally blocks the effects of a known glutamate receptor agonist and protected against the damage it caused since excessive glutamate is a key factor in excitotoxicity, as well as, seizure activity.

I have reactive glutamate receptors so i avoid any type of NMDA or AMPA agonists. But theanine helps keep me relaxed and chill. I tried NMDA as a sports supplement once and it was not ok. Thankfully after taking 1-2 grams of theanine (and some phenibut) I felt much better.
 
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I should get it next week looks like it's slowing getting through customs. My current plan is to try one leaf first and see how I respond. If all does well I'll try the powder slowing increasing the dose each day until I see an effect then stopping for 48 hours to review. I welcome anyone's suggestions.

I have some nasal naloxone ready on standby in case it's too strong and liver protective repairing substances so I think I have my bases covered.
 
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The consensus on all that ive read regarding l-theanine points to it having agonistic action on the NMDA receptor.

Behavioral and molecular evidence for psychotropic effects in L-theanine.
Abstract
RATIONALE: L-Theanine (N-ethyl-L: -glutamine) is an amino acid uniquely found in green tea and historically considered to be a relaxing agent. It is a glutamate derivative and has an affinity for glutamatergic receptors. However, its psychotropic effects remain unclear.
OBJECTIVES: To elucidate effects of L: -theanine on psychiatric disease-related behaviors in mice and its molecular basis focusing on brain-derived neurotrophic factor (BDNF) and N-methyl-D: -aspartate (NMDA) receptor.
METHODS: We examined the effects of L: -theanine on behaviors in mice by using the open-field test (OFT), forced swim test (FST), elevated plus-maze test (EPMT), and prepulse inhibition (PPI) of acoustic startle. By western blot analysis, we looked at the effect of L: -theanine on the expression of BDNF and related proteins in the hippocampus and cerebral cortex. To determine whether L: -theanine has agonistic action on the NMDA receptor, we performed Fluo-3 intracellular Ca(2+) imaging in cultured cortical neurons.
RESULTS: Single administration of L: -theanine significantly attenuated MK-801-induced deficits in PPI. Subchronic administration (3-week duration) of L: -theanine significantly reduced immobility time in the FST and improved baseline PPI. Western blotting analysis showed increased expression of BDNF protein in the hippocampus after subchronic administration of L: -theanine. In cultured cortical neurons, L: -theanine significantly increased the intracellular Ca(2+) concentration, and this increase was suppressed by competitive and non-competitive NMDA receptor antagonists (AP-5 and MK-801, respectively).
CONCLUSIONS: Our results suggest that L: -theanine has antipsychotic-like and possibly antidepressant-like effects. It exerts these effects, at least in part, through induction of BDNF in the hippocampus and the agonistic action of L: -theanine on the NMDA receptor.

Characterization of l-Theanine Excitatory Actions on Hippocampal Neurons: Toward the Generation of Novel N-Methyl-d-aspartate Receptor Modulators Based on Its Backbone.


Abstract
l-Theanine (or l-γ-N-ethyl-glutamine) is the major amino acid found in Camellia sinensis. It has received much attention because of its pleiotropic physiological and pharmacological activities leading to health benefits in humans, especially. We describe here a new, easy, efficient, and environmentally friendly chemical synthesis of l-theanine and l-γ-N-propyl-Gln and their corresponding d-isomers. l-Theanine, and its derivatives obtained so far, exhibited partial coagonistic action at N-methyl-d-aspartate (NMDA) receptors, with no detectable agonist effect at other glutamate receptors, on cultured hippocampal neurons. This activity was retained on NMDA receptors expressed in Xenopus oocytes. In addition, both GluN2A and GluN2B containing NMDA receptors were equally modulated by l-theanine. The stereochemical change from l-theanine to d-theanine along with the substitution of the ethyl for a propyl moiety in the γ-N position of l- and d-theanine significantly enhanced the biological efficacy, as measured on cultured hippocampal neurons. l-Theanine structure thus represents an interesting backbone to develop novel NMDA receptor modulators.
 
The consensus on all that ive read regarding l-theanine points to it having agonistic action on the NMDA receptor.

To determine whether L: -theanine has agonistic action on the NMDA receptor, we performed Fluo-3 intracellular Ca(2+) imaging in cultured cortical neurons.
RESULTS: Single administration of L: -theanine significantly attenuated MK-801-induced deficits in PPI.

This says theanine slightly modulated the effects of a NMDA antagonist drug. But does not indicate agonist receptor properties.

In cultured cortical neurons, L: -theanine significantly increased the intracellular Ca(2+) concentration, and this increase was suppressed by competitive and non-competitive NMDA receptor antagonists (AP-5 and MK-801, respectively).

Where this says it countered some of the effects of NMDA antagonist which suggest a modulation effect.

l-Theanine, and its derivatives obtained so far, exhibited partial coagonistic action at N-methyl-d-aspartate (NMDA) receptors, with no detectable agonist effect at other glutamate receptors, on cultured hippocampal neurons. This activity was retained on NMDA receptors expressed in Xenopus oocytes. In addition, both GluN2A and GluN2B containing NMDA receptors were equally modulated by l-theanine. The stereochemical change from l-theanine to d-theanine along with the substitution of the ethyl for a propyl moiety in the γ-N position of l- and d-theanine significantly enhanced the biological efficacy, as measured on cultured hippocampal neurons. l-Theanine structure thus represents an interesting backbone to develop novel NMDA receptor modulators.

It seems it may function as a partial agonist/antagonist or modulator rather than purely as one.

"Biosci Biotechnol Biochem. 2002 Dec;66(12):2683-6.
Inhibition by theanine of binding of [3H]AMPA, [3H]kainate, and [3H]MDL 105,519 to glutamate receptors.

In an investigation of the mechanisms of the neuroprotective effects of theanine (gamma-glutamylethylamide) in brain ischemia, inhibition by theanine of the binding of [3H](RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), [3H]kainate, and [3H](E)-3-(2-phenyl-2-carboxyethenyl)-4,6-dichloro-1-H-indole-2-carboxylic acid (MDL 105,519) to glutamate receptors was studied in terms of its possible inhibiting effects on the three receptor subtypes (AMPA, kainate, and NMDAglycine), with rat cortical neurons. Theanine bound the three receptors, but its IC50 of theanine was 80- to 30,000-fold less than that of L-glutamic acid."

It definitely binds to them and in this study the effect was inhibitory usually a function of antagonists. But a partial or mixed agonist may also apply. It does note it's very weak compared to glutamate itself.

"Neurochem Res. 2017 Oct;42(10):2686-2697. doi: 10.1007/s11064-017-2317-6. Epub 2017 Jun 9.
An L-Glutamine Transporter Isoform for Neurogenesis Facilitated by L-Theanine.

L-Theanine (=γ-glutamylethylamide) is an amino acid ingredient in green tea with a structural analogy to L-glutamine (L-GLN) rather than L-glutamic acid (L-GLU), with regards to the absence of a free carboxylic acid moiety from the gamma carbon position. L-theanine markedly inhibits [3H]L-GLN uptake without affecting [3H]L-GLU uptake in cultured neurons and astroglia. In neural progenitor cells with sustained exposure to L-theanine, upregulation of the L-GLN transporter isoform Slc38a1 expression and promotion of both proliferation and neuronal commitment are seen along with marked acceleration of the phosphorylation of mammalian target of rapamycin (mTOR) and relevant downstream proteins."

Hmm this could be the missing link that it also acts as a glutamate transporter uptake inhibitor.
 
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If I had a sample of the plant I'm sure I would conduct some trials with it (with probably fewer precautions than you're taking).

There's only so many entheogen shops out there worldwide I had to do a lot of searching to find it but I'm sure you can. It would be so great to have someone else's take on it as well. I think with any new source of anything testing is a must before taking it. Sure it costs but you covered yourself as much as you could.
 
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This says theanine slightly modulated the effects of a NMDA antagonist drug. But does not indicate agonist receptor properties.



Where this says it countered some of the effects of NMDA antagonist which suggest a modulation effect.



It seems it may function as a partial agonist/antagonist or modulator rather than purely as one.

"Biosci Biotechnol Biochem. 2002 Dec;66(12):2683-6.
Inhibition by theanine of binding of [3H]AMPA, [3H]kainate, and [3H]MDL 105,519 to glutamate receptors.

In an investigation of the mechanisms of the neuroprotective effects of theanine (gamma-glutamylethylamide) in brain ischemia, inhibition by theanine of the binding of [3H](RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), [3H]kainate, and [3H](E)-3-(2-phenyl-2-carboxyethenyl)-4,6-dichloro-1-H-indole-2-carboxylic acid (MDL 105,519) to glutamate receptors was studied in terms of its possible inhibiting effects on the three receptor subtypes (AMPA, kainate, and NMDAglycine), with rat cortical neurons. Theanine bound the three receptors, but its IC50 of theanine was 80- to 30,000-fold less than that of L-glutamic acid."

It definitely binds to them and in this study the effect was inhibitory usually a function of antagonists. But a partial or mixed agonist may also apply. It does note it's very weak compared to glutamate itself.

"Neurochem Res. 2017 Oct;42(10):2686-2697. doi: 10.1007/s11064-017-2317-6. Epub 2017 Jun 9.
An L-Glutamine Transporter Isoform for Neurogenesis Facilitated by L-Theanine.

L-Theanine (=γ-glutamylethylamide) is an amino acid ingredient in green tea with a structural analogy to L-glutamine (L-GLN) rather than L-glutamic acid (L-GLU), with regards to the absence of a free carboxylic acid moiety from the gamma carbon position. L-theanine markedly inhibits [3H]L-GLN uptake without affecting [3H]L-GLU uptake in cultured neurons and astroglia. In neural progenitor cells with sustained exposure to L-theanine, upregulation of the L-GLN transporter isoform Slc38a1 expression and promotion of both proliferation and neuronal commitment are seen along with marked acceleration of the phosphorylation of mammalian target of rapamycin (mTOR) and relevant downstream proteins."

Hmm this could be the missing link that it also acts as a glutamate transporter uptake inhibitor.

A partial agonist yes, but certainly not an antagonist as you had asserted. Language such as, "exhibited partial coagonistic action at N-methyl-d-aspartate (NMDA) receptors, with no detectable agonist effect at other glutamate receptors" is pretty clear in that regard.

Plus, ive aborted two unpleasant 2f-deschloroketamine experiences by taking 1000mg of l-theanine with remarkable efficacy. It totally abolished the dissociative experience.
 
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