• N&PD Moderators: Skorpio | someguyontheinternet

Pharmacology Why are SRI/SNRI not treated as 5HT2A agonists like how DRI/DNRI's are D2 agonists?

This thread contains discussion about a Pharmacology-related topic

bigjackaal96

Bluelighter
Joined
Nov 27, 2024
Messages
109
The study that had shroom users struggling to tell DXM & Shrooms apart, Had them having to use DXM's disso effects to tell them apart. Meaning If they did 400 ~ 600mg again with a DXO inhibtor they would fail instantlly. I noticed this doing 200 ~ 450mg but I view DXM more close to RC psychdelics that are 5HT2A full agonists but a very high quality one, Since It your own serotonin that getting you high.

I even noticed trippy effects with chlorphenamine at 8 ~ 24mg, It turns out It actually a SNRI.

 
Are reuptake inhibitors automatically ligands at the receptors?

I know medicines classed as dopamine agonists appear to have quite nasty side-effect profiles.

I'm uncertain as to what a DXO inhibitor is, as the compound appears to act in several distinct ways.
 
The study that had shroom users struggling to tell DXM & Shrooms apart, Had them having to use DXM's disso effects to tell them apart. Meaning If they did 400 ~ 600mg again with a DXO inhibtor they would fail instantlly. I noticed this doing 200 ~ 450mg but I view DXM more close to RC psychdelics that are 5HT2A full agonists but a very high quality one, Since It your own serotonin that getting you high.

I even noticed trippy effects with chlorphenamine at 8 ~ 24mg, It turns out It actually a SNRI.

I am sorry, but what? Your own serotonin getting you high with DXM?
The study that had shroom users struggling to tell DXM & Shrooms apart, Had them having to use DXM's disso effects to tell them apart. Meaning If they did 400 ~ 600mg again with a DXO inhibtor they would fail instantlly. I noticed this doing 200 ~ 450mg but I view DXM more close to RC psychdelics that are 5HT2A full agonists but a very high quality one, Since It your own serotonin that getting you high.

I even noticed trippy effects with chlorphenamine at 8 ~ 24mg, It turns out It actually a SNRI.

What are you even trying to say here? As expected, the study says that the participants largely were able to distinguish between the two. There was no struggle at all for most people. DXM feels nothing like shrooms and vice versa...

And what are you talking about DXM feeling like an RC 5ht2a receptor agonist? It absolutely does not share similar qualities. Its much more dissociative like mixed with a mild dopaminergic agent. No clue what you are talking about, and I am not sure you do yourself which is the concerning part lol
 
I am sorry, but what? Your own serotonin getting you high with DXM?
Reuptake transporters at 80 ~ 100% activity tell the brain to dump out it juices. Nutmeg is a eCBRI It forces your own cannabinoids the brain makes to flood out which then affects CB1 & CB2 receptors. CI-966 was a GABA-RI at 60mg It produced muscimol like trips despite not directly affecting GABA-A.
What are you even trying to say here? As expected, the study says that the participants largely were able to distinguish between the two. There was no struggle at all for most people. DXM feels nothing like shrooms and vice versa...

And what are you talking about DXM feeling like an RC 5ht2a receptor agonist? It absolutely does not share similar qualities. Its much more dissociative like mixed with a mild dopaminergic agent. No clue what you are talking about, and I am not sure you do yourself which is the concerning part lol
Only because of It NMDA antagonist effects which they state once they compare high dose shrooms vs 400mg DXM. Why are you calling me wrong when you seem to have no idea that DXM is a potent SNRI at 90mg?.

There a reason why DXM is called serotonergic PCP. It way too psychdelic to be from NMDA antagonism alone & Is far warmer in how It feels.
 
Are reuptake inhibitors automatically ligands at the receptors?

I know medicines classed as dopamine agonists appear to have quite nasty side-effect profiles.

I'm uncertain as to what a DXO inhibitor is, as the compound appears to act in several distinct ways.
They bind to transporters It when they are blocked by 80 ~ 100% the agonist effects appear. It stops the liver coverting DXM to DXO, Any CYP2D6 blocker would do fine.
 
They bind to transporters It when they are blocked by 80 ~ 100% the agonist effects appear. It stops the liver coverting DXM to DXO, Any CYP2D6 blocker would do fine.

So you are saying that they bind directly to the receptors?

It's such a long time since I studied all of this.
 
Reuptake transporters at 80 ~ 100% activity tell the brain to dump out it juices. Nutmeg is a eCBRI It forces your own cannabinoids the brain makes to flood out which then affects CB1 & CB2 receptors. CI-966 was a GABA-RI at 60mg It produced muscimol like trips despite not directly affecting GABA-A.

Only because of It NMDA antagonist effects which they state once they compare high dose shrooms vs 400mg DXM. Why are you calling me wrong when you seem to have no idea that DXM is a potent SNRI at 90mg?.

There a reason why DXM is called serotonergic PCP. It way too psychdelic to be from NMDA antagonism alone & Is far warmer in how It feels.
Oh, I see now what you are trying to say, and I am calling you wrong because the thing you linked to clearly states your interpretation is flawed. DXM results in a different signalling cascade than PCP is why DXM causes more serotogenic effects. I am having a very difficult time understanding the way you are phrasing what you are trying to say, coupled with the fact that you are misinterpreting how DXM affects neurotransmission as well as the fact the study is being misrepresented by you to try and "prove your point" (though I am not sure of why...?)

I don't really care to be involved in this discussion anymore to be quite frank as I don't think this is going anywhere quick, but I do hope you find your answers. Peace.
 
Oh, I see now what you are trying to say, and I am calling you wrong because the thing you linked to clearly states your interpretation is flawed. DXM results in a different signalling cascade than PCP is why DXM causes more serotogenic effects. I am having a very difficult time understanding the way you are phrasing what you are trying to say, coupled with the fact that you are misinterpreting how DXM affects neurotransmission as well as the fact the study is being misrepresented by you to try and "prove your point" (though I am not sure of why...?)

I don't really care to be involved in this discussion anymore to be quite frank as I don't think this is going anywhere quick, but I do hope you find your answers. Peace.
Then leave If your gonna being ignorant. SERT at 80 ~ 100% activity = Indirect 5HT2A full agonism just like how DAT at 80 ~ 100%(54 ~ 200mg Concerta) will do the same. Once again the study OUTRIGHT states the SNRI effects gave psychdelic effects that Nitrous & Ketamine can't do through NMDA blockade.

I highly doubt you read It and are just sore that DXM is actually a OTC psychdelic that also a Disso.
 
Then leave If your gonna being ignorant. SERT at 80 ~ 100% activity = Indirect 5HT2A full agonism just like how DAT at 80 ~ 100%(54 ~ 200mg Concerta) will do the same. Once again the study OUTRIGHT states the SNRI effects gave psychdelic effects that Nitrous & Ketamine can't do through NMDA blockade.

I highly doubt you read It and are just sore that DXM is actually a OTC psychdelic that also a Disso.
I am leaving because your ego is too big. You are being extremely disrespectful, and I never once said that it wasn't SNRI. I said you entirely misunderstand classification of drugs, and I did read the study. It states DXM and mushrooms could be distiguished from each other most of the time.

I suggest you do an actual psychedelic in adequate dose so you lose the ego problem you have, and then we can try to speak again. Until then, this is like me trying to talk to a teenage boy with an inferiority complex: pointless.
 
Top