Some sort of interaction between NMDA antagonism with acetylcholine antagonism?

[Ventrusii]

I made a post about my terrifying adventure when trying to reverse the antagonism of the NMDA receptor and conversion of Dextromethorphan into Dextrorphan, and, long story short, it ended up with me getting no or little antagonism of the NMDA receptor and (since I had taken CCC's), pretty bad muscarinic Acetylcholine receptor (mAChR's) antagonism, causing a pretty moderate state of delirium.

Since this delirium NEVER occurs even with doses up to 40mg chlorpheniramine when I take CCC's, but when I made it so the Dextromethorphan couldn't turn into Dextrorphan (and even if it did, I had an NMDA receptor modulator so it would decrease how much I felt), the delirium was pretty intense (with all the side effects, dry/red skin, difficulty urinating, tachycardia, delirium, paranoia, restlessness, and "Yuggeeeeee" pupils) even when I only took 24mg chlorpheniramine.

This caused me to believe that there's an interaction between mAChR's and NMDA antagonism.

One pretty much guess I have is that since NMDA antagonism prevents some communication to travel throughout your body, that the usual doses that I took of CCC's caused enough NMDA antagonism to either effectively dull the amount of signals that were being sent to my brain about incorrect information, or another guess is that because the NMDA antagonism caused by Dextrorphan could have caused my thought deceleration to the point that it became more of a logic puzzle for my brain, rather than acting on impulse. To explain what I meant by that last statement better, I think that because the NMDA antagonism causes though deceleration, that my brain had time enough to look at what was being said to it, and since it had time, so to speak, to process it, it decided that some or most of the information that was given due to impulse was false, and didn't alert me of whatever my body wanted me to be alert of.

Does anyone know a little bit more about NMDA receptors or mACh receptors and could either contribute to or help me solve my confusion?

I sometimes wonder how these questions even come to me.

 

[sekio]

The actual NMDA-mediated dissociative effect of DXM is mostly just the headspace and lack of muscular coordination, based upon my logic. DXM/DXO are not selective NMDA antagonists. DXM itself is mostly a SNRI, but also has anti-nAChR effects too. The huge pupils, tachycardia, restlessness etc can be attribted to the strong SNRI effects of DXM more than the antimuscarinic effects, I'd say. I would also wager that it potentiates the psychoactive effects of antimuscarinic/antihistamine drugs.

 

[Ventrusii]

Well, I know that DXM is a SNRI and that DXO is an NRI and the actual dissociative psychoactive. I just wanted to agonize the NMDA receptors so I prevented the conversion of DXM to DXO and also used Noopept to modulate the NMDA receptors.

I didn't know that DXM itself has anti-nAChR activity, but I thought it was only mAChR antagonism that caused delirium?

But thank you, I'll take that into account and do more research next time. I also think that the SRI effect of DXM wasn't what caused the large eyes, because I was feeling pretty bad dysphoria and I would think that my pupils would be big if I was in a state of euphoria, but still, it could have been overshadowed by the anti-m/nAChR action going on.

Thanks :D

 

[d1nach]

Why would triple cs have any effect on the conversion of dxm to dxo?

 

[d1nach]

Maybe its my double vision but the more I read this the more confused i am.

I think you mean noopept blocked the conversion of dxm to dxo? Dxm is ? Converted to dxo outside the brain by enzyme p450 2d6. Noopept might reduce the amnesia and cognitive effects of dxo but noopept doesnt act as do rectly as a uncompetitive antagonist of the nmda receptor. I believe there is direct and indirect competitive andd uncompetitive and various sub nmda sites like nmda polyamine and nmda glycine. Its highly likely you just got so many bad effects from using triple cs you couldnt even tell the dxm effects try using dxm only products or your basically just gunna feel poisoned trust me im a expert on that lol tried non dxm only dysphoria confusing heartpounding delirium everytime

 

[Cotcha Yankinov]

Haven't read the thread but noopept can act as an acetylcholine reuptake inhibitor so that could the thinking for using it to reduce delirium

 

[Mracid]

Chlorpheniramine inhibit the CYP2D6 ezyme, not as much as DPH but it does. Taking that into account you decrease the ratio DXO/DXM making it a more SNRI/nACh antagonist with little NMDA antagonistic activity. Also Chlorpheniramine act more of a SNRI than a mACh antagonist pileing on the SNRI effect of DXM. Taking noopept increase both the AMPA receptor activation which is useful in NMDA activation thus reducing the NMDA antagnonist activity due to more NMDA receptors activated allowing your brain through neuroplasticity to do act more normally, then noopet is a Choline enhancer, no matter how it does it, which does the same to ACh receptors as it does with NMDA receptors.

So more simply, Tripple C's are more SNRI than anything else, and adding noopept make your brain able to bypass the fact that some of your NMDA and ACh receptors are closed by using other neurons to create a different pattern that would end up doing the same thing, thus reducing the perceptual dissociative and delirious effect.

The combination of Tripple C's and noopept would most likely make a reduced dissociative/delirious state than DXM alone or DPH alone and a more pronounced SNRI effect, which can lead to heart issues, while remaining mostly clear minded due to the noopept..