Noopept as a painkiller, is it only me, and why?

[Cotcha Yankinov]

Basically AMPA provides a lot of input to NMDAr's. It takes a lot of stimulation to activate NMDAr's and ultimately NMDA is what is mediating a lot of the cognitive effects from ampakines. Generally there are a lot of studies that look for antagonism of something to be significantly reducing the effects of a particular drug to reason that the drugs effects are to whatever degree mediated through what they are antagonizing, and my question for a long time was that how do they know it's not related (after all you would expect NMDA antagonism to affect cognition regardless of whether racetams were working via NMDA) but ultimately it boils down to the authors of the study feeling that the antagonism's reduction of activity would not have been as significantly with placebo + antagonism.

I would actually expect people who take NMDA antagonists to be at lesser risk of pain amplification syndromes unless there is significant upregulation of NMDA with NMDA antagonism, NMDA upregulation is seen with NMDA potentiation if I recall correctly, but NMDA upregulation is definitely seen with ampakines.

Whether or not the upregulation of NMDAr's seen in the periphery with pain amplification syndromes is far far beyond what you would ever see with ampakines or NMDA antagonists is beyond me. I know the NMDA upregulation seen with ampakines is about 20% after a couple weeks I think...

 

[Cotcha Yankinov]

so is noopept contradicted for use in benzo or alcohol withdrawl or hangover? i think like all racetams it works on glutamate stimulation?

Assuming that it's glutamate potentiation is outweighing it's beneficial neurotrophic effects I would guess that it is contraindicated - the main issue with chronic benzo use is downstream compensation of glutamate.

 

[Mracid]

Is the pain relief acute? I almost assume it is since you seem to be associating the effect with particular doses?

AMPA does seem to control central sensitization and processing of peripheral information, and is involved with chronic pain. Antagonists and modulators have been suggested to experiment with, but it doesn't seem like any trials with them are actually taking place. Noopept is a modulator, so who knows? It seems like a connection?

Pain relief acute and short term you are right.

New informations and internal logical therory ! I like it ! I also think it might play a role. ( I also read it was regulating Ca++ in cells so that might be an impact too)

 

[Mracid]

so is noopept contradicted for use in benzo or alcohol withdrawl or hangover? i think like all racetams it works on glutamate stimulation?

WRONG, not a racetam, it is even a prodrug to Cyclopropylglycine which is an endogenous peptide involved in stabilisation of neuronal transmission and nerve cell. (has other effect but its its main). The only thing that is alike racetams in noopept is the skeleton.

Also It can protect brain cells from damage caused by abscence of inhibitory NT caused by Benzo or alcohol WD so I think it isnt contradicted but should be promoted at low dosage.

 

[Mracid]

Basically AMPA provides a lot of input to NMDAr's. It takes a lot of stimulation to activate NMDAr's and ultimately NMDA is what is mediating a lot of the cognitive effects from ampakines. Generally there are a lot of studies that look for antagonism of something to be significantly reducing the effects of a particular drug to reason that the drugs effects are to whatever degree mediated through what they are antagonizing, and my question for a long time was that how do they know it's not related (after all you would expect NMDA antagonism to affect cognition regardless of whether racetams were working via NMDA) but ultimately it boils down to the authors of the study feeling that the antagonism's reduction of activity would not have been as significantly with placebo + antagonism.

I would actually expect people who take NMDA antagonists to be at lesser risk of pain amplification syndromes unless there is significant upregulation of NMDA with NMDA antagonism, NMDA upregulation is seen with NMDA potentiation if I recall correctly, but NMDA upregulation is definitely seen with ampakines.

Whether or not the upregulation of NMDAr's seen in the periphery with pain amplification syndromes is far far beyond what you would ever see with ampakines or NMDA antagonists is beyond me. I know the NMDA upregulation seen with ampakines is about 20% after a couple weeks I think...

But what if pain is caused by wrong neural transmission like sending a message not because it was "asked to" but because if it did not something would happen like too much intracellular Ca++? would reducing intracellular Ca++ reduce the illusionary pain? Edited the post cuz I realized I was saying that low transmission can cause pain, while I know its present in quite unique cases..

 

[Cotcha Yankinov]

Generally over excitable nerves are what cause stuff like complex regional pain syndrome. If nerves are transmitting signals normally and there is still pain it basically means there is a genuine cause for the pain, as opposed to stuff like allodynia.

Part of what I'm getting at here is that not all types of pain are equal, I mean for example opiates makes pain amplification syndromes worse in the long run.

There are instances in which there is both nerve damage and pain sensitization (complex regional pain syndrome type 2 aka causlagia) but the pain sensitization is not an inherent property of lack of neurons capable of transmitting intact signals, except for phantom limb pain, which has more to do with the brain than the peripheral nerves.

As a caveat for all this and what noopept is doing, the metabolites and neurotrophic effects might be playing some role, but if we're just taking the ampakine effects into account we might have to assume some of the pain relief has to do with increased inhibitory projections running from the brain down into the spinal cord. One way you could test this is by using a more selective ampakine. There could also be modulation of sensory areas in the brain.

 

[Mracid]

Generally over excitable nerves are what cause stuff like complex regional pain syndrome. If nerves are transmitting signals normally and there is still pain it basically means there is a genuine cause for the pain, as opposed to stuff like allodynia.

Part of what I'm getting at here is that not all types of pain are equal, I mean for example opiates makes pain amplification syndromes worse in the long run.

There are instances in which there is both nerve damage and pain sensitization (complex regional pain syndrome type 2 aka causlagia) but the pain sensitization is not an inherent property of lack of neurons capable of transmitting intact signals, except for phantom limb pain, which has more to do with the brain than the peripheral nerves.

As a caveat for all this and what noopept is doing, the metabolites and neurotrophic effects might be playing some role, but if we're just taking the ampakine effects into account we might have to assume some of the pain relief has to do with increased inhibitory projections running from the brain down into the spinal cord. One way you could test this is by using a more selective ampakine. There could also be modulation of sensory areas in the brain.

Interesting theory ! But if I had money to finance experiments I wouldnt even need to come on these forums since every1 react slightly to greatly differently to various drugs due to over billions and billions of interactions between our cells.

Despite having accurate answer (which is nearly impossible in neuropharmacology) I got what I wanted, the confirmation that there is a theory with internal logic that would explain 1 or more way for noopept to relieve my pain, making me think its a light painkiller not much more potent than paracetamol for mostly everyone unless you have specific pattern in your neuronal system that would benefit from some if not all of the noopept effect even tho we did not find it exactly.