LONGECITY

How to increase the density of NMDA receptors? upregulate NMDA? I know one method, namely the use of piracetam, but this makes me irritable, plus longer use despite addition of choline causes chronic fatigue ...

Other ways to upregulate NMDA?

Sarcosine increases the activity of NMDA receptors via the co-agonist glycine, both by inhibiting glycine transporter 1 and by acting as an agonist at the glycine site itself.

sarcosine and glycine was tried and both cause in my depression, and increased receptor density is the same as increasing the activity of the receptor, because I think that there

By the way, allowed to stand nicotine patches, a few nights in a row broke off and I start to have trouble thinking clearly

I mention this because nicotinic receptors alpha-7 receptor stimulation with d1 glutaminergic puts it in the running, so to speak


it ... because what I care to stimulate nicotinic receptors alpha-7 and increased NMDA receptor density
Edited by scibor, 25 December 2012 - 06:47 PM.

I read somewhere that Alcohol temporatily downregulates NMDA , which causes an upreguation above baseline after a while.

always a hangover (alcohol) feel increased motivation, maybe it has to do with overactive NMDA at this time ...
other proposals yet ...?

of the NMDA receptors is often the case in different ways, such as quinolinic acid is an agonist of the NMDA, and contributes to many diseases and it would antagonize him, the question of whether the addition of glycine sarcosine, which operate over a calming ...

The kynurenic acid acts as an antagonist of NMDA and tyez contributes to the development of many diseases, even schizophrenia

Both kynurenic acid and quinolinic acid act generally bad for the human body, both of which are metabolites of tryptophan, in my opinion, tryptophan One has disposed of the block and not only was part of these changes, perhaps the only lock suitable enzymes, but what substances??


I would like to know how I can block the quinolinic acid, kynurenic acid and tryptophan?

This is the information you are looking for....OP --> http://area1255.blog...eptors-and.html

Edited by Area-1255, 14 February 2015 - 06:36 PM.

Though certainly weak, perhaps totally ineffective, magnesium is a safe option.  You could get 200mg extra daily with just a few changes of diet.

Magnesium up regulates nmda. Although it inhibits Nmda, once the cell is excited enough it fires, making the signal much stronger. Try magnesium oil spray, it is the best thing ever for going to sleep.
Edited by Arjuna, 14 February 2015 - 11:09 PM.

Are there any prescription medications that would help or regulate the NMDA issues some people have?

 

For example,

 

R̲i̲l̲u̲z̲o̲l̲e̲, M̲e̲m̲a̲n̲t̲i̲n̲e̲, A̲m̲a̲n̲t̲a̲d̲i̲n̲e̲, or L̲a̲m̲o̲t̲r̲i̲g̲i̲n̲e̲?

 

I appologize if my understanding is not correct, I am still in the process of learning about these areas.  Thanks for any help, corrections, and insight.

Are there any prescription medications that would help or regulate the NMDA issues some people have?

 

For example,

 

R̲i̲l̲u̲z̲o̲l̲e̲, M̲e̲m̲a̲n̲t̲i̲n̲e̲, A̲m̲a̲n̲t̲a̲d̲i̲n̲e̲, or L̲a̲m̲o̲t̲r̲i̲g̲i̲n̲e̲?

 

I appologize if my understanding is not correct, I am still in the process of learning about these areas.  Thanks for any help, corrections, and insight.

Yes, NEFIRACETAM.

 

Though it's not a prescription medication, its a nootropic/research chemical.

 

 

 

 

 

 

 

 

Mol Pharmacol. 2007 Feb;71(2):580-7. Epub 2006 Nov 9.

Nefiracetam potentiates N-methyl-D-aspartate (NMDA) receptor function via protein kinase C activation and reduces magnesium block of NMDA receptor.

Moriguchi S1, Shioda N, Maejima H, Zhao X, Marszalec W, Yeh JZ, Fukunaga K, Narahashi T.

Author information

 

Abstract

Nicotinic acetylcholine receptors and N-methyl-D-aspartate (NMDA) receptors are known to be down-regulated in the brain of Alzheimer's disease patients. We have previously demonstrated that the nootropic drug nefiracetam potentiates the activity of both nicotinic acetylcholine and NMDA receptors and that nefiracetam modulates the glycine binding site of the NMDA receptor. Because the NMDA receptor is also modulated by Mg2+ and protein kinases, we studied their roles in nefiracetam action on the NMDA receptor by the whole-cell patch-clamp technique and immunoblotting analysis using rat cortical or hippocampal neurons in primary culture. The nefiracetam potentiation of NMDA currents was inhibited by the protein kinase C (PKC) inhibitor chelerythrine, but not by the protein kinase A (PKA) inhibitor N-[2-(4-bromocinnamylamino)ethyl]-5-isoquinoline (H89). In immunoblotting analysis, nefiracetam treatment increased the PKCalpha activity with a bell-shaped dose-response relationship peaking at 10 nM, thereby increasing phosphorylation of PKC substrate and NMDA receptor. Such an increase in PKCalpha-mediated phosphorylation was prevented by chelerythine. Nefiracetam treatment did not affect the PKA activity. Analysis of the current-voltage relationships revealed that nefiracetam at 10 nM largely eliminated voltage-dependent Mg2+ block and that this action of nefiracetam was sensitive to PKC inhibition. It was concluded that nefiracetam potentiated NMDA currents not by acting as a partial agonist but by interacting with PKC, allosterically enhancing glycine binding, and attenuating voltage-dependent Mg2+ block.

PMID:   17095583   [PubMed - indexed for MEDLINE] 

 

Edited by Area-1255, 15 February 2015 - 08:26 PM.