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Will sarcosine lead to NMDA receptor downregulation?

sarcosine nmda downregulation

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#1 Strelok

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Posted 22 March 2014 - 07:11 PM


I've recently been trying to learn more about sarcosine. It is a co-agonist of the NMDAr. Many sources say that sarcosine "improves" NMDAr function, but another source hypothesized that it may:

Also, both potentially attenuate signaling through NMDA receptors, ketamine with single doses and sarcosine, with long-term administration, by evoking an adaptive down regulation of NMDA receptors."


If someone had NMDA hypofunction, wouldn't it be a bad idea to risk downregulation? Or perhaps long term benefits could be attained by short or medium-term use of sarcosine before downregulation occurs?
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#2 abcmanomandriepunt1

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Posted 22 March 2014 - 07:36 PM

I think if your schizophrenic sarcosine is mainly doing good. In my country it's even acknowledged by traditional medicine as one of the few things for improving negative symptoms. I think many people with cognitive dysfunctioning might contribute from it .

I also thought about the downregulation, but that's a difficult question. Same goes for many other supplements and medicines. I think it's the best to look at the research and it's so far so good.
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#3 Strelok

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Posted 02 April 2014 - 10:08 PM

I emailed one manufacturer of sarcosine (who markets it for the purpose of improving NMDA function) asking about the potential for downregulation of the NMDAr, and here is their response:

... Your questions are well informed and we're unsure if there’s even established research that addresses them. You are correct that Sarcosine is a Glycine agonist. It is a GlycineT1 Inhibitor, essentially a glycine reuptake inhibitor.

Unfortunately, we can’t provide any additional information on down-regulation. These questions would certainly be suited for a discussion with a physician. Perhaps your physician can consult with a colleague that is well-versed in integrative psychiatry.

Please understand that as a manufacturer, we are limited in providing any healthcare advice.

In other words, they have no idea if sarcosine can lead to NMDAr downregulation.

#4 Heraclitus

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Posted 03 April 2014 - 12:12 AM

In other words, they have no idea if sarcosine can lead to NMDAr downregulation.


If it does downregulate NMDA then it might be simply a matter of taking enough magnesium before bed to even things out. Pure speculation though, because I don't recall seeing anything that said magnesium could upregulate NMDA, although I'm fairly certain magnesium is a NMDA antagonist.

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#5 Mnemonicsmoke

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Posted 13 October 2014 - 03:04 PM

I do know for sure that it down regulates an NDMA sub unit that is involved with the sensitization for pain. 
( at least in rats )

http://www.ncbi.nlm....pubmed/24598217
and here's another study to give it some perspective
http://www.jpain.org...0796-7/abstract

However, I'm no expert but it doesn't seem like every single sub unit of NDMA receptors is going to be decisively influential in determining cognition. Also I read some more rat studies about pain and sarcosine and Sarcosine didn't affect ALL subunits, actually s'far as i know just this one, but I haven't read EVERY single study out there lol.

Looked into it some more here is the wiki article on NR-1

 

 

Glutamate [NMDA] receptor subunit zeta-1 is a protein that in humans is encoded by the GRIN1 gene.[1][2]
The protein encoded by this gene is a critical subunit of N-methyl-D-aspartate receptors, members of the glutamate receptor channel superfamily which are heteromeric protein complexes with multiple subunits arranged to form a ligand-gated ion channel. These subunits play a key role in the plasticity of synapses, which is believed to underlie memory and learning. The gene consists of 21 exons and is alternatively spliced, producing transcript variants differing in the C-terminus. Although the sequence of exon 5 is identical in human and rat, the alternative exon 5 splicing in rat has yet to be demonstrated in human. Cell-specific factors are thought to control expression of different isoforms, possibly contributing to the functional diversity of the subunits.[2]

I have been taking Sarcosine for OCD and this description definitely seems to hold true, maladaptive mechanisms that have made my OCD worse have definitely improved, as if my brain was more readily re-learning more healthy ways to think...but perhaps this is just the way our brains manage learning? You have to learn new things for a certain period to overcome...whatever... but at some point it has to consolidate and become more rigid, less flexible to change? (Thus the down regulation)

 


Edited by Mnemonicsmoke, 13 October 2014 - 03:13 PM.

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