NMDA receptor Puns

And at the same time NMDA antagonism like memantine works great for ADHD by reducing PFC glutamate release/excitotoxicity? As someone with ADHD who's unable to fall asleep I have no idea if I should be nuking my NMDA receptors or opening the floodgates 😔

I am looking into taking Agmatine to try to restore the GABA-Glutamate balance in the brain. Due to past substance abuse, I feel that my GABA levels are low and my glutamate levels are higher than what I want.

Since Agmatine is an NMDA receptor antagonist, I'm wondering if Agmatine will upregulate NMDA receptors in the long run, thereby raising glutamate and having the exact opposite effect of what I'm trying to accomplish (more GABA, less glutamate).

I'd be very grateful if anyone can chime in. Thank you!

https://pubmed.ncbi.nlm.nih.gov/1388081/

https://pubmed.ncbi.nlm.nih.gov/24656255/

VSS is an electrical synapses issue over a chemical one

I really liked the effect that D Aspartic Acid has on me and I believe that it must be because of its effect on the NMDA receptors, but I am not sure.

It makes me relaxed, less worried etc.

D serine apparently reduces paranoia and other substances that help people with schizophrenia include sarcosine, glycine and I have found D aspartic acid mentioned as well.

My guess is that D aspartic acid could be a substitute of D serine, but it is just a guess.

I am concluding that it is the NMDA hypofunction that gets addressed by D Aspartic Acid.

I find that after about 7 to 10 days it has bad symptoms that I believe comes from testosterone reducing effect that it apparently has. Is D serine likely to do the same?

Secondly, would other substances such as L serine which is more easily available help people with schizophrenia as well considering it would address NMDA hypofunction as well.

I was just googling 2-FDCK (a legal Ketamine analog) for my own attempted use of it in antidepressant treatment. Someone said something like "at low doses it's like alcohol", and I'm like, "hm... well alcohol is also a dissociative basically, sure feels like that", and I googled "alcohol NMDA" and voila, it seems that that is the main action of alcohol.

Come on people, how come noone thought of this earlier! :)

Disclaimer: I don't claim I've figured it all out, I just think this must play a role. I mean, NMDA antagonists are new antidepressant drugs.

I might end up antagonizing my NMDA receptors

Hi,

I suffer from something called dissociation and I have been taking Melatonin for over 2 years now ( I know, way too long), but since of yesterday I told myself that Im going to quit it. Now I read online that Melatonin actually blocks the NMDA Receptors which then can lead to dissociation and malfunctioning of some brain parts (just like Ketamine). And I wanted to ask you whether someone has any idea on how to open up the NMDA receptors, which then might make me dissociate less (I think?)

So i’m taking a break from dissos just wondering if there’s anything OTC I can take for the brain fog/ Agitation/ and just to feel good and heal receptors while i’m on the break ? anyone got tips?

Disclaimer: Formally diagnosed with chronic depression and generalized/social anxiety, but not under any course of treatment currently. I've tried various SSRIs, SNRIs, and TCAs but couldn't tolerate any of them. I'm not taking any other supplements or medications that are noteworthy, mostly things like vitamins and fish oil.

I have been taking Magnesium L-threonate 1000 mg daily (giving 75 mg elemental magnesium) for about 1 month now. The first 3 weeks I got the benefit of reduced anxiety and improved sleep (due to feeling more relaxed).

Coming closer to 1 month, I'm starting to feel dissociated and emotionless, characterized by flattening in mood and lack of facial expression. Sure, my anxiety has been totally eradicated, but the caveat is that I can feel that people are finding me unapproachable. I feel nothing and that affects my ability to become interested in people or in any activity at all, and people can see that.

My ability to recall knowledge, form coherent sentences and be spontaneous have been reduced. I can barely remember what I did the day before.

I've been waking up 2-3 times every night and that seems to be what's affecting my cognitive ability. I also don't feel tired when it's bedtime anymore.

I did some research on this and found these:

NMDAR activation regulates the daily rhythms of sleep and mood

Sleep deficits in rats after NMDA receptor blockade

This doesn't seem to be much of a nootropic to me.

Edit: To add more info -

• I'm in my mid 20s.

• Besides waking up in the middle of the night, I also sleep less. 6 hours vs the usual 8-9 hours.

Fully explained by Andrew Huberman in this segment from his podcast

"There are now several studies... pointing to the fact that creatine supplementation doesn't just have these positive effects on physical performance but can also be used as a way to increase mood and to improve the symptoms of major depression."

Hi fine people

Chronic pain, alzheimers, Parkinson's, depression, addiction.. everyone knows someone whos life is affected. Here is a few papers about the relationship between these conditions and LTP.

Its interesting to think about how important LTP is for learning, yet when its overactive it becomes one of the drivers for alzheimers. Biology is full of homeostasis mecanisms and there's often 2 sides to each coin

LTP and depression

LTP and chronic pain

LTP and Alzheimers

LTP and Addiction

LTP and Parkinson's

Long story short, I've been in love with dissociatives since my teens, used them every now and then with usually great results. Never had any hints of psychotic symptoms which would exceed the trip's duration.

Then life wanted me to lose my longterm gf and home, and I slipped voluntarily into a heavy disso addiction. Blew through a solid three figure number of arylcyclohexylamines with concomitant morphine use (don't know the relevance, opi + disso is a combination which I saw mentioned in reports from time to time usually with good results), every day multiple bumps of 2F- and DCK. During this time, something changed. Acoustic hallucinations would set in, beginning very subtle in form of whispering in the rushing of running water or the humming of a fan. This progressed into listening words or even complete conversations sometimes. Always only as long as I had the drug in my system but eventually a second stream of thought would manifest. While under the influence, over time the required dosage got lower and lower while general tolerance skyrocketed - I'd use dosages which a disso naive user would send into anesthesia while I still functioned more or less.This second stream of thought is difficult to explain - it has no sex, is clearly identifiable as originating in my head, under the influence or sometimes before falling asleep, complete conversations could be made yet it (of course) couldn't provide me any information which I didn't already know myself. Eventually I'd begin to see it as sort of a mirror of my own, a strange reflection.

Now this should clearly be a sign to stop, which I eventually did and with sobriety the phenomenon began to diminish. One low-dose 1cP-LSD trip was beautiful and well tolerated, no re-occurance of the thoughts/voices. But dissociatives, even memantine when dosed above the medicinal 20mg's, will trigger and while tolerance built down, it is somewhat incomplete (became more sensitive to certain aspects of the dissociative experience while others, unfortunately many of the positive ones, like boundless hypomanic energy and feelings of weightlessness/floating, etc, are gone almost completely).

-> So, afaik based on reading PubMed papers etc, dissociatives are used as a schizophrenia model (which I feel is flawed, as neither the acute, nor semi-chronic effects of dissociatives are anything like what the schizo folks experienced, was voluntarily in the mental ward and there you've got plenty of time to talk with each oth

https://www.sciencedirect.com/science/article/abs/pii/0166223687901779

Not sure if this kind of post is allowed here, but I think a lot of the members of dxm related communities have a wealth of knowledge relating to the NMDA receptor! r/NMDA is a place dedicated to answering questions about the nmda receptor! I would be happy to have all of you guys here to so we can all learn more about our body and brain!

I started LDN last night at only 1 mg and today I feel nauseous and extremely drowsy to the point where I’m really struggling to make it through the work day.

I tried LDN briefly before and remember having similar side effects in addition to some serious anxiety/depression, so now I’m wondering if maybe just just am someone who can’t tolerate it.

I seem to be able to tolerate most meds/supplements except the ones that I’ve tried for anxiety. Does anyone have knowledge of LDN and NMDA/GABA/glutamate? I did a quick Google search and it seems to act on NMDA receptors and all the supplements I’ve taken that are supposed to interact with glutamate/GABA/NMDA all seem to make me extremely drowsy and nauseous. I’ve had similar reactions to glycine, magnesium glycinate, 5htp. I don’t understand the science enough but there seems to be a connection from what I understand.

I’m wondering if I should even try and push through since I took such a low dose, feel pretty terrible and had similar experiences when I tried it before (I think I only tried it for 1 month before).

Hey guys I’m not sure if this kind of post is against the rules but here goes nothing. I’ve started a community called r/NMDA, it’s focused on the research of the nmda receptor. The dxm community and its members have a wealth of knowledge relating to this receptor and its mechanisms. I would like to invite everyone to check it out. Cheers!

I notice that NMDA is primarily responsible for the dissociative effects. Given 1st plat doesn't really have any, could it be the case that DXM is only an NMDA antagonist at higher doses?

I ask because i am taking a tolerance break from dissociatives, but have a nasty cold atm and am hoping to have a low dose of DXM without ruining my break. Curious to hear everyone's thoughts!

What happens when your body starts attacking its own NMDA receptors? The list of symptoms is scary but the good news: its treatable. I didnt know about it until today so i thought I'd share what i learned about Anti-NMDA Receptors Encephalitis

Anti-NMDA Receptor Encephalitis

This article refers to the interplay between CB1 activation and NMDAR inhibition, something I've read about in passing once or twice before. I'm trying to understand how chronic CB1 activation might effect glutamate transmission, especially upon cessation of chronic (heh) CB1 agonism. The reason for asking this is that I have observed that acute bipolar (manic) symptoms that arise following cannabis cessation can be temporarily halted via ketamine administration. Could this potentially be due to a buildup of extracellular glutamate, causing excess excitatory activity once NMDA receptors come back "online"? I would love if there were a more sustainable way to counteract this rebound.

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Pyroglutamic acid resembles the molecular shape of the piracetam.

Does it mean it gives piracetam like nootropic effects .

Searching it on PubMed ... Got me these conclusions :

• It increases Acetylcholine release
• It increases GABA release
• Protect against glutamate toxicity

Also .. it is added in alcohol hangover formulation. in order to prevent alcohol deleterious effects on NMDA receptors .

What is the role of Pyroglutamic acid in NMDA receptors ... ?

Does it agonize NMDA receptors like D-Serine/D-Aspartic acid ?