5 replies to this topic

[bawsh]

It has been hypothesised for a long time that NMDA hypo function can cause psychosis and there are links to several studies cited in this article.

 

http://www.nature.co...0912a.html#bib1

 

Would it be arguable that long term administration of Memantine, a NMDA antagonist could bring about psychosis?

 

There is an anecdotal case this happening on a social anxiety forum of someone who initially responded well to Memantine then experienced a sudden break with reality and paranoid delusions.

 

Could anyone hypothesise as to if daily intake of Memantine would have an accumulative effect on NMDA receptors or if it would simply have a stable effect by maintaining NMDA antagonism?

 

and Could anyone add anything to this or comment with their own experiance of taking Memantine or extended use of any other NMDA antagonists?

[ILIkeBeer]

Memantine blocks the NMDA receptors, isn't that the opposite of an antagonist?  Regardless I do not know much about this, but I would hope this isn't true because that could spell doom for GLYX-13 and the like.

[FW900]

Memantine is a weak, voltage-dependent, NMDA receptor antagonist that will not result in profound changes in brain glutamate levels that are theorized to cause psychosis. I would argue no, long term administration will not cause psychosis. Magnesium is also a weak NMDA receptor antagonist and long term use typically promotes brain health and does not cause psychosis.

 

The studies listed in the nature article you provided mainly detail antagonists that have a very high affinity toward NMDA receptors such as PCP.

 

 

Memantine blocks the NMDA receptors, isn't that the opposite of an antagonist?  Regardless I do not know much about this, but I would hope this isn't true because that could spell doom for GLYX-13 and the like.

 

No. Memantine is a voltage-dependent channel blocker rather than an "NMDA receptor blocker". It's action as a (voltage-dependant) channel blocker, mainly limits the influx of Ca2+ which is one of the ways NMDA receptors are activated. Even if this were not the case, what you describe would not produce the opposite effect of an antagonist.

[formergenius]

As I understand it, you needn't worry about GLYX-13. It's a partial agonist, which can be seen as a regulator / conditional modulator of sorts. If there are too much (endogenous) full agonists present at the receptor, it will compete with them, thereby causing a net decrease in receptor activation. If there are too little, it will act as an agonist. Hence its anti-psychotic value, and anti-excitotoxic potential.

[ILIkeBeer]

As I understand it, you needn't worry about GLYX-13. It's a partial agonist, which can be seen as a regulator / conditional modulator of sorts. If there are too much (endogenous) full agonists present at the receptor, it will compete with them, thereby causing a net decrease in receptor activation. If there are too little, it will act as an agonist. Hence its anti-psychotic value, and anti-excitotoxic potential.

 

Yeah ok I don't understand that, but I take your meaning!  Thanks for posting that... and you say you are a former genius!!

[medievil]

I took a high memantine dose the first time i ever had psychosis, i dont take nmda antagonists anymore but look into pro agonism for enhancement of cognition, negative and positive symptions.

 

Mem does reduce negative symtions combined with a atypical antipsychotic in shizophrenia.