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Nucleotides as NMDA antagonists?

(zonk)

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I was searching for novel NMDA antagonists when I happened to notice guanosine, adenosine, and inosine endogenous compounds as NMDA channel blockers but I'm confused as to there exact method of blockade. They're dose dependent and the most potent ones seem to be the triphosphates(ATP,GTP,ITP) and thiophosphates(ADP beta S, GDP beta S). I've seen some of these listed as direct antagonists, some as "modulators", and some as glutamate reuptake enhancers. They are effective at all NMDA receptors but seem more preferential toward NR1/2-A/B but many are quite effective at the non-NMDA receptors too.

My question(as with most)is how effective/powerfull would these be? They're neuroprotective effects are documented but like any typical BLer I'm also interested if there'd be a noticable mind-altering(dissociative type)effect and what the average dose(orally/IV). If there is a possibility of decent effects if/what kind of subs to these compounds might yield more potent/preferential compounds.

As a slightly unrelated(compound-wise)topic... I was reading on neurosteroids and found that the base for these was a potent endogenous product called Allopregnanolone which is used as an anesthetic and is a GABA-A agonist/modulator. The sulphate(also endogenous)is an NMDA antagonist, not sure if it still has effect on GABA receptors and again-not sure how strong of an antagonist it is? Seems estrogen related compounds are all antagonists but as a guy I'm obviously not cool with taking female hormones for a buzz but allopregnanolone sulphate seems like it would be safe to experiment with although oddly I couldn't really locate a CAS# let alone a supplier.

Are these worth looking into for ANY kind of relaxing or recreational effects??? Could different substitutions lead to even greater compounds?
 
I think those nucleotides would only cause CNS effects if injected directly in the brain... Oral administration would just lead to rapid metabolism or poor BBB penetration.

Allopregnanolone doesn't have a feminizing effect because it lacks the aromatic ring found in estrogen molecules. It binds to the neurosteroid site of the GABA-A receptor and causes sedative-hypnotic effects. Animals learn to self-administer allopregnanolone ( http://www.ncbi.nlm.nih.gov/pubmed/12062582 ), and it probably even leads to a withdrawal syndrome after cessation of chronic administration. Looks like something that could be used as a substitute for benzos/barbiturates.
 
The sulphates have very different profiles tho. I was hoping it would be nothing more than an NMDA antagonist but info on ALLOPREGNAS isn't as abundant as i'd like it to be and I'm not sure of it's effects on GABA
 
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