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questions about NDMA toxicity

T

thesomoan

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It appears that there is no conclusive data as to whether Olney's lesions occur in humans, and whether or not they would occur at low-moderate doses, however, there seems to be a general consensus that some dissociatives, such as PCP, are so neurotoxic because they are a highly selective NDMA antagonist. Yet other selective NMDA antagonists (and even PCP analouges) like ketamine exhibit very little neurotoxicity and are widely used in medicine. I am confused as to what determines a drugs NMDA toxicity, and what the link between the NMDA receptor and illnesses like schitzophrenia etc.
 
Really? i thought that PCP was discontinued because of its neurotoxic effects/links to mental illness. Ok thanks the 5-ht2 agonist seems interesting i will look into that.
 
atara said:
PCP is not terribly neurotoxic; however, it is strongly dopaminergic and can thus produce a hangover.

NMDA toxicity is quite easily preventable, incidentally, if it does exist. 5-ht2a agonists (psychedelics) prevent it
Click to expand...

as do gaba agonists


nmda antagonists are actually neuroprotective in the right doses as they interfere and prevent parts of the ischemic cascade
 
It is speculated that PCP's D2 agonism is connected to the many instances of psychotic behavior that have been reported under the influence. The D2 receptor is the site most commonly antagonized by antischizophrenia medication; the potency of a typical antipsychotic is directly correlated with it's potency at the D2 receptor.

Sorry, but I'm not buying it. PCP produces NMDA antagonism and dopamine reuptake inhibition. That is to say, you get drunkenness, and lots of energy. And whenever those effects are combined, you get lots of dumb shit. Anaesthesia doesn't help the situation.
 
Alright lol I am inclined to agree with you on that point, I found it very strange that PCP's NMDA antagonism was simultaneously condemned as being highly dangerous, while its weaker analouges are used in pediatrics. Do u know if anyone has experienced lasting psychotic effects from PCP or if "psychosis" only occurs in people strung out as fuck?
 
PCP was discontinued because it greatly FX a broader range of NMDA receptors including the Glycine sites, coupled with strong DRI including D2 which strongly contribute to psychotic FX, ketamine shares some of these properties aswell but to much more well balanced in the right direction but much more importantly it's short duration of action is why it's used and not pcp. Plus stimulant properties are also not good for the perpouses of anesthesia unless it's topical then it doesn't really matter.
 
BTW I've experienced PCP psychosis several times. This was not from being "strung out" or heavy usage, it can happen with one single use and is very real and can be very scary. PCP can b heavenly or demonic, i guess as is the case with any psychedelic other than DMT that is, i just cant see that drug ever being negative at any dose or in any setting, but that's just IMHO
 
i believe PCP does effect Gly NMDA sites. I wasn't saying it was discontinued cuz of how it works specifically, just that compared with ketamine those are the behind the scenes fx that create the psychosis(long duration/potent stimulation/broader range of receptors affected)
 
More and more, I'm beginning to believe that "NMDA antagonists" as a category is about as useful as "Narcotics" - that is to say not at all.

It really seems to me that the one thing all NMDA-antagonists have in common is that they are all active on several other sites with wildly differing effects, making it seem like NMDA-antagonism is a minor part of each of these drugs' actions.

As for toxicity, I personally don't even bother to look at research that lumps a medicine like Memantine together with a poison like Dizocilipine and comes up with conclusions about possible toxicity.
 
i agree with you Jamshyd. The effects are so varied its stupid to group them as such, specially in recreational sense. same as serotogenic drugs which affect multiple systems! i remember reading about a 5ht agonist that reversed pcp induced cognitive impairments via glutamergic system cascade
 
About the PCP videos: A dark, quiet room is supposed to be a better environment for recovery from PCP intoxication than those shown. But people like drama!
 
In the ignorance of youth I was a DXM addict for 6 years. I used an average of 3-4 times a week. During this time I also became addicted to crack. So on a lot of occasions I did both at the same time. I could tell a definite strong interaction between the two. I would get a burning headache and a sharp pain in my lower left abdomen. Now years later I know I caused some brain damage. Its nothing that is debilitating but small parts of my personality are suffering, In particular social situations. I've done a lot of searching but still can't find out what the mechanism is behind Cocaine and DXM. Maybe it is duplicating the mechanism that make PCP neurotoxic.
 
Rocknroll, 50-60% intrinsic activity at D2 is leaning more towards the full agonist end of the scale. Aripiprazole is much weaker I think, I remember reading somewhere there was some controversy over weather it was even a partial agonist or just an antagonist. Having trouble finding actual numbers now though...
 
i think aripiprazole is both, being a full modulater. I couldbe wrong but think that's its thing, it was a pretty relvolutionary chem
 
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