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25i excitoxicity via glutamate acceleration

jacktheripper42

Bluelighter
Joined
May 9, 2017
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62
If 25i NBOMe is a full agonist with ultra affinity for serotonin 5ht2a receptors then does this not mean that it leaves a person extremely susceptible to drug induced excitoxicity, considering that the 5ht2a receptors act as glutamate accelerators while the 5ht1a receptors act as glutamate inhibitors. Does 25i release a ton of glutamate since it is a full agonist of 5ht2a with super selective affinity, which causes excitoxicity?

Could this be why so many people suffer from HPPD after 25i? Glutamate induced excitoxicity damage?




Who here knows about biochemistry/neurology enough to answer this question?
 
I am not an expert on excitotoxicity but human cases of excitotoxicity are actually known, from a couple different exogenous sources (domoic acid and beta-methylamino-L-alanine), and don't particularly resemble HPPD.

Also I don't have a ref for this on hand, but IIRC the thing about 25I being a full agonist is a bit of an urban myth.
 
jacktheripper42, you've been posting for a while about this problem.:\

What have you tried to help yourself with it? Mindful meditation? Naturally derived GABAergics like, Valerian root extract, Magnolia Bark extract, Passionflower extract, Lemon Balm extract, Taurine? I'd start there. Also try N-Acetyl-L-Cysteine and Agmatine.

Maybe some Memantine or other mild NMDA-antagonist could be of help since they all reduce glutamate toxicity but make sure you understand what are you doing with them.
 
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