jacktheripper42
Bluelighter
- Joined
- May 9, 2017
- Messages
- 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?
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?