SugarFree88
Greenlighter
- Joined
- Apr 6, 2010
- Messages
- 33
The current consensus for the theory of HPPD amongst the researchers at Harvard medical is that theres been a loss of 5-ht2a receptor subtypes on GABAergic inhibitory neurons. Normally, when serotonin binds to these GABAergc neurons, it releases GABA. GABA output=inhibition=calm.
I found this on this site and i thought about the fact that i got HPPD after a really deep, almost anaesthetic K-Hole.
Now i'm pretty sure that Ketamine does not bind 5-HT2A receptors while it's pretty sure that it someway has an activity on sigma 1 receptors.
So i'm wondering if what i've been through those months (hallucinations, CEVs, moving walls) was just because of sleep deprivation and all the weed i smoked before that K-Hole (but not during it anyway).
Sorry for my english, and, btw, i'm fine now.
I found this on this site and i thought about the fact that i got HPPD after a really deep, almost anaesthetic K-Hole.
Now i'm pretty sure that Ketamine does not bind 5-HT2A receptors while it's pretty sure that it someway has an activity on sigma 1 receptors.
So i'm wondering if what i've been through those months (hallucinations, CEVs, moving walls) was just because of sleep deprivation and all the weed i smoked before that K-Hole (but not during it anyway).
Sorry for my english, and, btw, i'm fine now.



