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Je pensais que tu faisais une FMRI  

Demain je ferai le pet scan

Ok, so it would appear that its quite likely that the glutamate release is activated by 5ht2a/5ht receptors, and would pretty much solidify the neurotoxicity or any 5ht2a agonist, specific to interneurons. Here is the study that basically shows the link between glutamate and 5ht2a. https://www.nature.com/articles/1395430 So, I think everything really came around and connected everything together finally. 5ht2a agonism increases glutamate, we know already glutamate storms are neurotoxic. The neurotoxicity is mediated through reactive oxygen species leading to mitochondrial DNA damage/failure, which is going to cause them to signal apoptosis, leading to intraneuronal loss. Interneurons are regulatory neurons and without their involvement excitatory neurons will act unregulated giving the symptoms of HPPD. The only thing that can show otherwise at this point is if say classical hallucinogens like LSD or DMT etc do not show the same release of glutamate. But based on the study posted here I think its likely it will be the same.  What some people may be wondering then is why do some not appear to get HPPD and others do, but in this case the answer is simple. Because eventual neuronal loss is caused by reactive oxygen species its going to be mediated through various antioxidant profiles and according to one of the studies it looks to be glutathione, people who do not appear to get HPPD realistically are still probably losing neurons, however in the case of people with HPPD they likely have altered glutathione levels, which can occur for various reasons. Well I'll try and add some positivity for anyone reading this, cause even after studying this for 10 years now this is a pretty hard read. The positive side is, that interneurons as far as I understand are specifically close proximity neurons and have short connections, so recovery under stimulation of neurogenesis is likely to be higher than say if long distance axons were damaged/lost. To say that other neurons in the surrounding areas are not affected, I'm not sure, but when I have time I will look in to the possibility. I think though this most likely explains the cause and etiology of HPPD. Maybe we can get the information stickied so that people understand what it is that these compounds do, and will help to prevent the future use of them. It explains as well why benzodiazepines assist the best in the condition but do not mute the symptoms entirely, is that there are no receptors/synapses/neurons to exhibit GABA for excitatory neurons, and it is probably acting on downstream neurons that still have their interneuron connections. Big thanks to @MentholFlavoring for find those studies.