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Hear me out. There's lots of emphasis on here placed on NMDA antagonism. As far as I can tell the thinking goes MDMA, LSD -> NMDA agonism -> HPPD (help) --> how to fix --> NMDA antagonism (opposites). This makes sense and I know a lot of people have had success with antagonising the NMDA receptor in mitigating their symptoms. A good example of success with this thinking here. And here, we see Dextrorphan (an NMDA antagonist) prevents the neurotoxic effects of MDMA in rats. But this is administered with the MDMA. Of course, we don't have this luxury. But, what about NDMA agonism or selective NDMA agonism? Check out the profile of GLYX-13: GLYX-13 - partial NDMA agonist - enhances memory and learning - readily crosses the blood brain barrier - shown to increase Schaffer collateral-CA1 LTP in vitro - shown toelevate gene expression of hippocampalNR1, a subunit of the NMDA receptor, in 3-month-old rats - Neuroprotective effects have also been demonstrated in Mongolian Gerbils by delaying the death of CA1, CA3, and dentate gyrus pyramidal neurons under glucose and oxygen-deprived conditions - 'long lasting antidepressant' Comments from person here: Okay, now how I actually got to this compound, and the point I will charter into the lands of sounding like an idiot, but, if only to be better informed then that is okay. I am ready to get schooled (raising hands for ignorance) So my thinking and research generally adopts, like quite a few people I have seen here, a PTSD-esque template for HPPD. To simplify my thinking (which I am eternally trying to put more thoroughly into a document), the trip(s) that led us to HPPD were traumatic experiences, analogous to watching someone get blown up in a battlefield; the mind goes into overload, and you're left with damaged hippocampal and amygdalal regions, causing a stuck fight-flight response loop between the hippocampus, amygdala and other limbic regions and your visual cortex (of course there are other areas involved too). So the HPPD mind is in some sort of constant fight-flight response, hence, aroused sympathetic nervous system, the HPA axis is affected, neurotransmitters, hormones all over the place blah blah, hence you feel pretty messed up all the time. But you knew that. Anyway, so until the fight-flight response loop is resolved, I don't think anything is going to fix all this stuff successfully... so, we need a resolution from the top down, then everything else will hopefully figure itself out, or at least be able to. So I am proposing the amygdala and hippocampus as the core pathological areas that need targeting in treatment. On that I found out about D-Cycloserine. - Primarily it is used as an tuberculosis antibiotic. Otherwise; -It is also being trialed as an adjuvant to exposure therapy for anxiety disorders (e.g. phobias), depression, obsessive-compulsive disorder and schizophrenia. - Recent research suggests that D-cycloserine (d-4-amino-3-isoxazolidinone) may be effective in treating chronic pain. - The side effects are mainly central nervous system (CNS) manifestations, i.e. headache, irritability, depression, psychosis convulsions. Co-administration of pyridoxine can reduce the incidence of some of the CNS side effects (e.g. convulsions). - These psychotropic responses are related to D-cycloserine's action as a partial agonist of the neuronal NMDA receptor for glutamate and have been examined in implications with sensory-related fear extinction in the amygdala, and extinction of cocaine seeking in the nucleus accumbens. - D-cycloserine is a partial agonist at the glycine receptor, and has been shown to have cognition-enhancing properties for models of Parkinsons disease in primates.[5 Facilitation of Extinction of Conditioned Fear by D-Cycloserine In PTSD treatment, as many of you will know, exposure therapy does what it says on the tin; the subject is asked to face up to the traumatic experiences of their past with the goal of eventually being able to accept, emotionally process and then rid themselves of them and the anxiety and fear that comes with their avoidance. Only problem for us is how do you expose yourself to the ineffability of tripping without taking the same substances that brought us here, and, does that even count as exposure? It's hardly going to replicate that trip, especially with the chemical diversity of compounds bought on the street, and the extremely subjective nature of tripping. I have suggested the idea of exposure using the same substances as potentially beneficial around on this forum, but haven't founded my claims well, because something else would need to go on at the same time as this exposure (if my thinking works) and I can't figure out what. I have pondered on the idea of teaching your body to release certain chemical responses to overwhelm, for example, a bombardment of the visual cortex from a psychedelic substance- a kind of gene response conditioning. However, there appears to exist no such practice as far as my personal research goes. Besides, that all sounds a bit idealistic, futuristic, or stupid. Back to D-Cycloserine and exposure. Note some of the abstract from the study above; We see the same here; D-cycloserine augments exposure therapy. "Blockade of [the NMDA] receptor blocks extinction"... to my analysis, the persistent visuals are evidence for the brain trying to process emotional trauma - the emotional trauma of tripping - hence the reminiscent visuals. If the brain is trying to extinguish trauma, and the blockade of the receptor blocks extinction, why would you want to block it? And why would you in fact not want to help it with a compound such as D-Cycloserine, which, could potentiate the processing of the emotional data? I mean obviously this idea needs a deeper analysis, but I fail to see why it should fall at the first hurdle. Notes from http://www.ncbi.nlm.nih.gov/books/NBK2532/ (emphasis in bold) I fail to see how NMDA antagonists are beneficial (compare NMDA (partial) agonists above, 'improves learning', with the opposite of antagonists) , with a direction to full recovery anyway, are they not the opposite? And appropriate activation of the NMDA receptor plays a critical role in learning, memory LTP. Why would you want to block it/not aid it? It seems to me that antagonists would only skip over the core issue here without dealing with anything fundmental to a full recovery. They might mitigate symptoms due to messing up the learning/memory system in general (damaging it) rather than helping process the emotional information. I am prepared to be corrected as fallacious In the light of NMDA antagonism simulating schizophrenia and causing memory impairments, is this really even a line of treatment to be considered at all? And are the profiles of D-Cycloserine and GLYX-13 which facilitate the opposite, not in fact more helpful, in resolving more fundamental issues, helping process trauma? There's lots of anecdotal evidence against what I've said, clearly NMDA antagonists have helped many, I wonder how much relief overall their usage brings. I haven't heard of anyone approaching it from a different angle though, either I'm being stupid or it might be worth a shot I would like to go into more detail in this initial post, but it would take me ages. I will update accordingly.