Fawkinchit

Now this is significant

Yah I will as soon as I get some free time. I thought everything was pretty clear

Hur hur hur. Regardless, just because were amateurs doesn't mean we cant accomplish great things. Its all about gravity, and in the end, though highly accurate, its incorrect and has been shown to be wrong by Marko Rodin. And I was wrong Einstein did go to college.

In for beach resort job

False, the brain though vast is a complex yet simple vibromimetic resonator Also false, the brain will not heal itself, if you haven't noticed yet that the scars on your arms don't heal to normal skin tissue. And quadriplegics never walk again then you have ALOT of learning to do and seem like a dreamer. I also question whether you read the entire thread, this is no long "amateur" research it's become obvious fact. BTW einstein started without any degrees and never went to college, he's was given a degree. That should show you what "amateur" research does. BTW his theory on time is not correct. Time to hit the books.

They absolutely would I believe. But how would you begin to obtain them, and how would you get them in to the various parts of the brain. Its generally best not to make assumptions based off of no research. People do it alot for some reason though. Read this entire thread, its pretty much already been shown to be a case of neuroexcitotoxicity. Good! Not sure what the hppd campfire is though?

Does for me, if you take a really small dose, like REALLY small its not to bad. But I cant continuously take it.

To my knowledge this would only increase acetylcholine, with no other real benefits. There are supplements out there that already accomplish this, inositol being one, I cant remember the others.

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http://www.luisprada.com/protected/russian_dna_discoveries.htm Someone find the english version of that book.

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I could only assume that its cause its a precursor to serotonin, were you on any other meds? Were there any other supplements? BTW 15 years? Wow man im really sorry!

It can be presumed that the stimulatory effect of reuptake inhibitors could make symptoms worse.

If you go over everythimg that I have posted recently you can see that the excitotoxicity is from 5ht2a receptor activation, its all in the notes, it goes 5ht2a agonist > 5ht2a receptor > glutamate release > excitotoxicity > neuronal apoptosis. Im sure its hard to take on and alot of people are going to just be in denial about cause brain damage seems like a dead end, but its not, neurogenesis is possible, and can be proven easily to be so, its just figuring out how. Also damage to specific sites in the cerebellum is all Ive shown, im sure that there is damage to inhibitory cells also in the visual cortex, and there should be some in the lobes, Also didnt know that the cerebellum was involved with vision can you provide the information on that.

The excitotoxicity cascade is no longer present in the brain, it is present during the influence of the hallucinogenic compounds. Once the hallucinogens are out of the blood stream the excitotoxic event ends. HPPD is a result of neuronal apoptosis(death) during the excitotoxic event. The only way to fix HPPD is through neurogenesis, the only other method of having a significant effect would be to somehow mimic the inhibitory cells such as the perkinje cells, or the golgi, which I assume would be impossible, and that would only effect anxiety and balance I believe, so visuals would still be there etc.

Excitotoxicity is the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitterglutamate (glutamate receptors) such as the NMDA receptor and AMPA receptor are overactivated by Glutamatergic Storm. In post #414 you can see that 5ht2a receptors effect glutamate release, and AMPA receptors, this means that the everstimulation of the receptor will cause an over abundance of the release of glutamate, causing overexcitotoxicity and the death of selective inhibitory neurons. That basically seems to be it guys. All the connections seem to be made.

Wow this is awesome Golgi cells areinhibitory interneurons found within the granular layer of the cerebellum. They were first identified as inhibitory by Eccles et al. in 1964.[1] It was also the first example of an inhibitory feed back network, where the inhibitory interneuron was identified anatomically. This ties in with the inhibitory feedback that I was talking about in the beginning of this thread, that there may have been damage to these inhibitory cells, and the brain now lacks the ability to modulate anxiety! The question now just remains, do hallucinogens cause damage and burn out of these cells through excitotoxicity or are they turned off through receptor triggers. Personally im leaning towards excitotoxic burnout.

This is probably a piece of gold right here. Newer findings reveal that psychoactive effects of classic psychedelics are mediated by the receptor heterodimer 5-HT2A–mGlu2 and not by monomeric 5-HT2A receptors. The mGluRs perform a variety of functions in the central and peripheral nervous systems: For example, they are involved in learning, memory, anxiety, and the perception of pain.[3] They are found in pre- and postsynaptic neurons in synapsesof the hippocampus, cerebellum,[4] and the cerebral cortex, as well as other parts of the brain and in peripheral tissues.[5] Like other metabotropic receptors, mGluRs have seven transmembrane domainsthat span the cell membrane.[6] Unlike ionotropic receptors, metabotropic glutamate receptors are not ion channels. Instead, they activate biochemical cascades, leading to the modification of other proteins, as for example ion channels.[7] This can lead to changes in the synapse's excitability, for example by presynaptic inhibition ofneurotransmission,[8] or modulation and even induction of postsynaptic responses.

This is a whole list of connections that might possibly link to symptoms of HPPD in other disorders. Feel free to do research on all these to see what you can find. 5-HT2A is expressed widely throughout the central nervous system (CNS). It is expressed near most of the serotoninergic terminal rich areas, including neocortex(mainly prefrontal, parietal, and somatosensory cortex) and the olfactory tubercle. Especially high concentrations of this receptor on the apical dendrites of pyramidal cells in layer V of the cortex may modulate cognitive processes,[8][9][10] by enhancingglutamate release followed by a complex range of interactions with the 5-HT1A,[11]GABAA,[12] adenosine A1,[13] AMPA,[14] mGluR2/3,[15] mGlu5,[16] and OX2receptors.[17][18] In the rat cerebellum, the protein has also been found in the Golgi cells of the granular layer,[19] and in the Purkinje cells.[20][21] In the periphery, it is highly expressed in platelets and many cell types of thecardiovascular system, in fibroblasts, and in neurons of the peripheral nervous system. Additionally, 5-HT2A mRNA expression has been observed in humanmonocytes.[22]

In the rat cerebellum, the protein(5ht2a receptors) has also been found in the Golgi cells of the granular layer,[19] and in the Purkinje cells. ---> Purkinje cells, or Purkinje neurons(/pərˈkɪndʒiː/ pər-kin-jee), are a class of GABAergic neurons located in thecerebellar cortex. They are named after their discoverer ----> People with cerebellar ataxia may initially present with poor balance, which could be demonstrated as an inability to stand on one leg or perform tandem gait. As the condition progresses, walking is characterized by a widened base and high stepping, as well as staggering and lurching from side to side. Interesting line of connections there, symptoms of hppd sometimes have been known to exhibit balance disorders, seems to be linked to cerebellum purkinje neurons.

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Yah that would great if he would, he has some substantial research and evidence. Obviously intelligent. You missed the whole point of the response. Good job bro!