Fawkinchit

I did done reading the other day on gene expression, and this cannot be the cause. Hallucinogens do change gene expression, however, this is not permanent, and it does not change actual dna coding, it only increases/decreases a couple of gene expressions temporarily. I think it may be a large misconception that actual gene coding is changed?

Cool!

Well, is there anything else that hallucinogen have a direct connections with?

I agree, thats what this is about, making connections, and our first connection is the 5ht2a receptor. I dont think that will we be able to definitely prove a solid diagnosis for this but I believe that we can deduce to the most reasonable and probable cause. Something should make the most sense. So we need to just get ideas and make deductions based on those ideas, ideas made through connections.

Regardless of their action, they still down regulate 5ht receptors, all receptors in regards to down/up regulating act in the same manner.

Do some research on ssris and 5ht receptor down regulation, its very common and always reverts back to the norm after ssri use discontinued.

A good question to ask there is what are the effects of down/up regulations of 5ht2a receptors? Mainly is what this is showing is that receptor sites will minimize to counter the use of hallucinogens, however after a short time period the synapses will replace the receptors after agonist usage is discontinued. Everything seems to be pointing to specific localized 5ht2a rich neuronal apoptosis.

Alot of people never notice the outlining of the brain in this picture Depicting mind force, 9. Another cool tidbit is notice that the fingers are not touching, this may actually be significant.

The olfactory tubercle is a multi-sensory processing center due to the number of innervations going to and from other brain regions such as the amygdala, thalamus, hypothalamus, hippocampus, brain stem, auditory and visual sensory fibers, and a number of structures in the reward–arousal system as well as the olfactory cortex. Due to its many innervations from other brain regions, the olfactory tubercle is involved in merging information across the senses, such as olfactory—audition and olfactory—visual integrations, possibly in a behaviorally relevant manner. Thus damage to the olfactory tubercle is likely to affect the functionality of all these area of the brain. Examples of such disruption include changes in normal odor guided behavior, and impairments in modulating state and motivational behavior (Wesson & Wilson 2011) which are common in psychiatric disorders such as schizophrenia (Rupp et al. 2005), dementia (Murphy, Nordin & Jinich 1999) and depression (Negoias et al. 2010). The Olfactory tubercle is directly effected by 5ht2a receptors, more proof that there may be some form of brain damage.

This can be easily proven as wrong, maybe you are thinking of social anxiety? This is wrong because shown areas of damage to the cerebellum cause uncontrollable vertigo, stroke victims to this area can NOT consciously or subconsciously control their vertigo, or their anxiety. There are parts of the brain that regulate these things, If they are missing, they cannot function.

Id take VS over anxiety any day.

wanted to correct you on 5ht2a receptors and GABA, they are completely different receptors, they do have interactions but GABA has its own receptor sites. If the problem were a lack of GABA on receptor sites then benzos would be a fix it for HPPD.

Its a good idea, thats for sure. I will say though that under the circumstances of altered gene expression, how and/or why would there be varying levels of recovery? If a gene is silenced, then it will stay that way, and no changes would occur there after, so why would there be improvements in some people?

Never really had any other than visual snow and sometimes lighting would seem to get REALLY bright some times. Anxiety is the biggest issue for me.

Im starting to disagree with this, providing some information to show your idea would be nice, however, if it were from gene expression then everyone that did hallucinogens would get HPPD.

What do those areas of the brain effect/control?

I disagree that most make a full recovery, I feel that most dont, I believe that alot do get better, but so do stroke victims, just their damage is much more extreme and recovery for them is limited. In HPPD it seems very localized to specific sections of the brain dealing with 5ht2a receptors. My DR/DP, and visual snow is gone, I never get it anymore, and my balance has returned, but my anxiety is still there, any contact with to many stimulants makes it pretty bad. So even though yes it is better, its not a full recovery. But I think that most at the point where I am at would say they have recovered.

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A new potential cause that I think is the most logical route to take things is the idea that receptors activate the release of certain chemicals when they are stimulated. Hallucinogens create a very strong agonizing effect on 5ht2a receptors, meaning that, whatever these receptors cause the release of, will be in full effect under the influence of 5ht2a receptors. So there may be a chemical release that has done some damage, or even destroyed, specific localized neurons that are affected by 5ht2a receptors. Under the circumstances of this damage, certain areas of our brains then lack the regulation of neuronal activity, causing high energy flows of things like visual response, anxiety, the inability to balance ones self, etc. A good example of the effects can sometimes be likened to stroke damage to the cerebellum, where high anxiety, loss of balance, and vertigo are the usual symptoms. It may be the case that there are a large amount of 5ht2a receptors on the cerabellum, and if thats the case it would probably be safe to say that there are probably alot on the visual cortex as well. The information that I have found that helps this idea is from wikipedia stating what chemicals are effected in release by the activation of 5ht2a receptors. 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, by enhancing glutamate release followed by a complex range of interactions with the 5-HT1A, GABA, adenosine A1, AMPA,mGluR, mGlu5, and OX2 receptors. In the rat cerebellum, the protein has also been found in the Golgi cells of the granular layer, and in the Purkinje cells. Excessive levels of glutamate have been shown to cause neuronal apoptosis. We see 5ht2a activity in the cerebellum of rats Receptor activity in the neocortex, this will acclimate for a large amount of effects. Green Areas rich in serotonin receptors

I wanted to make a reversion of my last thread, a potential cure for hppd, which I feel has gone off track with randomized posts and a strong strife to find a cure than to find the cause. So this thread will have some guidelines and rules. Guidelines: We are searching for the cause. Even if the cause is brain damage we are not hopeless. When we find the cause we can find the cure. Make connections. Rules: If you post clinical trial information, there must be a brief/simplified description of the information that you have found and how it applies. Please talk in simplified terms if you can so that everyone can understand. We do have very smart people on this site but not everyone is well versed in biomedical science.. If you guys have any other ideas for the rules or guidelines let me know, or if you guys feel that you would like a rule change let me know as well. I think that so far we have made some really good progress are we are ALL LEARNING ALOT! Which is awesome. Post #2 will start off a new idea that is a very good lead for the cause.

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Ok for the meantime I think we need to start looking for traces of potential cns damage cause by the over activation of 5ht receptors. http://en.m.wikipedia.org/wiki/Excitotoxicity#section_2 If you take for example the overstimulation of ampk receptors by excessive glutamate we can see the damages effects by excessive release of calcium ions cause neuronal apoptosis. So, what happens with over excitation of 5ht receptors and what damage is cause?

Possible tissue damage excessive glutamate release. As these receptors activate the release of glutamate. http://www.dana.org/news/cerebrum/detail.aspx?id=7376

Possible tissue damage excessive glutamate release. As these receptors activate the release of glutamate. http://www.dana.org/news/cerebrum/detail.aspx?id=7376