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?

http://www.sci-news....ticle00701.html

something interesting...

"A gene that is associated with regeneration of injured nerve cells has been identified by a team of researchers led by Prof Melissa Rolls of Penn State University."

Cool!

I'm not going to say that this is the main area [5ht2a receptors] we should be looking at.

But for this thread only!, Yes.

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

Mr. Qaiphyx:

I would like to get people like Visual and David Kozin to affirm my statement: to see if what i am saying is valid.

The truth of the matter is: I do not know for sure. Our main focus, here, is the 5ht2a receptor.

I will make an effort to not make any tangential leaps, and concentrate my posts to these focuses.

-mg

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.

SSRIs work mainly with inhibiting the reuptake duct

[hence the name Selective Serotonin Reuptake Inhibitor].

The actual SSRI chemicals do not bind to 5HT2a receptors.

"Paradoxical Regulation" of 5HT2a is relegated to agonists, antagonists, inverse agonists, etc.

SSRIs [in general] do not agonize, antagonize, etc. 5HT2a receptors.

Show me the evidence for your claims.

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

I do not believe that necessarily. I think there are less post-synaptic 5ht2A receptors in HPPD.

[for longer than average terms]

[Note: There may be:

"more Glutamate receptors/less GABA receptors." also]

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.

Back looking at: , Serine, Alanine, and Cysteine

Ni

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.

qaiphyx i have had pretty bad anxiety since i was born,i have avoidant personality disorder and many other stuff. i beat it ,i think thats why i don't have hppd anxiety too. you just have to adjust your mindset. if you do that,anxiety fades away. first thing i did was accepting that i create the anxiety not something else. you consciously do it,not subconsciously.

i have full blown hallucinations like LSD when i stare at walls and surfaces like that. dealing with anxiety is almost always the same,be it a personality disorder,post traumatic or hppd. it is hard to not give a crap about something constantly happening but you have to.

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.

Visual snow now that's what I want to get rid of I think there's a lot of options out there worth trying to help deal with the anxiety side of things I don't get anxiety anymore really only tue visual snow light sensotivty and after images really wanna beat them 3 symptoms

Id take VS over anxiety any day.

It's definitely an alteration to the inhibitory interneurons in the visual cortex and probably elsewhere. The 5-ht2a receptors have been altered to the point where they dom't release GABA after the neuron reaches it's max excitatory point to stop the nerve signal so the excitatory currents stick around for much longer than they rightfully should. This is why afterimages linger for so long or why we all have tinnitus or why we see visual snow and etc. etc. etc. It's all evidence that the inhibition that should be occuring to calm the neuronal circuits isn't working like it used to anymore.

My personal opinion is that gene therapy is the only type of medicine that is going to have a sure fire chance at making any REAL permanent improvement to people with the disorder.

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.

http://hppdonline.co...ionepigenetics/

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?

do you still have visuals / hallucinations and other stuff? I've always had anxiety(hppd like) after using stimulants(even non stimulants / stim likes like atomoxetine , modafinil)

perhaps your anxiety is something like PTSD,exposure to HPPD for long time is kinda traumatic.

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.

my money is on altered gene expression

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.

I'll be honest, most of that went way over my head. But a few comments based on my own (extremely limited) understanding. The regions of the brain that are apparently overactive in HPPD sufferers are the occipital and temporal lobes. This seems to be similar to tinnitus (something many HPPDers experience) which shows activity in the temporal lobes caused by a loss of inhibition to auditory cortex neurons in which they 'misfire' and cause the person to hear sounds that aren't real. Is a similar misfiring causing HPPD visuals? The latest sound treatment for tinnitus is able ""reset" auditory nerve cells in the brain to stop them misfiring" and "brainwave alterations were also reversed by the therapy." It is believed that GABA drugs, which can increase inhibitory signaling, should be able to have the same effect. So in both cases could it just be the case of finding the right one?

What do those areas of the brain effect/control?

I highly doubt its brain damage. And there are reports of people who have fully recovered,their numbers would be very very low if it caused brain damage. I am thinking of some kind of change which could be reversed in 5ht2a receptors.

after getting HPPD,my iq scores,reflexes,eye-hand coordination stays the same. if i focus i don't even notice i got HPPD unless i stare at empty surfaces or walls. I still get LSD like visuals if i do it,it feels like i am stuck at the last stage of trip. I am thinking of some sort of chemical change.

I never had DP/DR,maybe it is because i am very introverted and materialistic,but sometimes i can't sleep at nights alone. I still got hope that my brain will fix it on its own,some days it is like 80% gone,on others it is worse. never got as bad as first day though,it's been a month since i got it. I am giving it 2 years max,i will post there if i heal completely.

I am going to take benzos next week or so,probably 4-5 times a week.not that i feel anxiety but i am entering an university exam,any distraction that happens in exam time could possibly ruin my life so i want it under control this year.

http://www.neurosoup...n_interview.htm

http://www.neurosoup...m_interview.htm

i've found these. seems like some people can't recover from HPPD or it takes longer. Perhaps it has to do with genetics or amount of drugs that has been used?

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.

asdf

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-HT_2A 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-HT_1A, 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.

asdf

asdf

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