Fawkinchit

asdf

5-HT2A is expressed widely throughout the central nervous system

 (CNS). It is expressed near most of the serotoninergic terminal rich areas, includingneocortex

 (mainly prefrontal

, parietal

, andsomatosensory 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 enhancing glutamate

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]

 andOX2

 receptors.[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]

Ah right, an overexcitation of specific neuron.

Mg could you elaborate on what you're posting

Retigabine is just a potassium channel opener. Not sure what the significance of this is?

Mildly..........................as long as tardive dyskinesia doesn't make anxious

You got that from the HPPD or already had it?

Edit nvm guess its caused by the antipsychotics

Mg did it help your anxiety at all?

asdf

Dr A: "Studies of HPPD patients with qEEG mapping show that the disorder is represented by disinhibition in the cerebral cortex". Disinhibition means without proper controls and restraints.

The thalamus is not part of the cerebral cortex. All sensory signals go through the thalamus (except pain).

Paraphrasing another paper posted on the forum, it did attribute many HPPD symptoms as cerebral hyperactivity can be from incorrect or insufficient information getting from the retina - which would implicate retina -> optic nerves -> thalamus -> etc.

There are lots of feedback and feedforward systems in the brain, and thus oscillation (brain waves are oscillations)

Certainly everything that visual (etc) signals go through experience some processing. Signals split, go all over the place, get sub-processed here-there-and-everywhere, and then eventually get pasted together in some meaningful way we call perception. http://en.wikipedia....wiki/Perception Perception starts at infancy as hardwiring. Then plasticity and memories begin forming. Eventually here we are now, "meaning-making-machine" with perception based on past experience (memory).

For whatever reasons we get scrambled, distorted info (snow, bending, ...) and either our brains learn how to integrate "the-new-way", or signals "clean-up", or we keep experiencing "the-light-show"


Note: Sorry, no further info about Orville P Vunder.

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Basically because recreational drugs aren't the only things that can damage neurons. Aside from myriads of environment 'toxins', chronic stress damages neurons (no out side toxin at all).

This is a good point as well. But maybe the damage is somewhere else that just damage to the nuerons, maybe it has to do with damage related to the synapses etc...

I have another question about this change in brain structure or damage to CNS or something like that. If you've ever visited DPselfhelp.com it seems quite a few people experience similar visual and mental issues without ever having touched any drugs. They don't typically mention stuff like things actually moving in their vision, like people on here......but I've read a number of cases where people mention visual snow, light sensitivity, seeing the world in frames, flat/2D vision, things looking 'cartoony' or like a videogame, and stuff like that. I know we have more pronounced visual symptoms than that in a lot of cases, but I definitely have an overlap of symptoms with a lot of people who've claimed they've never done any drugs. So if our problems are from legitimate brain damage or damage to CNS from drug usage then how is it that individuals that have never taken drugs can experience many of the same things???

Thats a good question.

We had tons of threads about research papers specifically having to do with the 5ht2 feedback loop in the visual cortex involving serotonin and GABA back on the old site. If I get some more free time this week ill try to dig them back up from the internet the repost some of them.

Thats awesome please do i would like to see that. That would explain why some people are getting these symptoms from SSRIs and why syrian rue become hallucinogenic

Yeah........We'll find out on some of its efficacy in November

Would you like to be more descriptive?

asdf

What are your symptoms to make you believe your problem is reduced concentration of dopamine?
Do you feel you are coming down with a little of the ADD ?

It grabbed my attention when reading the cognitive problems on advanced parkinson's. Then looking at 43 other neurological diseases (including MS), only PD had relevance. Of course the clincher has been the response to dopamine increasing meds. For example, contrast adjustment is done in the retina via dopaminergic neurons. Contrast problems were among the first symptoms. Some (in not all) negative afterimaging is due to 'recharge' time of photoreceptors coupled with the dopaminergic neurons 'deciding' how much of the signal is relevant.

As for ADD, always had problems multitasking but was able to bury self with extreme focus on the topic/job at hand. Now am vulnerable to the slightest distraction as well as vulnerable to complete exhaustion.


I don't believe in the "push/pull" model of transmission

Please explain. As the opening of this thread began, "Everything in our universe is quite simple, Push/pull concept, up down black white red blue north pole south pole day night sun black hole etc etc etc... "

ALL neuronal communication is pulses of electricity (due to the accumulation of ions through synapses). A neuron is just an integrator (add/subtract machine) that fires when the sum reaches a certain level (action potential) of about -55 millivolts.

There are two main types of neuronal communication responses. Klonic (continuous firing) which exists in a push/pull balance in larger circuits. And Phasic (one shot) that fires due to change of stimulus.

Brain wave are simply the rhythmic patterns of feedback systems (push-pull). In electronics you may be familiar with "phase-lock loops" ... same kind of thing.

Dopaminergic systems are often described as controlling "signal-to-noise ratio". This controls the relevance of information passing through. D1 family receptors activate [push] (like glutamate and often on glutamate neurons). D2 family receptors deactivate [pull] passing signals (like GABA). So, in short, dopaminergic neurons filter and decide what to pay attention too. So you can see how this affects movement and perceptions. Decisions are affected too but more the ability to make them rather than how conclusions are derived.

These systems are 'little programs' that form and operate at the unconscious decision level - such as how to grab a glass of water and drink it. And much is learned over time - watch an infant learn to grab and control fingers ... or a musician learn to play a piece. Much fine tuned coordination is through the Cerebellum which is not dopamine dominant but has some http://www.ncbi.nlm....pubmed/16035192


ADD/ADHD is often blamed on norephinephrine as well as dopamine. Norepinephrine is mainly used in the locus coeruleus (90%). These two blue dots are big switching centers for what parts of the brain are dominant. The 3 main modes are: sleep, vigilance and concentration. However the locus coeruleus is controlled by the front part of the brain thus more of a relay station. But again this system is measured by pulse rates and patterns - push/pull.

So unlike dopaminergic circuits which are at lower level functions, this center controls what parts of your thinking is dominant ... huge systems. When you think about it, vigilance is a type of attention ... not concentration but hyperawareness (is there a tiger behind those trees? ...)

The development and use of SNRIs is largely experimental ... "Let's see what happens when we change these chemical concentrations ..." And of course it does change the balance of certain systems.


At any rate, you can see how anything that affects dopamine and/or norepinephrine could have profound effects. While HPPD is largely described as cerebral disinhibition (and thus GABA/benzo help to quiet it), dopamine may also quiet overactivity by fueling the system to regain control of itself -- if low fuel is a factor. Or to filter out noise that the brain is trying to make sense out of.

I think the theory of a down regulated 5ht2s receptor in the visual cortex is the most accurate theory we have right now and it makes the most sense. Hallucinogens attach themselves to these receptors and begin to cause rapid firing of the neurons and this causes quite a bit of stress in the synapse so the neurons that are downstream and receiving the big wave of the neurotransmitters can definitely become overloaded, as we know now with HPPD cases, and cause some type of genetic mutation to downregulate certain receptors to protect brain tissue from oxidative stress.

Now say if this theory were true, the problem is that these receptors stay downregulated and create a big problem on those neurons that have lost the receptors. They can no longer properly respond to serotonin and this makes it impossible for them to fire off and release GABA to inhibit and stop the nerve signal. The result is that the neurons are constantly firing and I believe (this is just my uneducated opinion) that we are seeing all of these visuals now because there is nothing there to inhibit the visual excitatory stimuli in the visual cortex.

Wow, maybe thats it! maybe 5ht2a receptors become permanitly down regulated! hence the need for an inverse agonist to reverse the effect. Possible, but still a shot in the dark.

Hey guys i'm still here but don't have internet or much time due to work.

Hope - you don't HAVE to have a phd, right there you already failed in curing this, they have a brain, you have a brain, what's the difference? They've spent more time researching.

As for now the problem is somewhere in the CNS, we need to research everything about the CNS

ok what were the first drugs you were mentioning on this post?; the first few were golden. On further review of an old drug, seriously tell me if propranolol is possibly helpful.

Its just a beta blocker, it MAY treat symptoms.

5htp2a receptor Inverse agonists

asdf

No, i was just throwing some ideas up........Listen with science, you can be wrong and you back track and start again......We are all looking for the same truth, and i am sure we will find it if we continue to work together. I learned something today that i was dead wrong about (regen./recycle receptors). ....It's good to know.

Now to the Ambien-stuff, we both know it's a sleeping pill. People get terrible hypnopompic hallucinations when trying to stay awake on this drug. (And also supposedly the dreams are wild, and people sometimes can get into the state of mind between sleep and consciousness and sleep paralysis, i believe.) Certainly, no driving.

lol.....hahahhahahahahahhaha..........wait qaiphyx, i got some drugs for you to check out tell me what you think of these drugs, ptsd drugs: Minipress and propranonol. And also~ Nootropics (don't know much about them).

***I just looked it up----wow thats a lot of them lol------i'm on like 10 of them if you count nicotine lol

What? Im pretty sure youre reading my posts wrong...

asdf

It seems to me based on the evidence of trials and studies that genetic mutation/etc. is a non-issue. Also the inverse agonists seem to be ineffective, unless there is some loophole in there.

Please provide the evidence of claims, I have seen absolutely no usage of inverse 5HT2A agonists for the treatment of hppd. Nor have I seen that gene mutation is negligible.