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Hallucinogen Persisting Perception Disorder (HPPD) Support Forum
dasitmane

Bit of an idea for possible CURE. Has some weight to it.

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How do you explain GABA action which mediates in the synapse?

And how does that related to the tug-o'-war model aside from the result of an event being a plus (+) and 1 of possibly many different results being a minus (-) ?

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Let me let you into my world for a second: I am looking into Aromatics, Dyes, and Pigments. Brainwaves (1-70Hz). Circadian Rhythms. DNA: 3-dimensional wave structure.

Color Wavelengths. Spectroscopy. Fluorescence.

quinine-fluorescent-800x800.jpg

Why is Quinine Fluorescent? ........

Quinine is used to treat malaria.

Resonance, Resonance Structures, Delocalized Electrons, Ions, Negative Charges, Leptons, Quarks, Higgs Boson.

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wait i've got it!:

2012 Jan-Mar

Penicillium species present in Uruguayan salami.

Galvalisi U, Lupo S, Piccini J, Bettucci L.

Source

Laboratorio de Micología, Facultad de Ciencias-Facultad de Ingeniería, Uruguay.

Abstract

The surface coverage of certain dry fermented sausages such as Italian salami by some species of Penicillium provides their characteristic flavor and other beneficial properties. One of them is the protective effect by means of a uniform film of white mold against undesirable microorganisms. The aim of this work was to identify and to isolate the fungal species present in mature Italian type of salami and to evaluate if it is possible to obtain some of them as starters. In addition, the effects of temperature (14 °C and 25 °C), water activity (a w) (0.90, 0.95 and 0.995) and 2.5 % sodium chloride (NaCl) on fungal growth were determined. Similarly, the proteolytic and lipolytic activity and the ability to produce toxic secondary metabolites were evaluated in order to characterize some possible starter strain. All species found belong to the genus Penicillium, including a performing starter as Penicillium nalgiovense and some potentially toxicogenic species. All the strains showed a higher growth rate at 25 °C. The production of extracellular proteases and lipases was significantly higher at 25 °C than at 14 °C with and without sodium chloride. Only Penicillium expansum produced patulin. On the other hand, Penicillium griseofulvum was the only species that produced ciclopiazonic acid but none of the strains produced penicillin. The species present on salami, Penicillium nalgiovense, Penicillium minioluteum, Penicillium brevicompactum and Penicillium puberulum were unable to produce any of the evaluated toxins. These findings suggest that some fungal isolates from the surface of salami such as P. nalgiovense are potentially useful as starters in sausage manufacture.

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Wow. talk about brain trauma, most of this post is way over my head. The first step to a solution is to identify the problem. I think the problem is that we cant identify the problem. neurologically, we cant say that it's that portion of these neurons, or those neurons, Everything effects everything, it's part chemical, part physiological, and it really is neuro-soup (not that I dont totally appreciate the efforts here). 30 years of this and for me it still comes down to trial and error. Some things help, some dont, none seem to "cure". Thats not to say that we cant better identify and refine the proposed "trials", and I think thats what's happening here in this post. regardless, my newest proposed trial is to give the sinemet a whirl, if I can get dr. to prescribe it. Keep up the good work, and keeep the faith! ymmit

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Visual has some good stuff to say, i believe in most of what he says, but i felt the need to take another side of the debate. I was looking for answers and ran across the Uruguayan Salami study; it was so amusing i posted it. At this point it has no relevance in terms of HP treatment (aside from being tasty). ......Trial and error, that's right. We can propose all sorts of theories, but they have to be practical and work practically.

I have been on the indole-related tip:

Melatonin, Imitrex, Indomethacin, etc.

This seems to be one of the most wide-open "drug classes". And i believe it will show promise because it relates to precursors to neurotransmitters. Indole is the precursor to Tryptophan and subsequently Serotonin, Melatonin and Niacin.

indole.png

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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.

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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.

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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.


asdf

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Was thinking today and realized that because the 5ht2a receptor antagonists make symptoms worse, that is probably a good sign that there is SOMETHING array with the receptors or whatever is connected to the receptors, we need to start compiling all the information we can on receptors and especially these receptors. If anyone can get any info at all that is related to these topics please post. Lets compile everything we can.

Has anyone found any 5ht2a reverse agonists yet?

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.

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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???

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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).

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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

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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.

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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...

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