dasitmane

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

601 posts in this topic

I believe the receptors are there all the time, they don't get produced or killed (generally)<---this is wrong BTW. ......You are right though it is electro-chemical. I think that some neurons don't fire as much though with HPPD. DNA alteration i think could be possible, maybe probable. ......I think that some of the basics are that you have two main neurotransmitters: glutamate and GABA. Then you have serotonin. And then you have other neurotransmitters that have larger molecules: dopamine, epinephrine, norepinephrine, histamine. And you have peptides and other amino acids also. I think GABA is general inhibitory and glutamate is excitatory. Serotonin is 5-HT; made from tryptophan in the neuron.

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everything is not 100% back to normal. Or else we wouldn't be having these symtoms: visual disturbances among other things anxiety, depression etc. I am talking about SSRIs and how they may help, not about drugs that have long left our systems. Aside from other neuronal damage, with HPPD, i believe, the neurons are not firing on all cylinders. I haven't even gotten to the visual cortex; my knowledge there is somewhat limited.

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I believe the receptors are there all the time, they don't get produced or killed (generally). ......You are right though it is electro-chemical. I think that some neurons don't fire as much though with HPPD. DNA alteration i think could be possible, maybe probable. ......I think that some of the basics are that you have two main neurotransmitters: glutamate and GABA. Then you have serotonin. And then you have other neurotransmitters that have larger molecules: dopamine, epinephrine, norepinephrine, histamine. And you have peptides and other amino acids also. I think GABA is general inhibitory and glutamate is excitatory. Serotonin is 5-HT; made from tryptophan in the neuron.

The receptors do get wasted away and replaced, The only receptors at play here are the 5HT2A receptors, the nuerotransmitters glutamate and gaba effect completely other receptors, Hallucinogens effect only 5HT2A receptors, which activate only certain areas of the brain, so our focus is there, and only there. Messing around with glutamate or GABA is easy and has been done already with benzodiazapines and the effects are temporary relief of symptoms, if that.

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The point that i am making is that if you don't understand the basics how do think you are going to understand the rest?

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everything is not 100% back to normal. Or else we wouldn't be having these symtoms: visual disturbances among other things anxiety, depression etc. I am talking about SSRIs and how they may help, not about drugs that have long left our systems. Aside from other neuronal damage, with HPPD, i believe, the neurons are not firing on all cylinders. I haven't even gotten to the visual cortex; my knowledge there is somewhat limited.

I only said chemically it is all back to normal. If it werent the problem wouldnt be that hard to fix I would assume.

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These are some inverse agonist but unfortunately none have hit the market.

  • Nelotanserin (APD-125) - selective 5-HT2A inverse agonist developed by Arena Pharmaceuticals for the treatment of insomnia. APD-125 was shown to be effective and well tolerated in clinical trials.[46]

  • Eplivanserin (Sanofi Aventis), a sleeping pill that reached phase II trials (but for which the application for approval was withdrawn), acts as a selective 5-HT2A inverse agonist.

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We haven't even gotten to the amygdala, the sensory cortex, the high road and low road of emotional stimuli.

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I like your enthusiasm though, a lot. I can tell you want to find a cure. Your ideas are great: you are coming up with some interesting chemicals!

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I was looking at Mifepristone (not directly related to 5-ht though), an abortion drug found to be helpful with major depression.

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actually i was thinking of dexamethasone on the near the first onset of HPPD, with small dose SSRI, then a few week rest refraining from the steroids and then with continued SSRI, maybe add mifepristone. ........There's not enough money in the world to test out all these drugs ....lol

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I was thinking about what you were saying and i was interested in what you were saying about the "electrical" circuitry of the CNS. Perhaps the pH in the synapses (w/ Ca, K etc.) is at play and somehow causing some sort of electro-chemical impedance similar to ohm-age in standard electronics. not sure lol

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I was thinking about what you were saying and i was interested in what you were saying about the "electrical" circuitry of the CNS. Perhaps the pH in the synapses (w/ Ca, K etc.) is at play and somehow causing some sort of electro-chemical impedance similar to ohm-age in standard electronics. not sure lol


asdf
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More interesting information that shows that psychedelics dont use just 5HT2A receptors but also cause an interaction with mGluR2, not even sure what that is yet but its something we need to look in to.

This goes a long way to explaining one of the mysteries of serotonin which is this: if 5HT2A agonists like LSD are psychedelic, why aren't antidepressants the same? Almost all antidepressants work by increasing extracellular 5HT levels. That ought to mean that they activate 5HT2A receptors (indirectly). This explains why not - 5HT alone doesn't promote the crucial 5HT2A-mGluR2 interaction.

http://neuroskeptic....ale-of-two.html

Also, psychedelics are SUPERAGONISTS

this means that they are activated connectivity of the receptors beyond that that serotonin will. Possible further evidence on the burn out theory, that the synapses themselves have become damaged from to much electrical connectivity.

http://en.wikipedia....eceptor_agonist

interact.jpg

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Heres a good write up/explination of whats going on when hallucinogens or neurotransmitters enter the synapse.

The adjacent neuron’s postsynaptic membrane appears as an elaborate, thickened complex of interlinked proteins gathered on the surface of a dendrite, which is one of the many arborizing extensions of a neuron. Neurotransmitter receptor binding alters the electrical potential of the dendritic membrane, which processes spatially and temporally the incoming barrage of synaptic impulses to form a signal directed toward the cell body. The dendrite receives both excitatory and inhibitory synaptic inputs. Once a sufficient number of receptor binding events occurs and threshold is reached, the postsynaptic neuron then fires an action potential. That momentary electrochemical flux becomes one nod from one neuron among the brain’s hundred billion.1,2

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Approximately 20% of cortical neurons inhibit rather than excite their neighboring neurons.6 Synaptic inhibition is essential to cortical processing, and inhibitory neurons are especially diverse in morphology and function.7,8 Inhibitory interneurons in the somatosensory cortex, for example, selectively suppress irrelevant input, filtering out incidental distractions and unchanging sensory stimuli.9 This allows the brain to focus. The brain, it would seem, values restraint. It values restraint not with the goal of inaction, but rather with the aim of achieving a controlled balance of calmness and intentionality.

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Synaptic overstimulation can be as detrimental as understimulation. Cocaine, for example, interferes with the synaptic reuptake of the neurotransmitters dopamine, norepinephrine and serotonin, leading to an excessive amount of dopamine in the synaptic cleft, which causes intense stimulation of the central nervous system and extremely dangerous mental and cardiovascular effects. Another example of synaptic overstimulation is epileptic seizures, in which susceptible individuals experience episodes of hypersynchronization of cortical neurons, leading to convulsions or other involuntary brain attacks.
 

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Alright excellent man as peeviously mention im a drum n bass bmw and bmx guru...this medical stuff is a mystery. Your saying we know what aggrivates post hallucinogen visuals so we could find the opposite? Wait....cheese has calcium in it...i eat shit loads of cheese...particularly over the past few weeks....and iv worsened soooo much. Maybe calcium is fucking me up? Ie calcium is bad for hppd? I could live without cheese

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i believe that calcium channel blockers could be one of the importants drugs to fight HPPD. alot of people with PMA got cured because of them. i read a lot of german migraine boards where people confirm this.

and i also do believe that the prob is not only found in our brains it must be more global than this because alot of our symptoms are created in the eye itself(negative afterimages, halos, starbursts, floaters, ghosting). a while back i posted an article about visual disturbances (HPPD?) caused by cannabis:

http://ucsdnews.ucsd.edu/newsrel/health/potpnas.htm

calcium channels seem to play the major role here.

but also serotonin is found in the nerves of the eye they are responsible of the intraocular pressure. funny because my presure is a bit elevated since the onset of HPPD.

i also dont believe that "dopamine receptor burnout" or something like this is root cause because alot more peolpe who had only taken speed or coke would be members of this forum.

so in my opinion it seems to be a chemical imbalance maybe to much or less serotonin in the ratio to dopamin caused by something which controlls this maybe the calcium channel blockers.

also calcium channels are involved in the regulation of gene expression maybe this is the key

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Alright excellent man as peeviously mention im a drum n bass bmw and bmx guru...this medical stuff is a mystery. Your saying we know what aggrivates post hallucinogen visuals so we could find the opposite? Wait....cheese has calcium in it...i eat shit loads of cheese...particularly over the past few weeks....and iv worsened soooo much. Maybe calcium is fucking me up? Ie calcium is bad for hppd? I could live without cheese



Cheese is probably worsening your symptoms because of the tyramine. Wiki it and youll understand. I understand that you know alot about other subjects, but if you focus your time on medical things everything will come together, you just need to read and read and read. It can take years to start grasping the understand of things like this, but you have your whole life. So its best you start now cause from what Ive seen, no one in the medical industry wants to help.
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BTW afew people report some relief because of magnesium which is natures own calcium channel blocker but maybe to weak to cure us.

if HPPD is caused by gene expressions as we talked about a few times before than the calcium channel could play a role and maybe taking c-c-blockers could silence the expressed gene again.

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BTW afew people report some relief because of magnesium which is natures own calcium channel blocker but maybe to weak to cure us.

if HPPD is caused by gene expressions as we talked about a few times before than the calcium channel could play a role and maybe taking c-c-blockers could silence the expressed gene again.


asdf

320px-Efficacy_spectrum.png

the push and the pull

800px-Agonist_full_and_partial.svg.png
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