Fawkinchit

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I see, I still am skeptical of an imbalance chemically, if there is thought, then whats causing it? I still feel that in some way or another these neurons are out of balance and overexcited. We need to track down the effects of 5ht2a receptors, and glutamate receptors and see what they are effecting and how, etc, we need to get our hands on some inverse agonists for the 5ht2a receptors as well, or even for glutamate receptors. These are both potentials. And we need to look farther in to gene expression etc. We also need to try and get more people involved, we have some pretty smart people with this condition, we all just need to work together and focus together, once we all do that we will be unstoppable, but everyone needs to help and participate, itll be 1000x better than if we all do it on our own.

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asdf the push and the pull

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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.

Bump to this topic and would like to continue this research a thread that I made, obviously there is some connection here with the Na/K pump and overexcitation of neurons. heres the link to my thread http://hppdonline.co...e-weight-to-it/

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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.

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.

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

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

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These are some inverse agonist but unfortunately none have hit the market. AC-90179 - potent and selective inverse agonist at 5-HT2A, also 5-HT2C antagonist.[44][45] 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. Pimavanserin (ACP-103) - more selective than AC-90179, orally active, antipsychotic in vivo, now in human clinical trials.[47][48][49][50] Volinanserin

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

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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True, but im not sure what youre getting at.

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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... well with our receptors its the same concept, agonist inverse agonist, I was thinking that maybe these very potent agonist of the 5ht2a receptors cause such an extreme push that things become out of balance, just like if you decreased suns gravity the earth would fall away, maybe we can utilize inverse 5ht2a agonists to accomplish the rebalancing of our receptors. unfortunately these dont exist that are on the market today, only in clinical trials, for the treatment of insomnia. Anyone have any ideas? Update: Full documentation of this disease can be found on page 24 post #478