Question...

Where are dopamine, serotonin, and norephedrine actually produced, and how? Did I hit all the neurotransmitters generally implicated in ADD? I realize ADD is more than just neurotransmitter availability, but it seems to be one of the few things that can be externally affected.

I've read that these neurotransmitters can't cross the blood-brain barrier, so ADD stim meds can only make the neurotransmitters already present more available to the synapses, as opposed to actually increasing neurotransmitter production. Is this true? Would there be any distinguishing symptoms between the brain producing insufficient dopamine as opposed to overactive dopamine reuptake? Does a non-stim med like Strattera affect available dopamine levels as well, or is its effect limited to serotonin?

Somewhere I'm missing some essential info to make the whole neurotransmitter thing make sense. Any links to some solid basic info would be much appreciated!

Just as an aside, one of my friends just suggested an herb as an ADD treatment because (according to her) 'serotonin is produced in the gut' and is absorbed into the brain later, and this herb is supposed to stimulate serotonin production. My skepticism is fully engaged:cool:, but I realized I really didn't know enough about the whole process to even comment on the possibility.

I'm not an expert, but:

I've read that these neurotransmitters can't cross the blood-brain barrier

I wasn't aware that this was true. Maybe it is, but I know 5-HTP and L-DOPA (what L-Tyrosine is converted into) cross the blood/brain barrier.... Serotonin is found normally in your blood, as well as GABA I believe? Overdoses on 5-HTP can cause serotonin syndrome, I believe. L-DOPA is available by prescription only, and L-Tyrosone (as well as L-Tryptophan) do not cross the blood brain barrier directly (which are converted to L-DOPA and 5-HTP, as needed, using B-vitamins (B6 mostly, I believe) as well as other things...).

People do use 5-HTP to treat depression and insomnia. I suppose L-DOPA might help ADHD too, but most people don't have access to it (prescription only). ADHD is not a lack of amino acids though, and even though L-DOPA will cross the blood brain barrier, the problem is not actually a lack of L-DOPA.

I believe all the neurotransmitters you mentioned can be involved in adhd, perhaps even some you didn't mention.
I think strattera is a norepinephrine re-uptake inhibitor, that indirectly increases dopamine in the pre-frontal cortex.

Serotonin, and other neurotransmitters, are produced in the body in addition to the brain. Once tryptophan is converted to serotonin in the body, it does have a difficult time crossing the blood brain barrier. On the other hand, Tryptophan and other serotonin pre-cursers do cross the blood brain barrier more efficiently, then are converted into serotonin in the neuron.

I could be wrong, but these medicines used for adhd not only change neurotransmitter levels, they change neurotransmitter levels in areas of the brain involved in adhd.

Increasing production of neurotransmitters in the neuron, is not neccessarily enough to alleviate symptoms. For example, l-dopa increases dopamine production in the brain, however it doesn't appear to be an effective treatment of adhd.

Sorry, I'm acting like a "know it all".

As I like to say, "i could be wrong".:)

Somewhere I'm missing some essential info to make the whole neurotransmitter thing make sense. I've always found the idea of swilling a couple of chemicals around a 'precision' instrument like the brain - and this having an effect - to be surprising. Guess it's just not so 'precision' ...

I'm actually going to back up a bit and discuss what neurotransmitters are in general:

Neurotransmitters are chemicals that neurons (brain cells) use to transmit signals to each other. Many of the cells in your body use some form of chemical signalling during a wide variety of biological processes. Chemical signals are essential for a complex multicellular organism like yourself to function, as you have trillions of cells that all have to work together to stay alive. Chemical signalling can even be seen in unicellular organisms, even "primitive" bacteria and archaeans use chemical signals. Chemical signalling can also occur between individual multicellular organisms, such as when bees emit a chemical signal telling the rest of their hive that they are under attack, or when some plants emit signals when bugs begin to eat their leaves, which tell other plants of the same species to release toxic chemicals to avoid being eaten themselves.

In general, chemical signals work because cells have certain proteins on their cell membrane, called "receptors." Each protein has a specific shape that is determined based on how its constituent amino acids bind together. If you remember from high school biology class, DNA contains the "instruction" code, which the cell can convert into a string of amino acids, and these amino acids will fold together into different proteins based on the order in which they are put together. Mutations to DNA can cause a cell to produce more or less of a given protein, or small point mutations could create a protein where one amino acid has been substituted for another, which creates a slightly differently shaped protein.

Now, because each of these proteins has a specific shape, certain chemicals will fit into them. For an individual single-celled organism, this is an important sensory mechanism for understanding the world around them, they are essentially "smelling" what chemicals might be in their area, and so they might have a receptor that would be triggered by a chemical that implies that there is food around, or by a chemical that implies that a predator might be near.

In your brain, this system has been slightly modified. Neurons are special cells that exist pretty much solely for the purpose of receiving and transmitting signals. One area of these cells, called the dendrite, is covered with many different types of receptor proteins. Another area, called the axon, is packed with whatever neurotransmitter this particular cell uses to communicate. These chemicals are packed into little bubbles called vesicles. Generally, neurons try to line up so that an axon of one neuron bumps up against the dendrite of another. The axon doesn't actually touch the other cell's dendrite, there is a small space between the axon of one cell and the dendrite of another, this space is called the synapse, and it's where the really interesting stuff happens.

Neurons have one other interesting property: they can take in charged chemicals from their surroundings (sodium, potassium, calcium, and chloride ions) and thus alter their chemical charge relative to their surroundings. This charge is called a voltage potential. Many cells can do this, actually, and it may be related to one of the earliest forms of chemical metabolism used by the very first cells on Earth*, but it has been highly modified in neurons. When the voltage potential gets high enough, the neuron will fire, shooting the neurotransmitters in its axons out into the synapses where its axons meet the dendrites of other neurons.

Ok, so now I'm finally at the part where I can answer the original question. Many of the receptors for these neurotransmitters will alter the cell's voltage potential. Often, a receptor is connected to another protein that can allow specific charged ions to enter the cell, and these proteins are called ion channels. You could think of the ion channel as like one of those revolving doors outside of a building, and the ions as people trying to get inside. When a neurotransmitter hits the receptor, it causes the door to rotate, letting some of the people go inside. In this sense, a neurotransmitter is like a key, and the receptor is like a lock.

But here's where it gets interesting: while sodium (Na+), Potassium (K+), and Calcium (Ca++), are positively charged, there are also ion channels that will admit chloride (Cl-), which is negatively charged. Note that the chloride ion, which is a harmless component of table salt, is different from the electrically neutral chlorine, which is a toxic, corrosive gas. Some neurotransmitters, such as GABA, trigger receptors that are linked to ion channels that admit the negatively charged Cl- ion. This lowers the voltage potential, which can prevent a neuron from firing. Because this action inhibits the neural firing, these neurotransmitters are often referred to as inhibitory neurotransmitters (Serotonin is also an inhibitory neurotransmitter, I believe...dopamine is an odd one, from what I understand, some dopamine receptors are excitatory, some are inhibitory). If a neurotransmitter causes a cell to admit positively charged ions, which increase the likelyhood that a neuron will fire, then those neurotransmitters would be called excitatory neurotransmitters.

Some receptors can also be linked to proteins inside the cell that perform certain functions, and dextroamphetamine (Adderall, Dexedrine) actually binds to one such receptor, but to keep things simple, I've just focused on the more basic ion channel receptors.

So because neurotransmitters are important methods by which brain cells communicate with each other, it's important for your body to have tight controls over them. Neurotransmitters are produced within each neuron, and each neuron will generally make one neurotransmitter (although some neurons will make both dopamine and norepinephrine, as they are closely related). These cells contain enzymes, which are proteins that can caused a chemical reaction, and these enzymes usually just make really simple changes to existing chemicals. Serotonin is produced by making some very basic changes to the amino acid tryptophan, dopamine by altering the amino acid tyrosine. Once the enzyme alters the amino acid, it is packaged up into those vesicle bubbles I mentioned earlier, and then locked and loaded so it can be fired out.

Neurotransmitters cannot cross the blood-brain barrier, and for good reason, since they would seriously screw up the chemical signalling system if they did. However, the amino acids that can be used to form neurotransmitters do cross into the brain, where they enter neurons and are used to produce more neurotransmitters (and also to produce proteins, of course). Many drugs mimic the action of neurotransmitters, and since they cross the blood-brain barrier, they can be used to alter neurological signalling. For instance, Gabapentin is simply the neurotransmitter GABA, but slightly altered so that it will pass through the blood-brain barrier, and diazepam (Valium) is a chemical that will bind to the receptor for GABA. Both of these chemicals, because they mimic the action of GABA, can be used to mimic the inhibitory signals that this neurotransmitter causes.

ADHD drugs are obviously a little different in that they do not mimic dopamine or norepinephrine (although dextroamphetamine may do so in higher doses), but they increase the levels of these chemicals in the synapse. The axon has proteins on its membrane that take up the neurotransmitters it has just sent out, and pull them back into the cell, where they are often either re-used or broken down into their constituent chemical parts. This is the main way that a neurotransmitter exits the synapse. Methylphenidate (Ritalin) and Atomoxetine (Strattera) simply block the uptake itself, while dextroamphetamine (Adderall, Ritalin) binds to a receptor that activates a protein inside the cell that tells the uptake proteins to work in reverse...pushing more of the neurotransmitters out into the synapse instead of pulling them back in.

I'll post more later, meds are wearing off and Daily Show is coming on



*interesting fact: scientists have been able to take the inorganic chemicals that would probably have been around on early Earth, such as methane, CO2, hydrogen, etc. and combine them together to create protobionts...not true cells, but little "soap bubbles" that resemble cell membranes. One of the coolest things about these critters is that some of these membranes are capable of maintaining and modulating a crude voltage potential.

I won't quote from H's post - but there's a clear message therein of the importance of ion flux.

Now for the freaky bit.

I believe that the flux is the driver in the process and not the biological process which elicits the flux - though the relationship is intimate.

Ion channels pervade.

Ion flux generates an electromagnetic field.

http://en.wikipedia.org/wiki/Electric_field

->-
... the space surrounding an electric charge has a property called an electric field. This electric field exerts a force on other charged objects.
Electric fields contain electrical energy with energy density proportional to the square of the field intensity. The electric field is to charge as acceleration is to mass and force density is to volume.

A moving charge creates not just an electric field but also a magnetic field ... 'electromagnetic fields'.
... ... ... added to the quote ... ... ...

6 of one, half a dozen of the other

But keep in mind that the membrane voltage potential system is derived from other more ancient systems that are unrelated to chemical signalling. It is an excellent example of evolution by exaptation, whereby an ancient energy producing/storing system is converted into an efficient signalling process. Because changes in voltage potential can be carried out far faster than hormone-signalling or protein-kinase processes, it allows for faster response to stimuli.

I'd say that the ions are only the "driver" of the process in the sense that gasoline is the "driver" of a car. It is a tool that the cell manipulates to achieve a given function. And of course, it's not the only form of chemical signalling.

As I mentioned, the concept of chemical stimulus->receptor->response is a basic theme of all living organisms. The near-complete exaptation of systems designed to sense the outside world into systems that allowed cells to signal each other was a major advance that was required for true complex multicellular life to evolve. A colonial organism may need only a rudimentary method for distinguishing compatriot from prey or enemy, but true multicellularity requires more than just recognition, it requires cooperation.

But I think you're reading too much into the electromagnetic nature of this. There are plenty of signalling processes that do not involve ion channels, including some of the most powerful signalling methods whereby membrane receptors can actually trigger transcription factors (thus altering the functioning of the cell's genetic machinery). This is an essential process in embryological development, and may also play a role in some cancers (I do not know much more about this particular topic, but a friend of mine in undergrad did this for her thesis).

And don't forget, without the ability to use chemical signalling to orchestrate gene transcription factors, complex multicellular life could never develop at all, because embryological development would simply not be possible. Colonial eukaryotes (think seaweed) would be the most advanced life-forms on Earth...although I suppose some primitive fungi might be able to function.

... not in disagreement ...
... merely though - is it exaptation (as such) ...?...

for instance
~in the old days~
stimulus ->- a bit of ion flux
~nowadays~
stimulus ->- a lot of ion flux
...with energy density proportional to the square of the field intensity... a bit, a lot - no matter ... since the driver (*yes petrol, gasoline) ... continues to drive.
Exaptation not from the perspective of the ion (gas).
Exaptation only from the perspective of the biological process (older simpler process ->- newer more complex process) ... tied to ion flux (Fred ->- Jim the driver of the motor vehicle).

... Generally (then) ...

I'm placing the following context on the biochemical processes in your post ...

-response times-
neuro- v fast
kinase/phosphatase - v fast
endocrine- not so fast

-end effects-
neuro- v fast (neurotransmission)
kinase/phosphatase - protein activated and deactivated quickly - though delays may ensue due to the proteins being involved in transcription (not a millisecond(s) or even second(s) process)
endocrine - just plain slow compared to the other 2 guys

I'm painting all bodily subsystems as supportive of an increased
... field intensity- noting (as you mentioned) -
that neuro- comprises agonstic/antagonistic systems
kinase/phosphatase sets are agonistic/antagonistic
endocrine - particularly in the HPA (the major endocrine axis) - there's a sweet pattern of negative feedback (or in English) - high levels of hormones ->- reduced transcriptional rates of *themselves*.

0,1 pervades.
binary states.

Oh, a couple more things to mention about the original post:

Some neurotransmitters are also broken down in the GI tract by various chemicals there, such as monoamine oxidase (MAO), which also exists in the brain and can break down chemicals in the synapse. In fact, some older antidepressants work by inhibiting MAO, which is why patients taking monoamine oxidase inhibitors (MAOIs) are told not to eat certain foods or take certain drugs, because they are reducing the activity of the enzyme that would normally break down important chemicals in the gut and brain.

So yeah, in addition to the blood-brain barrier issue, you've also got the oral-activity issue.

Would there be any distinguishing symptoms between the brain producing insufficient dopamine as opposed to overactive dopamine reuptake? The scientific answer is "it depends." My speculative answer is "yes." ADHD is hypothesized to involve excess dopamine transporters resulting in overactive uptake, resulting in lowered synaptic dopamine levels, although it is entirely possible (and likely) that this may not account for all of the symptoms in all people. Parkinson's Disease is hypothesized to be caused by damage to the dopamine-producing neurons in the substantia nigra, resulting in a lowered production of vesicular dopamine. That's really the difference that we're talking about here, between synaptic and vesicular levels.

Now, obviously one main difference between Parkinson's and ADHD is that they're both occuring in different regions of the brain, but one thing that is noticeably different is how the brain responds. Parkinson's patients may have tremors when they try to move, because it's hard to raise dopamine levels on a moment's notice in their situation...but what you don't see are Parkinson's patients trying to move a little bit and then jumping up and down all over the place. When ADHD individuals try to overcompensate, they often wind up hyperfocusing, or something just becoming hyperactive. This is where we can see a major difference...if there the vesicular stores are depleted, it will be virtually impossible to overshoot, but you'll get those tremors which are sort of the beginning efforts of movement (this is not to be confused with the dyskinesia that is often produced by Parkinson's medication). But if the problem is excess uptake, then it actually is possible to overshoot and eventually get excessive activation...but it's generally not going to be too helpful, and you'll see swinging between extremes.

The other thing is obviously with which meds would be useful. ADHD meds are not overly useful for Parkinson's patients, because blocking reuptake or inducing reverse uptake isn't very helpful if there isn't enough vesicular dopamine available anyways. Similarly, L-DOPA and other Parkinson's drugs aren't going to be excessively useful for ADHD patients, because increasing vesicular stores isn't going to help if the neurotransmitters just gets pulled back into the cell anyways.

Does a non-stim med like Strattera affect available dopamine levels as well, or is its effect limited to serotonin?
Strattera's main effect is actually on norepinephrine reuptake inhibition. I do not believe that it has much of a serotonergic component, although I would not be surprised if there is a small amount of SERT inhibition, given that Strattera is somewhat similar to tricyclic antidepressants that inhibit the reuptake of all three chemicals. In some regions of the brain, dopamine also exits the synapse through the norepinephrine transporters, so Strattera probably also increases dopamine levels as well.

Just as an aside, one of my friends just suggested an herb as an ADD treatment because (according to her) 'serotonin is produced in the gut' and is absorbed into the brain later, and this herb is supposed to stimulate serotonin production. My skepticism is fully engaged:cool:, but I realized I really didn't know enough about the whole process to even comment on the possibility. Your friend is wrong. Any serotonin produced in the gut would be destroyed by the MAO in the gut fairly quickly. Even then, I don't think that it would pass the blood-brain barrier. In general, neurotransmitters are produced in the neuron that fires them into the synapse, since this is that neuron's raison-d'etre.

Now, the chemicals tryptophan and 5-hydroxytryptophan (5-htp) can be converted by the body into serotonin (5-hydroxytryptamine). One kinda cool thing is that "magic" mushrooms contain very similar enzymes, the only difference is that these enzymes converts tryptophan into 4-hydroxy dimethyltryptamine, or psilocyn. The fact that these two chemicals are so similar is why they produce their effects (and also tells us that the action of serotonin in the raphe nucleus plays some sort of role in sensory perception).

Anyways, back on topic, this would mean that it is possible that consuming 5-htp might cause your body to produce more serotonin, but I would doubt that this is going to have much of an effect, and it would be hard to predict what that effect might be, it certainly wouldn't be the same as SSRIs. I also don't know of any herbs off the top of my head that contain 5-htp, although that doesn't mean that they don't exist. However, just because an herb might produce a chemical similar to serotonin does not mean that ingesting it is a good idea...after all, as I mentioned earlier, "magic" mushrooms produce chemicals similar to serotonin, and while they won't kill you, they could be rather unpleasant in many situations ("We are gathered here today to join this couple in holy....*****, could someone tell the groom's carnation to stop making faces at me??? Oh wow man, the Bride does't have a face, SHE DOESN'T HAVE A FACE!!! Oh wait, that's just the veil, but why is it glowing?")

Also, serotonin and its cousin melotonin are thought to both play a role in regulating the sleep cycle, so I would be wary of taking anything that might alter serotonin levels without first speaking with a physician (if one is taking an anti-depressant by prescription, obviously you've already spoken with a physician).

Response to SB to follow in another post

Exaptation only from the perspective of the biological process (older simpler process ->- newer more complex process)
Well no, that's just the thing, the exaptation is that a pre-existing structure/function gets co-opted into a completely different use. So an ancient metabolic pathway used to drive energy production gets co-opted into a novel chemical signalling setup. You're looking at the final outcome, rather than the constituent parts. There are a lot of evolutionary developments of this nature, such as fish fins to arms and legs, gill arches to jaws...hell, the light-sensitive pigments in your eyes (rhodopsin) are very similar to the bacteriorhodopsin that some bacteria still use for a crude photosynthesis. The idea is that you can take a given structure, and use it for a completely different function.

It's not just that ion-channel neurotransmission is more complex (although you could make the case that it's actually simpler), or better, or any of that, but rather that it evolved from a different function. Because this chemical signalling method evolved from a different original function, it's going to have different properties than other methods. It's a matter of whether you're looking at the end outcome (chemical signalling) or the original function from which it evolved. Early in animal evolution, but probably right after the sponges split off from the crown group, some animals cells started using this mechanism to signal each other. This allowed these animals to process external sensory information faster, and to use that information to act immediately in response to stimuli. It also allowed for more fluid reactions to stimuli rather than a predetermined response. Because it offered an advantage, animals that had these cells had a better chance of survival, and animals whose neurons were arranged in certain layouts, depending on the needs of that particular species were also more likely to survive and reproduce. But looking at it from the end result that this mode of signalling created is putting the cart before the horse.

This - I believe - is the driver.

Originally Posted by SolarLife

... bandwidth ...

Eyes: 10,000,000 bits per second
Ears: 100,000 bits per second
Skin: 1,000,000 bits per second
Taste: 1,000 bits per second
Smell: 100,000 bits per second

Evolution of life towards lossless reality.

Why?

... because maxxing out on bandwidth- maxxes us out on 'energy' upload - makes for a 'fitter' organism.
The oft rejected but most often thought thought that evolution is generally towards complexity fits within this framework.

I'm suggesting a definition of complexity in terms of 'energy content' ... energy loading within the organism ... potential energyof the organism ... think how much RAM you would need to run an effective simulation of that organism.

The more RAM - the more evolved.

Noting that environmental considerations must apply,

Eyes: 10,000,000 bits per second
Ears: 100,000 bits per second pules can hear bats as well....
Skin: 1,000,000 bits per second
Taste: 50 bits per second
Smell: 8 bits per second.....<<


theres a lot more to porceing.... it could be that mreacodrain dna theres must be portins transfurrr as well..... the intrdatci offve infomation..beteewn dna an rna.........< nortranmiiters...an wounderfull thing but one must taken into accont the other transmitters that must be in the brain that we dont know about or have not beeen looked into we put lot trust an faith in the ones we know but there are well others that even if there very small have big impaticants....allso ieppergretics....the under laying layer to both dna rna expression what could hold the key to all thats been talked about in the therd....we talk about voltages pertenal....+ n - but what about inbeteewn the other focsesss have as biger role two,,,,no thory can be said to be total with out all the info being add tomghter great therd ,,,,,, drom

Receptors may also be involved in adhd. It could be a variation in recepter/s, or decreased/increased numbers of receptors that cause adhd. Post synaptic and pre synaptic receptors are intimitaley involved in neurotransmition. Altering sensitivity, or stimulating pre and post synaptic receptors can increase/decrease neurotransmitter turn-over. I've heard the D2 receptor discussed in potential causes of adhd. It's hard to imagine just one cause for adhd. Perhaps in one person it's D2, another MAO-B, another pre-synaptic receptors, and so on, and so on. In severe adhd it could be a multiple of mutated genes.

like you said, you can increase neurotransmitter stores in the neuron, but that doesn't neccessarily change synaptic neurotransmitter levels. From what I understand, pre/post synaptic receptors, second messenger systems are the key to it all.

Just Food for thought.:)

quote]chemical signalling) or the original function from which it evolved. Early in animal evolution, but probably right after the sponges split off from the crown group, some animals cells started using this mechanism to signal each other. This allowed these animals to process external sensory information faster, and to use that information to act immediately in response to stimuli. It also allowed for more fluid reactions to stimuli rather than a predetermined response. Because it offered an advantage, animals that had these cells had a better chance of survival, and animals whose neurons were arranged in certain layouts, depending on the needs of that particular species were also more likely to survive and reproduce. But looking at it from the end result that this mode of signalling created is putting the cart before the horse.[/quote]


I know what you people need in yet another opinion . . . . . . .how about giving the hoarse a ride a top his cart because after all it is Christmas!

If sufficient information were available it wouldn’t matter if we approached the subject from the top down or the bottom up, we could begin with the simple move to the complex or begin in global thinking fashion and begin with the entire complex concept and simplify it wouldn’t matter how the information was presented it would not change the information only the presentation thereof (IMHO)


The brain is affected by a multitude of chemical reactions both in the cell to cell exchanges, via neuro transmitters but the brain is also affected by endocrine hormone changes (just ask any one who has gone through metepause), physical activity and the price of tea in Boston. . . . . .if I drop a hammer on my foot it will affect my brain and defiantly influence my attention span and memory

Some4 ideas thown out here for comment, consideration, or to be ignored whichever suits the reader.

Nobel prize winners (http://www.wsws.org/articles/2000/oct2000/nob-o26.shtml)

Realizing that the nervous systems of mammals were too complex to serve as a starting point for investigating memory, Kandel conducted a series of experiments on an organism with a simple nervous system—the giant marine slug Aplysia, which measures 30 centimetres from head to tail. The slug has a simple protective reflex system—when a particular area was prodded, the gills would withdraw. By examining the operation of this reflex in detail, Kandel was able to get an insight into short- and long-term memory.
When Alpysia received a weak stimuli in the form of short prods, a series of interconnected chemical changes—a chemical pathway—would follow within the nerve cells. The neurotransmitter serotonin was released that would activate “protein kinase A” or PKA. In turn, PKA, modified other proteins producing a strong electrical connection between neurons that would last from several minutes to hours. There was, however, no long-term change as the proteins would return to their normal state.


But when the slug was continually prodded, it would stop responding completely and the effect would last for weeks. Kandel found that for this long-term memory to occur, certain genes needed to be “turned on” or activated through the release of a protein known as CREB 1. Once the genes were turned on, certain proteins would be released, which reshaped the end of the nerve cell or synapse and changed how it functioned for a lengthy period of time. Other experiments have confirmed that long-term memory cannot develop unless the particular genes in the nerve cells are switched on to produce these new proteins. If that process is blocked, nerve cells are only capable of short-term memory.***End Quote



Some simplified explinations (http://uk.encarta.msn.com/encyclopedia_781566624_2/Brain.html) of information which cover s in more detail some of the areas already touched upon briefly by previous post.


just an after thought (http://palgrave-journals.com/emboj/journal/v18/n7/full/7591600a.html) feel free to comment, ignore, what ever floats the ole boat.

The neurotransmitter serotonin was released that would activate “protein kinase A” or PKA.
last from several minutes to hours.
There was, however, no long-term change as the proteins would return to their normal state.

But when the slug was continually prodded, it would stop responding completely and the effect would last for weeks. Kandel found that for this long-term memory to occur, certain genes needed to be “turned on” or activated through the release of a protein known as CREB 1.
Other experiments have confirmed that long-term memory cannot develop unless the particular genes in the nerve cells are switched on to produce these new proteins. If that process is blocked, nerve cells are only capable of short-term memory.pka -> a from [ATP ->] cAMP

CREB -> CAMP Rsponsive Element Binding.

... more Nobels
http://www.addforums.com/forums/showthread.php?p=305464&highlight=ATP#post305464
(http://www.addforums.com/forums/showthread.php?p=305464&highlight=ATP#post305464)
Evolutionary psychology involves the study of the conscious mind, which itself is driven by the composite behaviours of all of our yesterdays (of our history, of our previous forms, of our evolutionary history).
If you'd like ... an observation ... the colours of my avatar reflect a certain time of day; that time of day (I wager) would have reflected a time of energetic activity in one of our evolutionary relatives. Just that ... and well, this'll be forever unproven ... but, well, anyway, here goes ... I have a suspicion that the colours which I adore - those colours (from my avatar), reflect a time of maximal energetic activity in our pre-cellular form (of ATP --- from earlier on in this thread); to be clear, I have this feeling that the transition from night to day - was a precursor in on the transduction of light (EM) energy into organic form, and the colours are a transition back into the key event in 'life' (noting that ATP is motor, energy, gene ... ... ... to life (*strictly* temporally ... from the dawn of life on earth) - it is unsurpassed in its utility - the ATP molecule acts like a battery, with ->->->- the protein ATP synthase ->->->-(the essential component of the mitochondrion (an intracellular multi-copy organelle (resident of each of our cells) which is inherited solely from the maternal line (~noting~ that we must return here at some point in the future, laying down a pointer 'mitochondrial genome' -> 'X chromosome') ... ->->->- the protein ATP synthase ->->->- as ballbearing and a subunit spinning on exposure (...) --- transduction of potential energy within wave (later matter) -> what matters to our physical form ... ... ...
---and that (Escher's vision of the waterfall as seen in ATP, the flux of electrons, seemingly moving up hill, except ... cheeky cheeky Escher ... the waterfall is in sunlight ... the waterfall is solar-powered ... cheeky, cheeky Escher ... 'go stand in the corner with Go..del and Bach, and no shooting the breeze ...:-)...') ---and that this was the key even in the generation of life---

Our most recent Nobel (Johnny Walker) won the Nobel for elucidating the structure of the engine of life --- the proton pump (ATP synthase) ... and sure enough ... energy is transduced into raw mechanical energy --- energy is captured by driving the spin in this protein (the rotor subunit) ... ... ... of ATP synthase.

...once a mechanism exists to pull down energy in the form of PE from KE.

Next - the mechanism will continue for only as long as demand is placed on its functionality

ie ATP is required

Thought and friends - the pattern of evolution of life towards an organism which uses ATP as highly as possible.

The most concentrated users of ATP represents the fitter more vibrant - more energetic organisms.

Processes favoured which lift our usage of ATP.

Of course - ADDer thought.

We evolve by rearrangement of our brains, mind to 'think' more - solely because thinking represents a better usage, higher usage, higher demand for ATP ->-

ADD

please not better ...

man is the only organism who can layer on better, worse

... this is nature ... working within our context - within the constraints of our context.

Maybee problems with ATP in certain areas of the brain is the final common pathway of adhd?:confused:

[QUOTE->-nzkiwi]Maybee {} with ATP in certain areas of the brain is the final common pathway of adhd?[QUOTE ENDS]
... just substitute the 'problems' for another word - more indicative of evolutionary change
... rather than a ~good~ or -bad- change ->- and we have it.

The experiential perspective of ADD is the experiential perspective viewed through our eyes - of a substrate of neurones (our brain) - rearranged into a form which utilizes ATP ~just~ *more* so than in previous neuronal configurations.

So - yes - ADD is ATP
- usage -
->->->- evolved.

Bit of a hit tv show called 'Lost'
Dr Marvin Kandel was the name of the host to our mind -
the presenter of the film which John Locke watched with the Dr guy.

We have covered Marvin here.
Marvin (Minsky) from the school of connectionism - please search for

{meadd823
connectionism OR connectionist}

{meadd823
... Kandel
also ...}

Combination of Kandel + Minsky ->- mind.

Minsky ->- mind as a logical model
Kandel ->- simplified physical functionality serving as substrate for Minskys' ideas.

... So ~to~ connect the two ...

The slug has a simple protective reflex system—when a particular area was prodded, the gills would withdraw. By examining the operation of this reflex in detail, Kandel was able to get an insight into short- and long-term memory.

When Alpysia received a weak stimuli in the form of short prods, a series of interconnected chemical changes—a chemical pathway—would follow within the nerve cells. The neurotransmitter serotonin was released that would activate “protein kinase A” or PKA. In turn, PKA, modified other proteins producing a strong electrical connection between neurons that would last from several minutes to hours. There was, however, no long-term change as the proteins would return to their normal state.

But when the slug was continually prodded, it would stop responding completely and the effect would last for weeks. Kandel found that for this long-term memory to occur, certain genes needed to be “turned on” or activated through the release of a protein known as CREB 1. Once the genes were turned on, certain proteins would be released, which reshaped the end of the nerve cell or synapse and changed how it functioned for a lengthy period of time.

Other experiments have confirmed that long-term memory cannot develop unless the particular genes in the nerve cells are switched on to produce these new proteins. If that process is blocked, nerve cells are only capable of short-term memory.... ... ...

Here's a shape

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which ->-
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first

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then
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within

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short term memory
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long term memory
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connectionism
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the mind (rrreality) is a logical model of RRReality

... a better RRReality simulation (rrreality simulator) {mind}

gives way to

increased thought (selection pressure)

... see posts above (within this thread) ...

eg

post 16

http://www.addforums.com/forums/showpost.php?p=370403&postcount=16

... of course - ADD thought ...

... Noting ...

ADDF link 1
(http://www.addforums.com/forums/showpost.php?p=318098&postcount=457)http://www.addforums.com/forums/showpost.php?p=318098&postcount=457

There is a pattern --- it's described in one of my posts here --- the long one ... it's the ... ... ...
(13)1 ... 3 ... 4 ... 13(1) pattern
... this pattern effectively describes evolution --- really it does ...

ADDF link 2
(http://www.addforums.com/forums/showthread.php?p=344032&highlight=eye#post344032)http://www.addforums.com/forums/showthread.php?p=344032&highlight=eye#post344032

http://images.google.com/images?q=tbn:-jdTCsVvoi_NfM:http://home.case.edu/%7Esjr16/media/stars_blackhole_anatomy.jpg<==> <==> <==>http://images.google.com/images?q=tbn:bg6R1iZOBcnfXM:http://pub.cozmixng.org/%7Egallery/pstickne/eye.jpg
external link 1
(http://www.crystalinks.com/eye.html)http://www.crystalinks.com/eye.html

http://www.crystalinks.com/12around1sm.jpg
12=1+2=...3...=third dimension - manifestation in 3D
12 around = ..13 ..= 4=...4...th dimension = time

external link 2 (http://www.crystalinks.com/eye.html)
http://www.crystalinks.com/eye.html

http://www.crystalinks.com/eyelephgalaxy.jpg

... that everything ~changes~ ...


... that more and more people are beginning to see ... ... ...
... that more and more people are beginning to see ... ... ...
... that more and more people are beginning to see ... ... ...

I believe that the long and short term processes represent the overarching process of forming an internal copy of external Reality - mirroring RRReality as closely as possible -an internal copy - as a substrate for thought to operate upon, with and alongside.

weeeeee

I have a suspicion that the colours which I adore - those colours (from my avatar), reflect a time of maximal energetic activity in our pre-cellular form (of ATP --- from earlier on in this thread); to be clear, I have this feeling that the transition from night to day - was a precursor in on the transduction of light (EM) energy into organic form,


Odd thing that occured to me as I read this,my avatar colors are the exact opposite. I am awake in my night time (late evening to early morning) which for you is morning into day so in essance our avatars are the same colors but being view from different sides of the planet. . . . .okay so a strange spin off I will admit but I think it is my turn any way- :p


I am being attracted to your shape / information relationship. How you connect shapes, very visual perceptions. Good thing I do those too.



The more complex information I will have to address after a bit of sleep.

Nite all.

... the comment during the days of Lautrec as avatar ... when yours was also - the negative (night waking), or maybe mine the negative to your positive.
Same difference.
If I were taken to rewriting a line from a PM written a coupla'seconds ago.
It'd probably go like 'just 0,1 - neither 'good' nor 'bad' *0* presupposing *1 * {and the converse also} - the ultimate jewel [holy] - dual [wholly] not duel [holey] {from ADDFt:metamind) and a coupla'other ADDFreakin't{s}.

shape / information

information -<- energy

Dual Motion (http://www.rwgrayprojects.com/Universe/DualMotion/dm.html)
dual [URL linked originally on ADDFt::Hyperactive mind {I think}]

The dual - two forms - one presupposing the other.
We have motion from one to the other.
The transition - motion - stored energy.
Perhaps kinetic energy and potential energy.
With the conveyor belt rolling counter to a black ball (black hole) - another view over PE.
We have the concept of more information content (energy) within a given space.
By evolution from 1 geometric structure to another - more complex.
The goal - most efficient usage of space.

An observation in line with this idea - the stable density of an iron core.