i was working with a person while doing a trial on stratera, they mentioned people who take ritalin (like me) have two chemicals that help control the hyperactivity, and depressed people have one chemical out of balance. for the life of me, i'd like to know what these are called?

I liking this forum, i've been reading several of the posts, from the comments I can relate to many of them. Its nice to know that I'm not the only one out in the world that thinks like this.

Dopamine, seratonin, epinephrine/norepinephrine are the chemicals.....Seratonin tends to be the depression chemical in most cases...Which are the hyperactivity chemicals??????? Not sure....:( Anyone?

No, SCS, you are certainly NOT alone in your thinking....:) Welcome to the Forums....:)

Yep those are the one, Dopamine, epinephrine/norepinephrine are the chemicals.....From what this quack was telling me, ritalin treats one of these where stratera will treat both. i was wondering if someone would know what i was asking in this post.

knowing what chemicals a drug is targeted will help with my family doc because he is more an internal family doc than a specialist.

Okay who here (on Ritalin or not) knows what neurotransmittors Ritalin targets??????????

And who here (on Strattera or not) knows what neurotransmittors Strattera targets???????

Originally posted by joanrdtobe

And who here (on Strattera or not) knows what neurotransmittors Strattera targets??????? [/B]

Stattera is a purely norepinephrine reuptake inhibitor. It does nothing to increase Dopamine.

Methylphenidate (the chemical name for Ritalin), is a dopamine reuptake inhibitor. It is technically called a dopamine agonist and is in the same category as Amphetamines and cocine and dextroamphetamine (adderall). Along with being a dopamine agonist is also stimulates the release of norepinephrine and dopamine from the neuron. English translation: it effects both Norepinephrine and dopamine, specifiically in the limbic and mesolimbic areas of the brain.

Strattera, from the information I have found is only a Norepinephrine reuptake Inhibitor (NERI), and does not effect dopamine levels. This, theoretically, is not immensely helpful for someone with ADD/ADHD because research shows that the disturbance is in the frontal cortex and limbic systems, both heavily reliant on dopaminergic receptors, not norepinergic receptors.

hope that helps.

MightyMouse

Originally posted by joanrdtobe
Okay who here (on Ritalin or not) knows what neurotransmittors Ritalin targets??????????

And who here (on Strattera or not) knows what neurotransmittors Strattera targets???????

This is NOT likely to be a production, inhibition, metabolic disorder.

it is most likely going to be recognized as a wiring disorder, and chemicials are simply part of the wiring in wetware. IMHO

The neurotransmitter impacted by Ritalin is dopamine. Ritalin creates more dopamine.Srtaterra blocks the reuptake of norepinephrine.Epinephrine is a different neurotransmitter and is not associated( to the best of my knowledge) with ADHD directly. All of these come inder the heading of catecholamines.

There is a theory called the Biogenic Amine Hypothesis which is very important to note here.The theory postulates that certain abnormalities in the physiology and metabolism of certain biogenic amines( organic substances divided into catecholamines and indoleamines (tryptophan and serotonin) are involved in the causes of certain psychiatric illnesses.This theory led to the discovery of the class of antidepressants we now know as SSRI's( Select Serotonin Reuptake Inhibitor's) , which includes Prozac, Zoloft and several others.

Why is this important? Well for one thing it links ADHD with depression, Tourette's, OCD, etc., in the sense that neurotransmitters are involved.Therefore, if ADHD isn't real , then neither are all these.I realize that this is complicated but there's no other way to describe what's going on inside the brain.

I'd be glad to go into more detail later about meds ; although keep in mind I am not a physician and claim no expertise in that area.I can relay what I learned at the Aug conference, which also touched on genetics.

http://www.webref.org/psychology/b/biogenic_amine_hypothesis.htm

http://www.vsppub.com/journals/jn-BioAmi.html

http://www.pickeringlabs.com/references/PCDBiogenicAmines.php4

http://www.ncbi.nlm.nih.gov/

http://www.ncbi.nih.gov/gquery/gquery.fcgi?term=Biogenic+Amine+Hypothesis

http://www.biopsychiatry.com/amine.htm

http://www.brucewoolley.com/HTML/rainbow/slide10.html

Indeed.

Then perhaps the number of co-morbid conditions, when separated out from the metabolic, will be a large number of understandably distracting forces, confusing the issue.

Perhaps much if not most of what is grouped under what it is to be ADHD will be excluded. Any sieve that requires only 4 or more of 20 issues is bound to be a heterogeneous population.

david

The symptoms of depression can be improved by agents that act by various mechanisms to increase synaptic concentrations of monoamines.

This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic and/or serotonergic systems and that targeting this neuronal lesion with an antidepressant would tend to restore normal function in depressed patients.

The hypothesis has enjoyed considerable support, since it attempts to provide a pathophysiologic explanation of the actions of antidepressants. However, in its original form it is clearly inadequate, as it does not provide a complete explanation for the actions of antidepressants, and the pathophysiology of depression itself remains unknown.

The hypothesis has evolved over the years to include, for example, adaptive changes in receptors to explain why there should be only a gradual clinical response to antidepressant treatment when the increase in availability of monoamines is rapid. Still, the monoamine hypothesis does not address key issues such as why antidepressants are also effective in other disorders such as panic disorder, obsessive-compulsive disorder, and bulimia, or why all drugs that enhance serotonergic or noradrenergic transmission are not necessarily effective in depression.

Despite these limitations, however, it is clear that the development of the monoamine hypothesis has been of great importance in understanding depression and in the development of safe and effective pharmacologic agents for its treatment.

Dare I ask if this "logic" was run past an expert in "logic?" at the college level? I suspect not!

http://www.biopsychiatry.com/monohypo.htm

Why do we bother to have logic classes in college, only to let pass all manner of technically bankrupt utterances, purported as support or challenge for positions when the fact is that there is no support for them being anything but the privately held opinions, based on no logic, of individuals? Yet paraded as something more?

Wheel,

It's always tough to sort out the comorbid features, however, you always try and look for what shows up first. Generally speaking, hyperactivity is the pre-school manifestation of the disorder. In my Diagnosis threads I talk a little about that and Inattention.It's not uncommon for example for ADHD kids to become depressed at some point as school gets harder and their best efforts fall short.

It's called a "hypothesis" because we don't know the origin, just as the "dopamine hypothesis" is associated with ADHD.The fact that these different meds work gives credence to these theories.No one ever said that this was an exact science.

I am fully aware that with a few well chosen radioactive tags, and some willing human guinea pigs, we could trace a number of chemicals through a bunch of metabolic pathways, and i trust, over time, we will completely map ALL the chemical reactions and metabolic transformations that occur.

My criticism wasn't about the distance between here and there, or the nature of hypothesis.

it was the readiness with which we abandon that which we know for sure! The readiness with which we accept any snake oil that comes down the pike.

There are those on this board whom I know stimulate in you a disdain, if not personally, at least for the "unscientific" or even counter scientific and therefore, from your point of view, unrealistic and therefore self limiting and delusional or phantasmagorical positions from which they demand to go forward, evidence be damned...

I simply have the same reaction when those doing the "sloppy thinking" are our best educated, and our best scientists. It becomes for me, the story of "the emperors new clothes." If the King is obviously naked, why does it take a small boy to say so? But it does!

Hypothesis does not cover for needlessly sloppy logic, ever. Hypothesis is an educated guess, not a WAG (Wild Awful Guess). IMHO

In computer programming, while attempting to model behavior a person could do, errors are generated. Experience demonstrates that it is most fruitful to address and correct all KNOWN errors beofre hunting for the "interesting" and dificult. It turns out that often those other errors are phantoms. And even when they are real, having them isolated rather than hidden in among others makes them easier to work. this is a principle of braod applicablity not restricted to computers, but applicable to process analysis as a whole.

I am particularly pained to have set myself, somehow, opposite you on such matters. I had hoped to work synergistically in a direction you have already set as your life's work.

And if I am to be set in opposition to you, I would prefer it to be along lines of substance leading to enlightenment, not the rehash of positions wherein we actually do not disagree. I do not argue with you for the direct benefit of others watching, but in service of a larger view, a refinement process of what is know.

I regret my failure to appropriately engage you, and any and all negative impact any of my criticisms take in collateral damage.

phantasmagorical

adj : characterized by fantastic imagery and incongruous juxtapositions; "a great concourse of phantasmagoric shadows"- J.C.Powys; "the incongruous imagery in surreal art and literature"; " [syn: phantasmagoric, surreal, surrealistic]

:confused:

Educated guesses just about cover it for all of medecine, not just psychiatry.

BTW,I really liked Mighty Mouse's reply to the original question.It was very well done.

You must read Amen, because one of the (several) complaints leveled against his SPECT Scans is the ethical issue of exposing test subjects to radiation.

I wish we weren't so imprecise but that is the nature of the discipline right now.Having said that, we have come so far since my Master's thesis in 1977 of a drug withdrawl study. The Human Genome Project will open so many doors for discovery that I hope to live long enough to see quite a few of them.

As always, I value your insights.

At the same time, how much radiation?

My mother stood on floroscopes as a kid in SHOE STORES. They used to wiggle their toes and watch them through the shoes!

She is dead, from metastatic kidney cancer... very rare in women....

we still give our children nuclear power plants with nowhere to restore the waste...

I really was pressing, not so much for the state of our science to be other than it is, but to avail ourselves of the logical tools of good logic and formal arguementation, to help guide our current understanding and short term progess, as well as we can.

It is the same everywhere. We have the ability to formally consider things, as a society, in ways we choose not to, for no good reason and to no good end.

Examples availabel on request.

Though I think there are perhaps 6 or 7 very distinct axis of operation in ADHD, I fit all six types of Amen's profiles. Personally he holds nothing for me.

I personally prefer, when possible, to construct by meeting ALL the requirements, conservatively, and then embellishing to acheive detail.

The Neurotransmitter Collection


Epinephrine

The Neurotransmitter Collection

http://micro.magnet.fsu.edu/micro/gallery/neurotrans/epinephrine.jpg Epinephrine

Neurotransmitters

All organisms must deal with a wide spectrum of different environments and be able to react to various factors such as danger, stress, and other organisms in order to survive. In bacteria, for instance, a major concern is determining the origin of a food supply. This problem is usually handled via the chemotactic response mechanism, which enables bacteria to sense and swim toward food sources and away from noxious conditions. Multicellular organisms, however, have evolved a more complex system that responds to external stimuli through the use of specialized sense organs and the communication of the information from these sensors to other parts of the organism. This type of communication falls into two categories. The first category is the transmission of chemical messengers between one tissue and another. The second is a more multifarious mechanism that involves the generation and transmission of impulses through the central nervous system.

http://micro.magnet.fsu.edu/micro/gallery/neurotrans/ltdopam1.jpg (http://micro.magnet.fsu.edu/micro/gallery/neurotrans/neuro1.html)
Dopamine In higher organisms, the chief unit of the central nervous system is a highly specialized cell termed a neuron, which serves to transmit impulses. In the human brain there are approximately 10 billion neurons, each with its own identity and function. The communication processes carried out among such a large body of cells is complex and the basic cellular structure for neurons differs radically from that of different types of cells. Most neurons have a cell body somewhat like that found in other somatic cells, however, they also exhibit a variety of projections (or processes) called dendrites and axons. Dendrites are branched protoplasmic extensions that receive neural signals from adjacent cells and conduct them inwards toward the body of the neuron. A single neuron may feature multiple dendrites. Typically, however, neurons each only possess a single long, threadlike axon, which carries signals away from the cell body and is capable of transmitting them to a dendrite on an adjacent cell. The connection between the axon terminals of one cell and the dendrites of an adjacent cell is called a synapse. The transmission of signals across a synapse is initiated by the presence of an electrical impulse and is accomplished by the use of small chemical messengers that are termed neurotransmitters.

http://micro.magnet.fsu.edu/micro/gallery/neurotrans/ltserotonin.jpg (http://micro.magnet.fsu.edu/micro/gallery/neurotrans/neuro2.html)
Serotonin A considerable number of chemical substances are believed to act as neurotransmitters, but the identification of only a few have been widely accepted. Among these, the earliest to be discovered was acetylcholine, which was first broadly recognized as a neurotransmitter in the 1920s largely due to the work of Austrian researcher Otto Loewi, who produced direct evidence of a sympathetic neurotransmitter by stimulating the autonomic nerves of a frog heart, resulting in the release of a chemical that decreased the beat rate of a second heart suffused with fluids from the other organ. Loewi's achievement was largely inspired by the earlier efforts of British physiologist Henry Dale, and a number of other scientists are also believed to have contributed significantly towards the modern understanding of neurotransmitters. Gaining knowledge about neurotransmitters has been a relatively slow, difficult process, however. Many of the early concepts regarding the chemicals have since been proven wrong. For instance, Dale purported that a neurotransmitter released at one axon terminal of a neuron was also released at other axon terminals of the same cell, though subsequent studies suggest that this is not necessarily the case. Nevertheless, over time a serviceable amount of knowledge about neurotransmitters has been accumulated, some of the most heavily researched of the chemicals being serotonin, dopamine, epinephrine, and norepinephrine.

http://micro.magnet.fsu.edu/micro/gallery/neurotrans/ltacetyl.jpg (http://micro.magnet.fsu.edu/micro/gallery/neurotrans/neuro3.html)
Acetylcholine The increasing availability of information about neurotransmitters in the latter half of the twentieth century resulted in massive changes in the medical and pharmaceutical fields. Indeed, conditions such as amyotrophic lateral sclerosis, also known as Lou Gehrig's disease, and Parkinson's disease, a degenerative brain disorder originally described by British doctor James Parkinson in 1817, came to be understood in new ways. Found to be associated with decreased levels of dopamine in the brain, Parkinson's became the first disease for which a neurotransmitter-based treatment was utilized. Today, drugs that contain metabolic precursors of dopamine, which can be converted into the neurotransmitter once within the body, continue to be used as an effective way to decrease symptoms of the disease and slow their onset, but do not provide a cure, suggesting that other unknown factors are the real cause of Parkinson's. Mood disorders are another good example of a kind of condition that has come to be widely treated with drugs that affect neurotransmitter release and function. Indeed, as early as the 1950s, depression began being attributed to deficiencies in certain neurotransmitters, and an array of pharmaceuticals that could help correct this problem soon appeared on the market.

http://micro.magnet.fsu.edu/micro/gallery/neurotrans/lnorepi2.jpg (http://micro.magnet.fsu.edu/micro/gallery/neurotrans/neuro4.html)
Norepinephrine The majority of early anti-depressant drugs produced were not designed to affect specific neurotransmitters, but rather had an influence on many or all of them. A variety of pharmaceuticals known as Monoamine Oxidase Inhibitors (MAOI), for example, function by inhibiting the activity of oxidases, substances that are able to break down neurotransmitters in the brain. The idea behind treatment with the drug is that as a result of its action, increased levels of neurotransmitters build up in the central nervous system and help individuals come out of a depressed state. While MAOI drugs are still available, they can cause severe side effects in some cases and have become significantly less popular as pharmaceuticals with activity restricted to influencing only certain neurotransmitters have been developed. The most prominent of this new variety of anti-depressants is the drug known as Prozac, which is Specific Serotonin Re-uptake Inhibitor (SSRI) that functions in a way that results in the prolonged presence of serotonin in the synapses of the brain. Avid Carlson, a Swedish scientist, was responsible for making many of the advances that resulted in the eventual development of Prozac, which became one of the top-selling drugs worldwide by the mid-1990s.


("borrowed" off http://micro.magnet.fsu.edu/micro/gallery/neurotrans/neurotrans.html)

How come ritalin with more than simply dopamine action works on ADD & dopamine specific meds are not known for treatment of ADD?

...Ritalin), is a dopamine reuptake inhibitor.... also stimulates the release of norepinephrine... English translation: it effects both Norepinephrine and dopamine, specifiically in the limbic and mesolimbic areas of the brain.

Strattera, from the information I have found is only a Norepinephrine reuptake Inhibitor (NERI), and does not effect dopamine levels. This, theoretically, is not immensely helpful for someone with ADD/ADHD because research shows that the disturbance is in the frontal cortex and limbic systems, both heavily reliant on dopaminergic receptors, not norepinergic receptors.

hope that helps.

MightyMouse