So after all my recent research, I've realized ADD is mostly a neurotransmitter problem, and it's mostly caused by either Catechoalmines (http://en.wikipedia.org/wiki/Catecholamine), most likely dopamine (http://en.wikipedia.org/wiki/Dopamine) or norepinephrine (http://en.wikipedia.org/wiki/Norepinephrine) why these chemicals - and what exactly they do - is a matter worthy of discussion, but not here.

Anyway it seems that virtually all the ADD drugs discussed at length in this forum act on these two nuerotransmitters in some way, and for almost all of them they act to increase the level. The stimulant medications (dexedrine, ritalin, adderall and so on) all do (though their method of action isn't entirely clear to me right now). Strattera is a SNRI - so it by definition inhibits norepinephrine reuptake. Wellbutrin/Bupropion is a Catecholamine reuptake inhibitor. Even lowly Clonidine acts on the system - however, it causes catacholamine production to fall, rather than rise. Rather unsurprising then that the clonidine prescription I got was to help reverse the effects of dexedrine so I could sleep!

It would seem then that the question with these drugs is how much dopamine and norepinephrine there is in the synapses after taking them. It would seem at a glance that the most "effective" treatment is one that boosts the levels the most.

But I discovered something interesting today. It would seem that while Amphetamines boost overall dopamine levels (quite a bit), they do so at cost - they really rip apart stimulation-specific response, causing it to drop as much as 82% in a study (http://amphetamines.com/dopamine/reverse.html). I'm having a hard time finding other studies or really much more than that abstract, but that abstract is all over the web - and implies that there are more studies indicating similar things.

This makes me wonder. To what effect do other, non-stimulant drugs enhance or diminish the stimulation-specific response?

It seems like this problem might be at the root of many people's ADD. I have noticed, for instance (in my experience as well as reading) that the response to stimulant medications for most people is best the first day they take them, and declined thereafter. To me it seems that this a result of the dampening of the stimulation-specific response. As a result, the people find that they can focus, but things just seem less interesting, and they often wind up focusing on mundane tasks - unsurprising given that their brain may well be soaking in dopamine levels that don't seem to change with the task, giving the brain hardly any reason to change task.

On the flip side of the coin are those people who are just taking strattera or wellbutrin, or etc. I can't really say for certain what strattera does to stimulation-specific response, or what it does in the long run. Definitely seems to work differently, though. It doesn't have that initial flood of dopamine that amphetamines cause. What dopamine changes do they cause? How does this change with dosing and time? I'd like to know.

It seems, from a casual viewpoint, that the key to medically mastering ADD is to get both the dopamine stimulation response and the overall dopamine levels right. If the response is okay but you have low levels overall, then you wind up with what I find typical ADD symptoms - rapid-fire focus changes, a desire for very stimulating material, etc. If the response is bad but you have high levels overall, it seems you become a zombie, just mindlessly doing tasks with no motivation to change your course.

Anyway I'm considering drugs outside of the stimulant tree and so I'd like to know people's thoughts, or much better, research they've found comparing these things.

My first take?......I don't like the feel of the study http://amphetamines.com/dopamine/reverse.html which linked to->http://amphetamines.com/
It has the look of being scientific yet it tastes like bleached flour and sugar.

Better Living through Chemistry -> what the hell is that? There is a link from the page above to -> http://www.bltc.com/

Hmmm..and now look at this page. How did the BTLC get in there??
http://www.worldandi.com/public/2000/november/sax.html

Here is another link from that original page.
http://www.wireheading.com/

As I dig deeper I smell Scientology or Breggin's ICSPP. This looks like a new generation of misinformation webpages. Looks like they are getting more sophisticated with the message. It is not so obviously biased and for the first timer, can easily scare and confuse. The last two traits are definite trade mark of Scientology and Breggin et al.

It is true that the parent page from which that site derives looks a little sketchy. Maybe even a *lot* sketchy. But you can find the paper from better sources. I've found it in full on columbia.edu:

http://cumc.columbia.edu/dept/neurology/sulzer/pdf_articles/Schmitz_AMPH2001.pdf

It references a lot of studies that I could track down, if I had the time and willpower to set up all the stuff I'd need to be able to access my former university's paper catalogs online. Of course, I'm as wary as anyone of Scientology bull**** (drugs are stored in fat?!), but I think this is legit.

I don't think that the hedweb site and it's related links are scientology related. I'm familiar with them, they have been around for years. I don't think that there is an anti-psyc agenda either. I rather enjoyed reading the page at http://www.biopsychiatry.com/
"The good drug guide: new mood brighteners and anti-depressants"
It's a really good over-view. The point the fellow is making is that we can't find happiness in a pill - yet - but they can help.
I think it's legit too.

It's difficult to say what the study in question - re stimulation-related dopamine release - means. I think they are saying that less dopamine is released from stimulation when amphetamine is present - which could be why stimulants help with impulse control(?) If stimulation - acting on the impulse - isn't releasing as much dopamine it's not as attractive to the brain(?). Hard to tell what the dosage is or if it has anything to do with theraputic use. Interesting in that it gives insight into how amphetamines work in the brian - which is what was being researched, after all.

I don't think that the hedweb site and it's related links are scientology related. I'm familiar with them, they have been around for years. I don't think that there is an anti-psyc agenda either. I rather enjoyed reading the page at http://www.biopsychiatry.com/
"The good drug guide: new mood brighteners and anti-depressants"
It's a really good over-view. The point the fellow is making is that we can't find happiness in a pill - yet - but they can help.
I think it's legit too.

A really good over-view??? It's more like a piece of propoganda. They have spent a lot of time and a lot of money here. But lets be clear, it is a strong antidrug message.


"One spectacularly incompetent route to a lifetime of happiness involves taking unsustainable psychostimulants such as cocaine or the amphetamines. In the short term, their activation of the sympathetic nervous system tends to elevate mood, motivation and energy. Users tend to talk a lot. Self-confidence is enhanced".

and

..."Some people continue to take psychostimulants casually for years without serious harm. Yet the potential risks of adverse physical, psychological and social ill-effects are high. Hence their use is best discouraged".


"Ill effects" is highlighted and when clicked, a full screen image of crack cocaine comes up. The whole thing(Amphetamine.com/ BLTC / the studies/ biopsychiatry.com/ ) is one LAARGE controlled and connected message. The first four pages of the Amphetamine.com webpage is up close pictures of stimulants. You can't roam..you have to go from one page to the next. It is a clear and controlled message, all stimulants are dangerous drugs. The last page is the "ice" page. -> http://amphetamines.com/ice.html. It looks scientific but reeks to high hell. There are links to pages that look like scientific studies and in fact some probably are. Yet, I'm certain that they are taken out of context and that no respectable scientist would want their work in what looks to be an elaborate deception.

Another thing, one scientific paper does not make something a fact. What was the scientist trying to discover? Does it mean what I think it means or am I drawing conclusions which I shouldn't be making? As mctavish23 said, "From the stanpoint of strict research methodology, you CANNOT make any inferences from this study".

Personally, I have seen so much FAULTY inference in the discourse on ADHD. That is, to make inferences from ONE study. Yet science doesn't work like that. Others must be able replicate your results. You should look for that, a BODY OF KNOWLEDGE. Just because someone has demonstrated something, it doesn't mean that you can draw conclusions about something related to what was demonstrated. When you see faulty inference happening, you know these people really know nothing about the subject.

The BLTC link looks to be strongly related to Scientology...but I have spent about 2 hours falling down the rabbit hole. The Scientology/ BLTC connection will have to wait for another day, for when I have time to post links so it is obvious to everyone.

scuro, thanks for starting a new thread, bltc.com, biopsychiatry.com, hedweb.com, and Amphetamines.com (http://www.addforums.com/forums/showthread.php?t=17462).

i found myself falling down that rabbit hole as well (love that image btw) , though, my focus shifted in the nick of time. :)

Maybe I've looked at it as a diatribe against recreational use - and I am not one to recommend amphetamines for that. I know nothing of scientology so I wouldn't recognize something with a scientology look if it was in front of my face. I'll check out that thread - I hate being duped by people with alterior motives.

It seems like this problem might be at the root of many people's ADD. I have noticed, for instance (in my experience as well as reading) that the response to stimulant medications for most people is best the first day they take them, and declined thereafter. To me it seems that this a result of the dampening of the stimulation-specific response. As a result, the people find that they can focus, but things just seem less interesting, and they often wind up focusing on mundane tasks - unsurprising given that their brain may well be soaking in dopamine levels that don't seem to change with the task, giving the brain hardly any reason to change task.

I am not a scientist, nor have I ever taken a stimulant meditation on a daily basis. But I would like to generalize here. I have drank coffee for 25 years. I have never experienced a noticable dampening of the stimulation-specific response. Perhaps different stimulants vary in their long term responses but my daughter has been on meds for 2 years at the same dose. I notice none of the symptoms you describe, in her.

I had also thought that the nurotransmitter uptakes had a large role to play in ADHD. That they were overactive and sucking up nurotransmitters before they crossed the synaptic gap. That it's not really a question of being "starved" or being "soaked" with nurotransmitters but rather if they are allowed to achieve their function properly.

It's been a while since I have looked at this so it would be interesting to hear more.

But I discovered something interesting today. It would seem that while Amphetamines boost overall dopamine levels (quite a bit), they do so at cost - they really rip apart stimulation-specific response, causing it to drop as much as 82% in a study (http://amphetamines.com/dopamine/reverse.html). I'm having a hard time finding other studies or really much more than that abstract, but that abstract is all over the web - and implies that there are more studies indicating similar things.

This makes me wonder. To what effect do other, non-stimulant drugs enhance or diminish the stimulation-specific response?

Taking a closer look at this study it appears that they used mutant mice lacking the D2 receptor, decapitated them, then sliced their brain open, put amphetamines directly into this cell area, and then measured the results with a voltmeter.

Jimbo, I think you may have jumped to some conclusions that could be correct but could also be incorrect.

Here are my intial thoughts about your ideas.
1)Humans don't apply amphetamines directly to any brain cell.
2)Humans are not mice.
3)What does the missing mice D2 receptor have to do with adhd in humans? Adhd may likely involve several receptors.

More study, especially with humans and specifically with humans who have adhd would need to done before a body of knowledge could conclusively prove anything relating to stimulant drugs and their outcomes in humans who have adhd.

Yeah, you are right on that, scuro. Plus dextroamphetamine, ritalin, and amphetamine aren't even the same.

I still wish I had some reliable studies on the topic of tolerance, though =\

Yup, I forgot to mention that point, thanks!!

From practical experience I have observed that people who take drugs like Ritalin do not need ever increasing doses to get the same effect. They do sometimes need a change in dosage as their body mass increases with time, like during a growth spurt.
I have also drank coffee for 25 years and it has been a real crutch for me. I have been on two cups of coffee for about 15 years and never felt the need to increase the dosage of this stimulant.

I thought you would also enjoy this. If your a one study guy, here is your proof! From the webpage the which you linked to, amphetamine.com, comes this study.
http://www.amphetamines.com/adhd/index.html
"When used in the therapeutic dose range, there is no evidence of the development of significant tolerance or sensitization".


Does potential tolerance for drugs like ritalin worry you that much? Where has this fear come from? You must have been trolling too many Scientology/ antipsych websites. ;)

McTavish23 has said. "THE US SURGEON GENERALS REPORT ON MENTAL HEALTH:CHAPTER 3(DISORDERS OF INFANCY, CHILDHOOD & ADOLESCENCE ) has the most complete history of the use of stimulants to treat behavior problems that I've seen. It goes all the way back to the original medication study done by a Rhode Island physician names Bradley in 1937. You can also find that mentioned in You Mean Im Not Lazy, Stupid Or Crazy? and Taking Charge of ADHD.

To quote Dr Barkley, "Stimulants are the most benign drugs in psychiatry." He also said that the "only" was a person with ADHD can become addictive to Ritalin (which remember isn't an amphetamine) is by grinding it and snorting it. THAT CHANGES THE METHOD OF DELIVERY".

Actually I have found in my research that stimulants are the most benign drugs around. They're nicer than alcohol. I've never taken two dexes and then felt like I need to take one more, which eventually becomes 10 and leaves me feeling like death the next day. I've never woken up and felt like **** until I got some dex into my system.

I still sometimes get worried when I wake up and I can't get **** done without my medication. But then a recent, multi-month long "drug holiday" showed to me that it has nothing to do with dependence and everything to do with the return of unmedicated ADD symptoms. It's in my nature. I have this incredible ability to spend a whole day and have *nothing* to show for it.

It does seem though, that the high you get the first few times taking Dex does diminish. If you're taking it to get high, a tolerance can develop. After the first few times, the "I am invincible and can take on the world" feeling drops off.

While I haven't been trolling scientology websties, I have been reading prescribing information. It's typically covered in notes and caveats about addiction and tolerance.
An example is here (http://www.healthyplace.com/medications/dextroamphetamine.htm#adverse), and let's not get in anrgument about that source, since there are many more like it.

Sources are oh so important to me because a good source will not post faulty info or be biased. Hate to do this but your link brought me to this webpage in two clicks-> http://www.stayfreemagazine.org/archives/17/screeningtest.html
I'm sure there is more biased stuff there but I'll leave it at that.

Anyways, lets take the info you posted at face value. The major complaint I would have with the symptoms on the website is that it appears that some of the symptoms posted would be associtated with chronic drug ABUSE and not theraputic drug use. Again, it looks like what we have here is a website that creates fear.

You do make some good observations and it is probably true that, "the high you get the first few times taking Dex does diminish. If you're taking it to get high, a tolerance can develop. After the first few times, the "I am invincible and can take on the world" feeling drops off".

I get the same thing off of coffee. If I have been off coffee while on vacation I do notice a high or buzz when I start again...and that goes away after the first few times. But the ability of coffee to focus me stays over the long run and my dependcy is slight and tolerance is not an issue. from what I have read in the literature, it is the same for Dex and Adderall for the general adhd population.

Found a better source for you - the official adderall XR website (http://www.adderallxr.com/default.asp?mode=SI) says "Abuse of amphetamines may lead to dependence. Misuse of amphetamines may lead to serious cardiovascular adverse events. A patient should report any new psychological symptoms to his or her physician."

Yes, it does say abuse. It also says dependance. I doubt Shire would make this up if it wasn't true; they're the drug company. Of course, "abuse" is taking it to get high - we agreed this won't work. Another thing it won't work on, according to my P-Doc today, is weight loss. You can take some and at first it helps supress appetite, but apparently, with time, the body adapts to this,

Or, take the word of the little packet of information I got with my new Adderall XR prescription (from CVS) -
"When used for an extended period, this medication may not work as well and require different dosing. Talk with your doctor if this medication stops working well."
My personal feeling is that at least part of the problem is not getting high any more. If you're not getting high any more, it doesn't feel like it's working, and so...

Abuse of an amphetamine would cause drug dependence, no disagreement there. What is meant by dependence, is drug addiction.
http://www.nlm.nih.gov/medlineplus/ency/article/001522.htm#Definition ...and yes the company is right to warn against this possibility misuse of their drug because it is a very serious matter.
Typically, when they talk of abuse of Amphetamines they mean a different delivery system (snorting it or injecting it ). Barkley has said that you can't create dependency from theraputic levels used as directed. It's very silly to equate drug dependency with any stimulant used as directed as a medication for adhd. This is what you would expect from the Scientologist or Baughman camp.

I can't really comment on the high of Adderall. I can tell you that my coffee buzz disappeared decades ago. It may not feel like I have the "zip" that I used to get and I must admit that at times I drink coffee and feel little difference yet I know I do better work then. Feelings have a wonderful way of being subjective and that is why I would tend to trust clinical studies on this matter and there are plenty.

i wonder, if the "high" i felt when first taking dexedrine wasn't really a high at all....

it's just that i felt *so* good because the medicine was working, it felt so good that the symptoms were being treated. so, the "buzz" was a psycological effect of me being so pleased that the symptoms of ADD abated. the thrill of completing a project, or being on time made me feel like i was on top of the world.

and, as with anything i became acclimated to feeling like i could accomplish a given task. so, my medicine didn't give me that psycological rush because the "medicated feeling" became the norm.

a friend just built a big, new house. his dream house. he was so excited and whitling even the entire time his house was being built. he'd go out to the work site and just dream. reality, though, is that the mortgage is a stinker and it is just a house....

just as in that situation, the medicine works on the symptoms -- now we feel like the impossible tasks are at least possible. they are no more desirable though. now we're just like non-ADDers, though, we don't want to do it, but we are able. it just takes some addititional time to get past the roadblocks our mind and experience places based on our history ....

anyway, i've really enjoyed following this conversation. and i *do* appreciate your concerns jimbo. i have similar concerns when i want to treat my child's infection and am worried that the anti-biotics prescribed may cause an unwanted reaction or lead to a resistant strain of whatever bug they currently have.

but, i do a mini-risk analysis and almost always end up treating the infection. i'm by the book, though. so i can make sure that it's not the virus that's making the miserable....

i'm a bit scattered today. hope you can follow my line of reasoning. haven't taken my dextrostat yet this morning... :D

really lovely discussion you guys. thanks!

wheezie

Ok, ok, I have to work, but before I do...

We just have to make sure we read the right things the right way. A word or prefix ("antag" vs. "ag", for example) can swing us in the wrong direction (in the example, a mixup would take us from "helpful for ADD, horrible for schizophrenic psychosis" to "helpful for schizophrenic psychosis, horrible for ADD.") They can all sound very similar, especially when you get into the D1, D2, D3...receptors, GABAA, etc. If your eyes start to blur take a break.

Most of us are on some form of dopamine agonist (Dex is included in this.) Dopamine receptor agonists act by either blocking the brain's attempts to metabolize dopamine (the word metabolize seems odd, but basically it makes the dopamine stick around) or making the brain produce more dopamine.

Norepinephrine deficiency, as well, aggravates the symptoms of ADHD, but we knew that too.

I have to go for now, but here are some articles which (should) illustrate the metabolism and actions of meds:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?term=dopamine+agonists&db=pmc&cmd=search&pmfilter_Fulltext=on&pmfilter_Relevance=on
Chrys

The dopamine "thing" is not quite as simple as agonists being good for ADHD and antagonists being bad. Many people may take both an agonist - like amphetamine - and an antagonist - like the atypical mood stabilizers Respirdal or Zyprexa. I believe that they work at different receptor sites (there are several, denoted D1, D2, etc) and possibly in different areas of the brain(?) Parkinson's disease is dopamine related, and yet ADHD patients don't take Parkinson's meds and vice versa.
Don't use PubMed searches as a primary research tool - I find that the research can be so esoteric as to be useless in understanding what's happening in my brain or how a drug works.

I believe that they work at different receptor sites (there are several, denoted D1, D2, etc) and possibly in different areas of the brain(?) Parkinson's disease is dopamine related, and yet ADHD patients don't take Parkinson's meds and vice versa.
Don't use PubMed searches as a primary research tool - I find that the research can be so esoteric as to be useless in understanding what's happening in my brain or how a drug works.
Different receptor sites AND different areas of the brain. And maybe ADD/ADHD has more than one neurological cause, further complicating matters.

Apt contrast between ADHD and Parkinson's disease (which is prompted by cell destruction in a very specific area of the brain stem).

I know your job is hard, Greg. Please just delete my post next time instead of putting any energy into my degredation. You're exhausted enough, man, and there are just too many ways to degrade me.

I was being rather vague. But I don't believe I ever said "Dopamine thing." I know it's not that simple, and I did mention receptors. D2 is the primary receptor concerned with amphetamines, if memory serves (kind of an ironic thing for an ADDer to say in discussing the mechanism of ADD meds.)

I'd have to politely decline your advice on PubMed...for one thing, I just spent four months studying things with the specific order that articles should be obtained from PubMed whenever possible. Doctors use PubMed. But this is not an ad for PubMed, and there is a word of caution I'm always forgetting, which is that if you don't know the basics, you might not be able to filter out any inconclusive, outdated or incomplete articles that may have slipped into your search...some journals seem to produce these articles repeatedly. J Clin Psy was silly a lot of the time, I remember. At any rate, yes, you're right, there's a drawback to using PubMed. Beginners can have accidents.

One more thing--stanzen's confirmation of your point that the two (ADD and Parkinsons) are different is, of course, on target. However, I'm afraid you are mistaken on one part. Amphetamines can prove useful for Parkinson's patients. It is simply logical when one considers the symptoms of disorders marked by damage to the extrapyramidal tract. Movement difficulties in Parkinson's are in large part due to deterioration of the substantia nigra pars compacta, after all. In truth, as much as we ***** about the ineffectiveness of our meds and treatments, they have it much worse.

Sorry...I am apparently of no use when discussing this Dopamine "thing."

The dopamine "thing" is not quite as simple as agonists being good for ADHD and antagonists being bad. Many people may take both an agonist - like amphetamine - and an antagonist - like the atypical mood stabilizers Respirdal or Zyprexa. I believe that they work at different receptor sites (there are several, denoted D1, D2, etc) and possibly in different areas of the brain(?) Parkinson's disease is dopamine related, and yet ADHD patients don't take Parkinson's meds and vice versa.
Don't use PubMed searches as a primary research tool - I find that the research can be so esoteric as to be useless in understanding what's happening in my brain or how a drug works.

Hey KJ,

Don't be so hard on yourself. I learned things reading your post.

KJ,
I really did not mean any offense - please don't take anything I say the wrong way. I genuinely enjoy your posts and wouldn't want to discourage your posting in any way. The ONLY reason I posted was that I didn't want anyone to think they might be on the wrong medication if they are taking a dopamine antagonist like Respirdal or Abilify - I'm paranoid that someone would stop taking meds without talking to their doctor first. There is lots of confusion with regard to dopamine and other neurotransmitters - I don't pretend to know how it all works, I barely know the basics- if that! :-)
I'm not a pubmed basher either - I look at it myself - but I think a lot of people - and I don't mean you - read things "into" the abstracts they see on Pubmed and make presumptions that aren't valid - the amphetamine "brain damage" type threads come to mind. Doctors have the advantage of having access the entire text of the papers and they are trained to judge the implications of the research on the real world health of their patients.

So please don't take offense KJ - if my posts seem short or harsh it's likely because I haven't had the time to write much 'cus I've been busy at work, and just posted what I had - when I have the time, I write more and am more careful not to make spelling mistakes or offend anyone.

Regards,
Greg

Yeah, Gregster, I agree with you. Often, however, pubmed and abstracts are the only port in the storm of slop that is medication discussion.

Do a search for any medication, and half of the links will be "Dexedrine Adderall Ritalin XL XR SP No Prescription Required!" - an internet spam that works by pumping in as many keywords as is possible. Another 45% will be some other form of crap, often lurking in sheep's clothing. I've read sites that seem to be reasonable discussions, then they spring their herbal remedy of choice on you (Such as Attend and those types). There's a lot of general ADD and/or medicine hate around the net too - a lot of "ADD isn't real, it's just invented for Pharmacueticals to make money". There are a lot of sites that seem to say "These medicines leave you mentally empty and could kill you too." There's also the really weird stuff like David Pearce's doings.

Generally that leaves the average person to only trust stuff which is very clearly scientific in origin. It's hard for most of us to interpret these studies properly, but it's all we've got.

As for the matter at hand: I don't think most stimulant medications are Dopamine *agonists*, or if they are, this isn't their main method of action. Agonist has a different (and not strictly opposite) definition than antagonist.

Dopamine agonists are a different form of drug - see here (http://www.mirapex.com/A/b/dopamine.asp)

An agonist activates nueroreceptor sites directly. This is why you see "D1 Agonist", referring to the site being activated - not the chemical it's working on. It might be referred to as a "dopamine agonist" when it's acting to activate all the dopamine receptor sites. But it's still acting as a kind of "fake" dopamine, *not* a reuptake inhibitor, which all our medications are. It doesn't increase dopamine levels.

An antagonist blocks another chemical. Sometimes it can act similar to an antagonist, by blocking at the nueroreceptor site by binding and not letting anything else come in. This what Clonidine does, in my understanding - it acts as a sort of fake nueorepiniphrine/dopamine that convinces the body to release less of its own, while not actually working as nueroepiniphrine/dopamine would.

In any event, stimulant medications work through 4 different means, of which I can't remember all of them right now. The primary method is as a reuptake inhibitor. This means that when a nueroreceptor releases dopamine, the medication prevents it from being reabsorbed, so the level remains higher in the synapse.

There are also a couple other things it does. It prevents vesicular retention, and I'm not too sure what that means. However, it has been shown to "actively" transport dopamine from the receptor into the synapse, further increasing the amount of dopamine present.

It's action on dopamine transport is the core of how it functions. It does not, by contrast, act to "replace" dopamine.

Other medications, like Wellbutrin and Strattera, also act to inhibit reuptake, but aren't nearly as aggresive about it as stimulant medications, or, in the case of Strattera, don't seem to particularly effect dopamine. This seems to be why they're less effective.

KJ,
I really did not mean any offense - please don't take anything I say the wrong way. I genuinely enjoy your posts and wouldn't want to discourage your posting in any way. The ONLY reason I posted was that I didn't want anyone to think they might be on the wrong medication if they are taking a dopamine antagonist like Respirdal or Abilify -
Just to clear things up... Abilify is a dopamine D2 agonist, not antagonist. It is unique in this regard among the atypicals.

Didn't know that about Abilify - I have to do some research on that drug in particular.

In this thread I describe how amphetamine and methylphenidate work - according to my textbook on the subject - I typed in the text word for word!http://www.addforums.com/forums/showthread.php?t=7701
I think that there is some "agonist" action with amphetamine too, but the primary mechanism of action is reuptake inhibition. It is certainly a complicated subject!

JimboOmega...

Actually, Dexedrine is a (synthetic, exogynous) dopamine agonist, though it's classified as a CNS stimulant.
You're right, not all the medications listed in this section are actually agonists--like I said, some unnaturally raise levels of dopamine, and some prevent dopamine from "metabolizing" quite as much as it should--in other words, it makes it "stick around longer." They are different.
That said, "agonist" and "antagonist" are, in fact, antonyms/opposites.

Chrys

Gregster...

Sorry, you're right, I get it now. Thinking from the frame of mind you described, of course, the very generalized phrasing of my initial statement might have upset some people. (Those who are on multiple meds, as you described.)

Misinterpreted the wording, thought you were being condescending, though we've never had a problem before to my knowledge...hopefully you get it. ;)

Chrys

Huh--I didn't know that either! Thanks. Cool, I'll have to check that out.
Chrys
Just to clear things up... Abilify is a dopamine D2 agonist, not antagonist. It is unique in this regard among the atypicals.

Adderall is to dopamine/norepinephrine receptors as tryptophan is to 5HT receptors. Now look at it this way, Straterra/Wellbutrin is to dopamine/norepinephrine receptors as SSRIs are to 5HT receptors.

In other words, Adderall boosts the amount of dopamine/norepinephrine in the brain as does tryptophan does to serotonin. On the other hand, Straterra/Wellbutrin changes the way existing dopamine/norepinephrine in your brain is utilized. In this case, more of your own natural catecholamine neurotransmitters (dopamine/norepinephrine) remain in the synapse. This works the same way as an SSRI such as Prozac where your existing sertonin is used.

Hope this makes sense.