![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 1 to 23 of 23. This is the beginning of the thread.
Posted by Janelle on September 21, 2001, at 15:47:07
... the basic differences between re-uptake (blockage?) of SEROTONIN vs. NOREPHINEPHRINE vs. DOPAMINE? What I'm trying to ask (even this question is not easy to phrase!) is what beneficial effects is each of these re-uptakes supposed to have?
Also, for what "conditions" (e.g., depression, anxiety, pyschosis) is each re-uptake *supposed* to be aimed at. Well, I guess I *know* that Serotonin is for depression, but I don't understand the other two as well.Thanks to whoever can help explain this in layperson's terms!
-Janelle
Posted by susan C on September 21, 2001, at 16:37:22
In reply to In PLAIN English, can someone please explain..., posted by Janelle on September 21, 2001, at 15:47:07
There is so much information on the internet, where to start, as Janelle says, in plain english...thank you.
> ... the basic differences between re-uptake (blockage?) of SEROTONIN vs. NOREPHINEPHRINE vs. DOPAMINE? What I'm trying to ask (even this question is not easy to phrase!) is what beneficial effects is each of these re-uptakes supposed to have?
>
>
> Also, for what "conditions" (e.g., depression, anxiety, pyschosis) is each re-uptake *supposed* to be aimed at. Well, I guess I *know* that Serotonin is for depression, but I don't understand the other two as well.
>
> Thanks to whoever can help explain this in layperson's terms!
> -Janelle
Posted by shelliR on September 21, 2001, at 17:45:49
In reply to In PLAIN English, can someone please explain..., posted by Janelle on September 21, 2001, at 15:47:07
> ... the basic differences between re-uptake (blockage?) of SEROTONIN vs. NOREPHINEPHRINE vs. DOPAMINE? What I'm trying to ask (even this question is not easy to phrase!) is what beneficial effects is each of these re-uptakes supposed to have?
>
>
> Also, for what "conditions" (e.g., depression, anxiety, pyschosis) is each re-uptake *supposed* to be aimed at. Well, I guess I *know* that Serotonin is for depression, but I don't understand the other two as well.
>
> Thanks to whoever can help explain this in layperson's terms!
> -Janelle
Janelle & Susan,My pdoc wrote this for the Washington Post. It is a bit simplistic, but I think a good starting point:
http://www.washingtonpost.com/ac2/wp-dyn?pagename=article&node=digest&contentId=A25065-2000Jun20.
Shelli
Posted by Cruz on September 21, 2001, at 19:53:00
In reply to In PLAIN English, can someone please explain..., posted by Janelle on September 21, 2001, at 15:47:07
I am not saying they are for everybody. But they could be useless. I know with my form of depression. Levels of seretonin,dopamine and NE are not a factor. Its a dysfunction in my circadian rythmn. Monominergic theories have been around for 50 + years and they are no closer to being proven than ever. Keep well, look after yourselves.
> ... the basic differences between re-uptake (blockage?) of SEROTONIN vs. NOREPHINEPHRINE vs. DOPAMINE? What I'm trying to ask (even this question is not easy to phrase!) is what beneficial effects is each of these re-uptakes supposed to have?
>
>
> Also, for what "conditions" (e.g., depression, anxiety, pyschosis) is each re-uptake *supposed* to be aimed at. Well, I guess I *know* that Serotonin is for depression, but I don't understand the other two as well.
>
> Thanks to whoever can help explain this in layperson's terms!
> -Janelle
Posted by Janelle on September 21, 2001, at 23:43:49
In reply to Re: In PLAIN English, can someone please explain... » Janelle, posted by shelliR on September 21, 2001, at 17:45:49
Shelli - Thanks ever so much for posting that link to your pdoc's article in the Washington Post. You are fortunate to have this person as your doctor; he sounds amazing, and I could really understand his excellent analogy of the three neurotransmitters to three tenor voices, needing to be in harmony.
I even took notes on the short, concise and PLAIN ENGLISH explanations that he gave for each neurotransmitter. The article provided just the type of answers I've been searching for - in simple phrasing, which aspects of emotions/moods does is each of those three neurotransmitters involved! Thanks to your link, now I know and understand the very basics of each of the neuros! And it gave me insight into my *own* condition(s) and why certain meds have worked and others have not! Thanks a MILLION!
Posted by shelliR on September 22, 2001, at 1:39:39
In reply to SHELLI: wow, thanks-just what I needed...more: » shelliR, posted by Janelle on September 21, 2001, at 23:43:49
> Shelli - Thanks ever so much for posting that link to your pdoc's article in the Washington Post. You are fortunate to have this person as your doctor; he sounds amazing, . . . .
Actually in person my pdoc is often difficut to work with (schedules 2 people every fifteen minutes and does not return calls). Other than that, I have not found him as creative in working with him as I would have anticipated from reading the article. He's rep is that he is brilliant, and I have not seen brilliance so far. But the article is a good starting point, I think, and I'm glad it helped you with what you were trying to understand.
Shelli
Posted by SLS on September 22, 2001, at 1:46:44
In reply to In PLAIN English, can someone please explain..., posted by Janelle on September 21, 2001, at 15:47:07
> ... the basic differences between re-uptake (blockage?) of SEROTONIN vs. NOREPHINEPHRINE vs. DOPAMINE? What I'm trying to ask (even this question is not easy to phrase!) is what beneficial effects is each of these re-uptakes supposed to have?
>
>
> Also, for what "conditions" (e.g., depression, anxiety, pyschosis) is each re-uptake *supposed* to be aimed at. Well, I guess I *know* that Serotonin is for depression, but I don't understand the other two as well.
>
> Thanks to whoever can help explain this in layperson's terms!
> -Janelle---------------------------------------
Hello one and all.I'll give it a shot. I know it looks like a lot of words. You asked for specific details and a simple way of describing them. Hopefully, you'll find both. I had nothing else better to do after Bruce, so it's no big deal if I've failed. I just like to waste bandwidth.
The most important thing to remember is that trying to break down these illnesses into a simple recipe of the known chemicals has not worked very well. To a great degree, calculated trial-and-error is still necessary when trying to figure out which drugs will work for each individual. Even though two people's depressions look exactly alike, they can be very different chemically (and psychologically).
You can skip the next paragraph if you like and move on to the one succeeding it.
Using various methods, scientists have tentatively mapped out which brain regions and their associated chemical messengers (neurotransmitters) are involved with specific functions: locomotor (movement), thought, mood, drive, sleep, sensory, hormonal, control of organs, and other such stuff. Many of these regions use the same neurotransmitters. For instance, regions known to be composed predominantly of dopaminergic (using the neurotransmitter dopamine) neurons include those that participate in locomotion, drive, reward, organization of thought, and the perception of emotion. Areas rich in norepinephrine neurons include those that initiate movement, direct thought, and increase mental energy and level of alertness. Areas containing serotonergic (serotonin) neurons can regulate and influence the activity of those listed above. It seems that OCD might involve an imbalance in the relationship between norepinephrine and serotonin pathways. Glutamate neurons activate dopamine neurons if stimulated by norepinephrine neurons and not inhibited by GABA neurons.
Now, if this stuff seems to be getting more complex as we continue to try figuring out the way the brain works, you are looking at but the tip of the ice-berg. There are literally hundreds of different chemical messengers both inside and outside the neuron. And this doesn't take into consideration enzyme systems and control of gene activity.
So, what causes depression? How do antidepressants work?
Cruz has pretty much captured the flavor.
Neuroscience has positioned us closer to unlocking some doors. Psychiatry is beginning to find the information evolving from neuroscience useful in constructing associations between what drugs do chemically and what they do clinically.
Example: Antipsychotics reduce dopamine activity in the frontal cortex by blocking the dopamine receptors (neurotransmitter = key; receptor = keyhole; ion-channel = door). The frontal cortex, high in dopamine neurons, is responsible for organizing thought. Disorganized thinking is a feature of schizophrenia. The frontal cortex of schizophrenics and siblings of schizophrenics have abnormally high numbers of dopamine type-1 receptors in the frontal cortex. This yields a hypothesis that certain features of schizophrenia are produced by excessive or erratic dopaminergic neuronal activity.
Psychiatrists can also use their experience with people and drugs to witness trends in the associations between specific illnesses and their subtypes (symptom clusters), the drugs that work for them, and the biological activities of these drugs. Some drugs increase the number of neurotransmitter molecules available to stimulate neuron_2 by preventing them from being absorbed and recycled by neuron_1 after it has released them to send its message to neuron_2 - reuptake inhibition. Other drugs increase the stimulation of neuron_2 receptors by acting as a fake neurotransmitter. Still other drugs reduce the stimulation of neuron_2 by blocking or hiding these receptors from the real neurotransmitter. Some drugs allow for a build up of neurotransmitter levels in neuron_1 by preventing it from getting rid of the excess normally accomplished by a disassembly enzyme - MAO-inhibition. Anticonvulsant mood stabilizers block ion-channels and/or increase GABA activity, which usually results in reducing the excitability of norepinephrine and dopamine neurons and influencing the overall balance of activity. Lithium? Well, it does so many different things that are relevant to neuronal function, that it's hard to know where to start. It pretty much acts inside neuron_2 to produce changes on its outside.
So, now we finally arrive at the point where we started. (You can now reread the first paragraph if you like).
How's that?
Please don't ask me to do it again. My brain hurts. Besides, I'm sure there are plenty of factual errors for others to correct. Please forgive me for not proof-reading. I'll let that be your job. :-)
I had fun.
:-)
Silly.
See ya'...
- Scott
Posted by v on September 22, 2001, at 7:44:15
In reply to Re: In PLAIN English, can someone please explain..., posted by SLS on September 22, 2001, at 1:46:44
scott..
i just want to thank you for your information. it is quite frustrating not having at least a decent rudimentary understanding, hence the original post by janelle... and BTW, thanks janelle for asking the question!and it was a great follow-up to "making the three tenors sing" (i love that phrase!) which gave just the basic info
thanks again,
v> Hello one and all.
>
> I'll give it a shot. I know it looks like a lot of words. You asked for specific details and a simple way of describing them. Hopefully, you'll find both. I had nothing else better to do after Bruce, so it's no big deal if I've failed. I just like to waste bandwidth.
>
> The most important thing to remember is that trying to break down these illnesses into a simple recipe of the known chemicals has not worked very well. To a great degree, calculated trial-and-error is still necessary when trying to figure out which drugs will work for each individual. Even though two people's depressions look exactly alike, they can be very different chemically (and psychologically).
>
> You can skip the next paragraph if you like and move on to the one succeeding it.
>
> Using various methods, scientists have tentatively mapped out which brain regions and their associated chemical messengers (neurotransmitters) are involved with specific functions: locomotor (movement), thought, mood, drive, sleep, sensory, hormonal, control of organs, and other such stuff. Many of these regions use the same neurotransmitters. For instance, regions known to be composed predominantly of dopaminergic (using the neurotransmitter dopamine) neurons include those that participate in locomotion, drive, reward, organization of thought, and the perception of emotion. Areas rich in norepinephrine neurons include those that initiate movement, direct thought, and increase mental energy and level of alertness. Areas containing serotonergic (serotonin) neurons can regulate and influence the activity of those listed above. It seems that OCD might involve an imbalance in the relationship between norepinephrine and serotonin pathways. Glutamate neurons activate dopamine neurons if stimulated by norepinephrine neurons and not inhibited by GABA neurons.
>
> Now, if this stuff seems to be getting more complex as we continue to try figuring out the way the brain works, you are looking at but the tip of the ice-berg. There are literally hundreds of different chemical messengers both inside and outside the neuron. And this doesn't take into consideration enzyme systems and control of gene activity.
>
> So, what causes depression? How do antidepressants work?
>
> Cruz has pretty much captured the flavor.
>
> Neuroscience has positioned us closer to unlocking some doors. Psychiatry is beginning to find the information evolving from neuroscience useful in constructing associations between what drugs do chemically and what they do clinically.
>
> Example: Antipsychotics reduce dopamine activity in the frontal cortex by blocking the dopamine receptors (neurotransmitter = key; receptor = keyhole; ion-channel = door). The frontal cortex, high in dopamine neurons, is responsible for organizing thought. Disorganized thinking is a feature of schizophrenia. The frontal cortex of schizophrenics and siblings of schizophrenics have abnormally high numbers of dopamine type-1 receptors in the frontal cortex. This yields a hypothesis that certain features of schizophrenia are produced by excessive or erratic dopaminergic neuronal activity.
>
> Psychiatrists can also use their experience with people and drugs to witness trends in the associations between specific illnesses and their subtypes (symptom clusters), the drugs that work for them, and the biological activities of these drugs. Some drugs increase the number of neurotransmitter molecules available to stimulate neuron_2 by preventing them from being absorbed and recycled by neuron_1 after it has released them to send its message to neuron_2 - reuptake inhibition. Other drugs increase the stimulation of neuron_2 receptors by acting as a fake neurotransmitter. Still other drugs reduce the stimulation of neuron_2 by blocking or hiding these receptors from the real neurotransmitter. Some drugs allow for a build up of neurotransmitter levels in neuron_1 by preventing it from getting rid of the excess normally accomplished by a disassembly enzyme - MAO-inhibition. Anticonvulsant mood stabilizers block ion-channels and/or increase GABA activity, which usually results in reducing the excitability of norepinephrine and dopamine neurons and influencing the overall balance of activity. Lithium? Well, it does so many different things that are relevant to neuronal function, that it's hard to know where to start. It pretty much acts inside neuron_2 to produce changes on its outside.
>
> So, now we finally arrive at the point where we started. (You can now reread the first paragraph if you like).
>
> How's that?
>
> Please don't ask me to do it again. My brain hurts. Besides, I'm sure there are plenty of factual errors for others to correct. Please forgive me for not proof-reading. I'll let that be your job. :-)
>
> I had fun.
>
> :-)
>
> Silly.
>
> See ya'...
>
>
> - Scott
Posted by stjames on September 22, 2001, at 14:40:57
In reply to Monominergic theories could be horse hockey, posted by Cruz on September 21, 2001, at 19:53:00
> I am not saying they are for everybody. But they could be useless. I know with my form of depression. Levels of seretonin,dopamine and NE are not a factor. Its a dysfunction in my circadian rythmn. Monominergic theories have been around for 50 + years and they are no closer to being proven than ever. Keep well, look after yourselves.
James here.....
Monoamines have everything to do with one cause of depression. Given that every AD effects them, clearly Monoamines have something to do with mood. No question here. It is "horse hockey" to
say that is a lack (or too much) of a Monoamine that causes mood problems, by themselves. This is where the theory fails as it is not complex enough.james
Posted by SLS on September 22, 2001, at 15:38:46
In reply to Re: Monominergic theories could be horse hockey, posted by stjames on September 22, 2001, at 14:40:57
> > I am not saying they are for everybody. But they could be useless. I know with my form of depression. Levels of seretonin,dopamine and NE are not a factor. Its a dysfunction in my circadian rythmn. Monominergic theories have been around for 50 + years and they are no closer to being proven than ever. Keep well, look after yourselves.
>
> James here.....
>
> Monoamines have everything to do with one cause of depression. Given that every AD effects them, clearly Monoamines have something to do with mood. No question here. It is "horse hockey" to
> say that is a lack (or too much) of a Monoamine that causes mood problems, by themselves. This is where the theory fails as it is not complex enough.
>
> james
Hi James,I agree.
I know I've said this before, but for monoamine neurotransmitter-type stuff, I get the feeling that pushing the system in one direction or another might be forcing a "reset" of a synaptic equilibrium that, if one is lucky, results in a better reflection of the system's genetically intended functional design.
Examples:
fluoxetine - > 5-HT reuptake inhibition
tianeptine - > 5-HT reuptake accelerationfluoxetine - > increases 5-HT2 receptor stimulation
nefazodone - > decreases 5-HT2 receptor stimulationWhat do you think? Simplistic, I know, but perhaps worthy of provoking thought?
- Scott
Posted by jay on September 22, 2001, at 17:55:13
In reply to Re: Monominergic theories could be horse hockey, posted by stjames on September 22, 2001, at 14:40:57
In Andrew Solomon's new book "The Noonday Demon", he mentions that both the monoamine *and* receptor up/downregulation theories are questionable. You will have to look at the book for sources, but he mentions that within one day of starting anti-depressants, both the neurochemical *and* receptor changes occur...yet they say it still takes a month or two for your symtoms to lift.
He mentions that it likely has to be some major shifts in massive amounts of bodily hormones, as well as things like areas of brain activity, that eventually change after much repeated a.d. use.
As he lastly states, using simple theories like the monoamine theory is like the ancient theories that mental illness was caused by "vapours".
Jay
> > I am not saying they are for everybody. But they could be useless. I know with my form of depression. Levels of seretonin,dopamine and NE are not a factor. Its a dysfunction in my circadian rythmn. Monominergic theories have been around for 50 + years and they are no closer to being proven than ever. Keep well, look after yourselves.
>
> James here.....
>
> Monoamines have everything to do with one cause of depression. Given that every AD effects them, clearly Monoamines have something to do with mood. No question here. It is "horse hockey" to
> say that is a lack (or too much) of a Monoamine that causes mood problems, by themselves. This is where the theory fails as it is not complex enough.
>
> james
Posted by SLS on September 22, 2001, at 20:08:51
In reply to Re: Monominergic theories could be horse hockey » stjames, posted by jay on September 22, 2001, at 17:55:13
> You will have to look at the book for sources, but he mentions that within one day of starting anti-depressants, both the neurochemical *and* receptor changes occur...
He is wrong.It is well documented that the turnover rate of neurotransmitter receptors along the cell membrane is approximately two weeks - just about the time it takes for downregulation to occur in response to antidepressants - just about the time it takes for someone to respond to these antidepressants. Whether or not some types of receptors are changed in some way immediately, it is indisputable that changes in the binding characteristics of many monoamine receptors (NE beta-1, NE alpha-1, NE alpha-2, 5-HT1a, 5-HT2, etc.) and the behavior of many postsynaptic second-messenger events are latent and associated with the chronic, but not acute, administration of antidepressant drugs.
- Scott
Posted by Janelle on September 23, 2001, at 0:55:16
In reply to Re: Monominergic theories could be horse hockey » jay, posted by SLS on September 22, 2001, at 20:08:51
Wow, I sure appreciate the knowledge that is being shared here, although I must admit that much of it has gone over my head! Now, what are monoamines??? Just a basic, simple definition would be fine. Thanks.
-feeling somewhat lost, Janelle!
Posted by jay on September 23, 2001, at 8:12:56
In reply to Re: Monominergic theories could be horse hockey » jay, posted by SLS on September 22, 2001, at 20:08:51
> > You will have to look at the book for sources, but he mentions that within one day of starting anti-depressants, both the neurochemical *and* receptor changes occur...
>
>
> He is wrong.
>
> It is well documented that the turnover rate of neurotransmitter receptors along the cell membrane is approximately two weeks - just about the time it takes for downregulation to occur in response to antidepressants - just about the time it takes for someone to respond to these antidepressants. Whether or not some types of receptors are changed in some way immediately, it is indisputable that changes in the binding characteristics of many monoamine receptors (NE beta-1, NE alpha-1, NE alpha-2, 5-HT1a, 5-HT2, etc.) and the behavior of many postsynaptic second-messenger events are latent and associated with the chronic, but not acute, administration of antidepressant drugs.
>
>
> - Scott
Well, that is your view. Read Peter Whybrow's "A Mood Apart" for discussion on the immediate changes of receptor sensitivity after a.d. administration. You are talking about the *complete* process of regulation, but that is old news. Why do some a.d.'s work, that don't even touch NT levels? More questions than answers.Jay
Posted by Mitch on September 23, 2001, at 10:51:44
In reply to In PLAIN English, can someone please explain..., posted by Janelle on September 21, 2001, at 15:47:07
> ... the basic differences between re-uptake (blockage?) of SEROTONIN vs. NOREPHINEPHRINE vs. DOPAMINE? What I'm trying to ask (even this question is not easy to phrase!) is what beneficial effects is each of these re-uptakes supposed to have?
>
>
> Also, for what "conditions" (e.g., depression, anxiety, pyschosis) is each re-uptake *supposed* to be aimed at. Well, I guess I *know* that Serotonin is for depression, but I don't understand the other two as well.
>
> Thanks to whoever can help explain this in layperson's terms!
> -JanelleHi,
Really, there are two questions to ask: 1) *What* does a med do once it is in your body-where does it go, how is it broken down, how does it effect other systems, hormones, etc. in your body. 2) *Why* is it working to solve the problem it is being used for. Number #1 can take a while to find out-and you may never find everything out about it, but this information is the most objective. Number #2 is speculation by humans about what is happening based on the information that has been collected answering number#1. The "monoamine" theory is just that-a theory, a best guess, something you work with until some other idea offers a better working explanation. We know that antidepressants affect neurotransmitter levels and receptor densities (as a response to the increased levels) in your brain, and you take an antidepressant and it appears to be effective, *therefore* people are depressed because (i.e.)they have a shortage of these chemicals, and to support that theory you have some "evidence"-they have looked at brains of suicides and found a very high density of serotonin receptors-antidepressants tend to decrease the density of serotonin receptors. So, until a *better* explanation has been found we will stick with this one with all its flaws for the time being. Hope this is of some help, I am not a pharmacologist.
Mitch
Posted by stjames on September 23, 2001, at 13:19:17
In reply to Re: Monominergic theories could be horse hockey, posted by jay on September 23, 2001, at 8:12:56
Why do some a.d.'s work, that don't even touch NT levels?
James here....
Could you list these rogue AD's ? never heard of them.
Posted by Janelle on September 23, 2001, at 15:18:08
In reply to In PLAIN English, can someone please explain..., posted by Janelle on September 21, 2001, at 15:47:07
Posted by Mitch on September 23, 2001, at 16:32:19
In reply to Can SOMEONE just DEFINE what is a MONOAMINE?! (nm), posted by Janelle on September 23, 2001, at 15:18:08
Janelle,
Sorry, obviously you are looking for the trees not the forest. Here is a link from a good online medical dictionary:
http://www.graylab.ac.uk/cgi-bin/omd?monoamine+neurotransmitters
Posted by SLS on September 23, 2001, at 19:06:45
In reply to Re: Monominergic theories could be horse hockey, posted by jay on September 23, 2001, at 8:12:56
Hi Jay.
continued...Regarding the mechanisms of action of antidepressants:
> > > You will have to look at the book for sources, but he mentions that within one day of starting anti-depressants, both THE neurochemical *and* receptor changes occur...
> > He is wrong.
> >
> > It is well documented that the turnover rate of neurotransmitter receptors along the cell membrane is approximately two weeks - just about the time it takes for downregulation to occur in response to antidepressants - just about the time it takes for someone to respond to these antidepressants. Whether or not some types of receptors are changed in some way immediately, it is indisputable that changes in the binding characteristics of many monoamine receptors (NE beta-1, NE alpha-1, NE alpha-2, 5-HT1a, 5-HT2, etc.) and the behavior of many postsynaptic second-messenger events are latent and associated with the chronic, but not acute, administration of antidepressant drugs.> Well, that is your view. Read Peter Whybrow's "A Mood Apart" for discussion on the immediate changes of receptor sensitivity after a.d. administration. You are talking about the *complete* process of regulation, but that is old news.
It really has little to do with any view. Although it may be old news, it is quite well established news. I think it is still relevant and important when describing the biological events known to occur when the brain is exposed to many antidepressants.
This is why I reacted to you the way I did: I know this is going to sound picayune, but your use of the word "the" in your original post infers that the receptor changes responsible for the clinical effects of antidepressants occur immediately. I doubt this is true. I capitalized your use of the word "the" that I found so critical to the meaning of your sentence as I it quoted above. No hard feelings, I hope.
> More questions than answers.
Unfortunately.
I wish they'd find the answers before the day my brain becomes part of the NIH archives.
What precisely are the immediate changes that Peter Whybrow describes to occur with receptors? In what ways does he feel these changes participate in the way antidepressants produce their therapeutic effects? I would like to learn more about it. I probably won't buy his book right away, but I would be very interested to know what are the things in it that you find most salient. How does he go about treating difficult cases?
Thanks.
> Why do some a.d.'s work, that don't even touch NT levels?
Which ones in particular? I know trimipramine is a bit of a black sheep. I think iprindole might fit into that category, but I'd have to check on that. For that matter, Wellbutrin probably belongs in this category as well.
If I remember correctly - and it's been a long time - I think some experiments showed that there are actually some receptor changes that occur latently in laboratory animals (poor things) in response to a single dose of an antidepressant. In other words, you take one dose of imipramine, and two weeks later, changes in receptor function appear. Like I said, it's been a long time, but it is entirely conceivable that things like this can occur.
Sincerely,
Scott
Posted by Janelle on September 23, 2001, at 22:52:04
In reply to Re: Can SOMEONE just DEFINE what is a MONOAMINE?!, posted by Mitch on September 23, 2001, at 16:32:19
Thanks for the link to that online dictionary; the definition there basically answered my question. However, you also wrote "Sorry, obviously you are looking for the trees not the forest" -- I know what this expression means in general, but could you please explain what you mean by it in reference to my requests for explanations of serotonin/dopamine/neurephinephrine and then my question about what monoamines are ... what am I missing in terms of the *big picture* by asking these specific type questions??!?? Thanks!
Posted by SLS on September 24, 2001, at 0:10:40
In reply to MITCH: thanks and I've got a question 4 U: » Mitch, posted by Janelle on September 23, 2001, at 22:52:04
> Thanks for the link to that online dictionary; the definition there basically answered my question. However, you also wrote "Sorry, obviously you are looking for the trees not the forest" -- I know what this expression means in general, but could you please explain what you mean by it in reference to my requests for explanations of serotonin/dopamine/neurephinephrine and then my question about what monoamines are ... what am I missing in terms of the *big picture* by asking these specific type questions??!?? Thanks!
Hi Janelle.I think the point of the comment was that asking "what is a monoamine" is precisely the right question to ask if one is eventually to understand the big picture. It was a great question. My complements.
- Scott
Posted by Mitch on September 24, 2001, at 0:42:17
In reply to MITCH: thanks and I've got a question 4 U: » Mitch, posted by Janelle on September 23, 2001, at 22:52:04
> Thanks for the link to that online dictionary; the definition there basically answered my question. However, you also wrote "Sorry, obviously you are looking for the trees not the forest" -- I know what this expression means in general, but could you please explain what you mean by it in reference to my requests for explanations of serotonin/dopamine/neurephinephrine and then my question about what monoamines are ... what am I missing in terms of the *big picture* by asking these specific type questions??!?? Thanks!
Oh, I just clearly overlooked your need to have something very *specific* explained or rather defined. I also have ADHD and sometimes I don't quite "get it" at times! I tend to paint big pictures of stuff by nature instead of getting focused on details. In other words I tend to get way "outside" what is being required at any given moment. The forest and trees thing is just analogy-nothing else really meant by it. I guess the "forest" I was speaking of has to do with the whole "process" of scientific evaluation, data collection and measurement, and formations of hypothesis-more of a philosophy of science approach, so to speak. The "trees" could be the specific nuggets of information/data/knowledge used to form a hypothesis-more of a "working knowledge" if you will.
Posted by Janelle on September 24, 2001, at 0:50:11
In reply to Re: MITCH: thanks and I've got a question 4 U: » Janelle, posted by Mitch on September 24, 2001, at 0:42:17
I'm the opposite of you in that I am a very DETAIL-oriented person, who often overlooks the broader picture! Thanks for taking the time to return here and explain where you were coming from with the forest-trees analogy. I understand that very well now!
-Janelle
This is the end of the thread.
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Dr. Bob is Robert Hsiung, MD,
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