![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 3 to 27 of 38. Go back in thread:
Posted by bulldog2 on February 22, 2010, at 1:20:57
In reply to Re: Dopamine not the magic answer folks, posted by linkadge on February 6, 2010, at 10:26:44
> I don't know where this whole idea of dopamine being the magic cure comes from. So many people come on this board and say "I've got a dopamine problem because I have yadi-yada symptoms".
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> Fist off, there are virtually no AD's that target dopamine. Wellbutrin (contrary to popular belief) has only very weak effects on the dopamine transporter.
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> Mirapex is also not a miracle antidepressant.
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> Animals studies also show that if you increase dopamine in the pleasure centres of the brain it activates BDNF in that area. BDNF in the neucleus accumbens produces behavioral depression.
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> Long term admistration of many drugs of abuse often increases feelings of craving and of depression.
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> You can block the behavioral depressant effects of accumbal dopamine by administering antipsychotics. This is why antipsychotics probably have a better record of being adjuncts for depression than do stimulants.
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> D3 receptor activation likely produces the depressant effects as mice lacking the d3 receptor do not respond this way to dopaminergic drugs.
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> Infact mice that have been administered dopamine precursors or dopaminergic drugs behave like they have been defeated in social models of depression. Serotonin on the other hand facilitates social dominance.
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> There is a difference between pleasure and an antidepressant effect. For instance, smoking weed. Sure you get a hit, then you just feel like a looser.
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> We need drugs that address dopamine. Maybe that is the missing link. We address the other two neurotransmitters so why not dopamine? I believe it is because of the fear of addiction because of its connection to pleasure.Read and enjoy
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>http://www.webmd.com/depression/news/20050728/dopamine-may-play-new-role-in-depression
http://www.acnp.org/g4/GN401000093/CH.html
http://www.utexas.edu/research/asrec/dopamine.html
http://www.news-medical.net/news/2008/01/16/34383.aspx
http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=1525
http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=1525
http://depression.about.com/cs/brainchem101/a/brainchemistry_2.htm
http://www.ncbi.nlm.nih.gov/pubmed/16051151
http://www.journals.elsevierhealth.com/periodicals/bps/article/PIIS0006322305012436/abstract
Posted by bleauberry on February 22, 2010, at 1:20:57
In reply to Re: Dopamine not the magic answer folks, posted by linkadge on February 6, 2010, at 10:26:44
Just to casually jump in the conversation, I share Link's views on this topic. Brain chemistry is so much more complicated. One neurotransmitter cannot be impacted without also causing downstream impacts on all the others, secondary messengers, enzymes, and genetic coding. Also, the region of the brain in which the drug targets will contribute to the outcome. Most meds are region specific, a region that may or may not be involved in that person's symptoms, a region that may worsen symptoms, or a region that will cause untoward side effects.
Anhedonia can be relieved with serotonin meds. NE meds. DA meds. Gaba meds. Antipsychotics. Stimulants. We often think anhedonia is a hypo-dopamine thing, but what about the person who has get-up-and-go on Xanax, or the person who becomes alive again on Prozac or Lexapro?
Trying to correct a "supposed" dopamine deficiency can result in psychosis, fear, agitation, and depression. Indeed, longterm dopamine stimulators usually end in depression.
Cocaine gets much of it's action from the serotonin system.
In reality, it is a complex interplay of all the neurotransmitters and their receptors, not any single one.
It's just aint that easy. More complicated than we will ever know in our lifetimes.
The only real way to find out what does what for a particular person, is to try it and see what happens.
Back to the start of this thread, if they are looking for a balanced antidepressant with potential to help even someone who failed ECT, it's already here. Describing the mechanism of that antidepressant or any other however is rather futile, except in terms of predicting common side effects.
Personal trial is all that matters. Someone can find the absolute best thing on paper for their symptoms, and it turns out to be a drug from hell. Ya just can't predict.
> I don't know where this whole idea of dopamine being the magic cure comes from. So many people come on this board and say "I've got a dopamine problem because I have yadi-yada symptoms".
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> Fist off, there are virtually no AD's that target dopamine. Wellbutrin (contrary to popular belief) has only very weak effects on the dopamine transporter.
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> Mirapex is also not a miracle antidepressant.
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> Animals studies also show that if you increase dopamine in the pleasure centres of the brain it activates BDNF in that area. BDNF in the neucleus accumbens produces behavioral depression.
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> Long term admistration of many drugs of abuse often increases feelings of craving and of depression.
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> You can block the behavioral depressant effects of accumbal dopamine by administering antipsychotics. This is why antipsychotics probably have a better record of being adjuncts for depression than do stimulants.
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> D3 receptor activation likely produces the depressant effects as mice lacking the d3 receptor do not respond this way to dopaminergic drugs.
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> Infact mice that have been administered dopamine precursors or dopaminergic drugs behave like they have been defeated in social models of depression. Serotonin on the other hand facilitates social dominance.
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> There is a difference between pleasure and an antidepressant effect. For instance, smoking weed. Sure you get a hit, then you just feel like a looser.
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Posted by floatingbridge on February 22, 2010, at 1:20:57
In reply to Re: Dopamine not the magic answer folks, posted by linkadge on February 6, 2010, at 10:26:44
Hi Link, this is a good discussion.
> I don't know where this whole idea of dopamine being the magic cure comes from. So many people come on this board and say "I've got a dopamine problem because I have yadi-yada symptoms".
I don't know enough to have come up with the term 'dopamine responder' on my own. I was told this by two separate doctors who came to their conclusions without my knowledge of dopamine.
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> Fist off, there are virtually no AD's that target dopamine. Wellbutrin (contrary to popular belief) has only very weak effects on the dopamine transporter.This is what I've been told; it has also been in accord with my treatment experience. I did not respond to wellbutrin.
> Mirapex is also not a miracle antidepressant.
>The doctors I spoke of said as much--that it was a long-shot adjunct. Therapeutic dosages often create intolerable side-effects.
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> You can block the behavioral depressant effects of accumbal dopamine by administering anti-psychotics. This is why anti-psychotics probably have a better record of being adjuncts for depression than do stimulants.Personally, I tanked on abilify--horribly so. Seroquel, too.
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> D3 receptor activation likely produces the depressant effects as mice lacking the d3 receptor do not respond this way to dopaminergic drugs.
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> Infact mice that have been administered dopamine precursors or dopaminergic drugs behave like they have been defeated in social models of depression. Serotonin on the other hand facilitates social dominance.Okay, the above is way over my head.
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> There is a difference between pleasure and an antidepressant effect. For instance, smoking weed. Sure you get a hit, then you just feel like a looser.
>Ummmm. I'm not sure I understand you here. I was told that some respond best to dopamine agonists--stimulants, maoi's. What do I know--these were a psych and a psych/pharamacologist. Everyone has their opinion and interpretation of data. Meanwhile, I respond to stimulants so far--kinda' scares the cr*p out of me, to be honest. I wouldn't have come up with this on my own, that's for sure. I'd love another course of treatment....
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Posted by linkadge on February 22, 2010, at 1:20:58
In reply to Re: Dopamine not the magic answer folks, posted by bulldog2 on February 6, 2010, at 11:46:20
>Amineptine targeted dopamine and was an >effective ad.
Amineptine had some effect on the dopamine transporter. So whats your point?
>Dopamine is needed to experience pleasure and >that is a piece of the whole depression pic.
Its all a bunch of theoretical B.S. at this point. Dopamine is not the magic pleasure chemical. Recent studies show that dopamine is more involved in motivation to seek reward but not actually in the process of experiencing reward. In the latter case, opiates appear to be more involved in experiencing reward.
>SSRIS often cause downregulation of dopamine and >a state of anhedonia.
If dopamine was the cure all, you could just take a dopamine precursor and bam everything would be fine. Its much more complicated than that. In parkinsons patients, ldopa can actually induce depressive states as well as mood swings and mental instability.
Many studies have been initiated to connect dopamine levels with depression. The results are equivocol. For instance, in this study, dopamine levels were higher in patients with depression and psychomotor retardation.
>Some people may truely lack enough dopamine.Yes, the word is may. Show me one scientific study that links low dopamine to depression.
>If some are lacking in serotonin and >norepinephrine than one cannot be low in >dopamine? Why is that?
I'm not saying you cannot be low in dopamine, but depression is MUCH more compex than that. There are hundreds of neurotransmitters, neuromodulators, neuropeptides etc that may be out of ballance in depression.
What is nonsensicle and non logical is when people come on this board and say oh, I have symptom x therefore I need more of chemical x. It just doesn't work that way.
Depression may not even be related to abnormal neurotransmiters, it may be a result of abnormal protein kinases, neuropeptides or epigenic factors that we are just beginning to understand.
The point is that we just don't know.
>We certainly need ads that preserve dopamine >function and do not lower it. That is why some >ads create so many sides including sexual >function.
Maybe we do maybe we don't. Seeing as we don't have a friggen clue what causes depression....
>Again you cannot compare stimulants that cause a >massive release of dopamine and there depletion >of dopamine with drugs that would maintain >healthy dopamine function.
Show me one study that proves dopamine is low in depression. How did people arive at the conclusion that dopamine is low in depression? Because of amineptine? Amineptine is no more proof that dopamine is low in depression that SSRIs are proof that serotonin is low in depression. SSRI's have many targets. Also, SSRI's do not consistently raise serotonin levels. They increase it initially but studies show that after about 2 weeks there is no increase in serotonin levels - so how can this be the mechaism?
Linkadge
Posted by linkadge on February 22, 2010, at 1:20:58
In reply to Dopamine May Be The Missing Link - Not Magic, posted by bulldog2 on February 6, 2010, at 12:16:08
A quote from THE VERY FIRST STUDY YOU POSTED:
"In laboratory tests with mice, researchers found prolonged exposure to dopamine through this pathway inactivated a regulatory protein in the brain known as Akt and caused the mice to behave like they were depressed in response to stress."
This is my point. I'm not even going to read the others cause I'm assuming you havn't either.
Linkadge
Posted by linkadge on February 22, 2010, at 1:20:58
In reply to where the idea comes from...one view » linkadge, posted by floatingbridge on February 6, 2010, at 16:49:18
>I don't know enough to have come up with the >term 'dopamine responder' on my own. I was told >this by two separate doctors who came to their >conclusions without my knowledge of dopamine.
WFT does that mean? Tell me one possible way that a doctor would come to the conclusion that a patient is a dopamine responder?
I've heard doctors say that a depression is "purely serotonergic". Again, WFT does that mean? Seeing as there are no clincal tests for neurotransmitter levels, and SSRI's don't consistently raise serotonin levels there is virtually no way to know that either.
I think basically doctors are still separating patients into two categores (for lack of better knowledge of depression). Those with sadness / high anxiety, and those with apathy, low interest / energy.
The former is said to be a product of serotonin dysfunction and the latter of norepinephrine or dopamine dysfunction. However, this is a gross oversimplification that doctors use to make them feel that they actually understand depression. This oversimplification has been around for the past 30 years.
Apathy in depression can respond to antipsychotics and anxiety / sadness can respond to stimulants. There are very little *useful* predictive tests as to what medication will work for what patient.
Linkadge
Posted by conundrum on February 22, 2010, at 1:20:58
In reply to where the idea comes from...one view » linkadge, posted by floatingbridge on February 6, 2010, at 16:49:18
My psychiatrist said that about 80 percent of patients respond to SSRIs and then a portion of those need NE boosted, and a smaller portion of those need dopamine. In his experience if someone needs dopamine he does a test with ritalin and says they should feel something.
Posted by floatingbridge on February 22, 2010, at 1:20:59
In reply to Re: where the idea comes from...one view » floatingbridge, posted by conundrum on February 6, 2010, at 17:35:12
> My psychiatrist said that about 80 percent of patients respond to SSRIs and then a portion of those need NE boosted, and a smaller portion of those need dopamine. In his experience if someone needs dopamine he does a test with ritalin and says they should feel something.
Well, guess that's what happened to me....
Posted by conundrum on February 22, 2010, at 1:20:59
In reply to where the idea comes from + a small link » conundrum, posted by floatingbridge on February 6, 2010, at 17:38:47
Yes if that link is about you, you needed all 3 boosted.
Posted by floatingbridge on February 22, 2010, at 1:20:59
In reply to Re: where the idea comes from...one view » floatingbridge, posted by linkadge on February 6, 2010, at 17:34:19
Really, Link, there's no need to shout :-)
I've agreed with you in advance on a main point--the complexity of pharmacology and depression treatment.
Other than that, I'm relating my experience as a patient patient.
Now, am I hearing you say that dopamine is being adequately addressed in current treatment regimes?
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Posted by floatingbridge on February 22, 2010, at 1:20:59
In reply to Re: where the idea comes from + a small link » floatingbridge, posted by conundrum on February 6, 2010, at 17:44:14
Well, it could be. Though unlike the woman studied, I was given a cns for my depression. And I guess I am having all three boosted. Nothing worked until a stim was on board.
pristiq
xanax
dexwe are considering a lithium adjunct
and fyi, I am on a lower dose of xanax now than before stim addition. go figure.
I've been asking for an maoi trial--one doc suggested the patch (Emsam--yeah, I know--don't all yell at once....)
(I really wouldn't mind some solid information about long term amp usage. My doc acts like it's not a big deal....)
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Posted by conundrum on February 22, 2010, at 1:21:00
In reply to Re: Dopamine not the magic answer folks, posted by bulldog2 on February 6, 2010, at 11:46:20
I thought ritalin was mostly a reuptake inhibitor not a substrate that releases DA. Just a shorter acting reuptake inhibitor.
Posted by conundrum on February 22, 2010, at 1:21:00
In reply to Re: where the idea comes from + a small link » conundrum, posted by floatingbridge on February 6, 2010, at 17:51:24
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448202/
Many people say that stimulants are mostly DA enhancing but if you look at that study you can see they increase NE a bit more than DA. I wonder what would happen if NE was antagonized? BTW many people attribute NE to the physical effects of stimulants, like increased heart rate, but I think that is too simplistic.
I'm glad that no matter what it is, these drugs are helping you.
Posted by conundrum on February 22, 2010, at 1:21:00
In reply to Re: where the idea comes from + a small link » floatingbridge, posted by conundrum on February 6, 2010, at 18:24:16
sorry I meant to say "amphetamines" not stimulants. Obviously they dont' all increase NE more. Ritalin doesn't and MDMA doesn't.
Posted by bulldog2 on February 22, 2010, at 1:21:00
In reply to Re: Did you actually read the studies you posted?? » bulldog2, posted by linkadge on February 6, 2010, at 17:22:20
> A quote from THE VERY FIRST STUDY YOU POSTED:
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> "In laboratory tests with mice, researchers found prolonged exposure to dopamine through this pathway inactivated a regulatory protein in the brain known as Akt and caused the mice to behave like they were depressed in response to stress."
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> This is my point. I'm not even going to read the others cause I'm assuming you havn't either.
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> LinkadgeOf course I read all the studies. It is not valid to cherry pick when the study actually backs up the dopamine theory.
The reality is I use what works for me and that is what is my study. We all have to figure out what works for us as individuals.
Many of us are dopamine responders and that is a fact for us even if you believe it is not true.
You always complain how horrible the current drugs are yet you deny that dopamine may be a player in depression.
You were also very rude to Floatingbridge. That is a reality for her and her doctor's conclusion. You owe her an apoligy for your response.
I'm not saying that dopamine is all that has to be tweeked. I know you despise ssirs. We are saying that drugs that lower dopamine or do not raise it may be missing a piece of the puzzle. Obviously since dopamine is a neurotransmitter in our brains it must have a function. If we tinker with se and ne why is dopamine off limits. ? Even sjw by some accounts raises dopamine.
Read And Enjoy from "The Good Drug Guide"
THE DOPAMINE CONNECTION
What's missing, crucially, is the therapeutic enrichment of hedonic tone via a combination of mu opioid pathway enhancement and prolonged stimulation of meso(cortico-)limbic dopamine function.This is really much more fun than it sounds. Yet the socially responsible use of reward pathway enhancements/remedial therapies is a technical, bioethical and medico-legal minefield. Complications aside, the currently available experimental evidence has persuaded many - but not all - investigators that the mesolimbic dopamine system serves as the final common pathway for pleasure in the brain. Enhanced responsiveness of post-synaptic dopamine D2/D3 receptors is vital to long-term emotional well-being. Insofar as they work, all "serotonergic" and "noradrenergic" mood-brighteners eventually act on the mesolimbic dopamine pathway, albeit in differing degrees and with varying delay. Even SSRIs depend on sensitization of the mesolimbic dopamine D2 receptors for their (modest) mood-lifting effect. New anti-Parkinsonian agents, notably the neuroprotective dopamine D3 receptor subtype selective pramipexole (Mirapex), ropinirole (Requip), and cabergoline (Dostinex) owe their potential role as fast-acting pro-sexual antidepressants to their dopaminergic action. Likewise, the possible mood-brightening effect of low doses of the dopamine receptor antagonist amisulpride (Solian), more commonly considered an antipsychotic agent, is explicable because amisulpride preferentially blocks the presynaptic dopamine D2/D3 autoreceptors; dopaminergic transmission is thereby enhanced.
The full story is inevitably complex. Dopamine agonists and reuptake inhibitors are often inadequate long-term mood-brighteners by themselves. The mesolimbic dopamine system mediates reward-signalling, incentive salience and a sense of urgency and significance, not the essence of pure bliss. Dopamine isn't itself the magic pleasure-chemical, though its functional role in conjunction with glutamate and mu opioid agonists in regulating medium spiny neurons of the rostromedial shell of the nucleus accumbens is critical. Researchers into affective disorders can prematurely become over-attached to one particular neurotransmitter system, its receptor sub-types and their signal-transduction cascades. Traditionally, serotonin and noradrenaline have attracted the fiercest rival partisans in antidepressant research. "Dopaminergic" (and opioid) agents, by contrast, are suspect. They are politically incorrect since they are potentially "abusable". Moreover it can be argued that the research and development of safe and sustainable Ecstasy-like empathogens and sociabilisers is at least as morally urgent as the license of safe and sustainable euphoriants. At any rate, enhanced mesolimbic dopamine release, exclusively or otherwise, enriches the intensity of experience; increases pleasure and libido, and potentially boosts cognitive performance. Even better, whereas some dopaminergics are potentially toxic, some dopamine-enhancing agents may have neuroprotective properties as well.
So what are the other contemporary options for chemical life-enhancement?
METHYLPHENIDATE (RITALIN); MINAPRINE (CANTOR); NOMIFENSINE (MERITAL)
A SSRI can be combined ("augmented" sounds more soothing to the official medical ear) with a dopaminergic such as methylphenidate. As Ritalin, methylphenidate is prolifically dispensed to American schoolchildren for different purposes altogether. It is sometimes abused as an instrument of social control. In spite of its structural relationship to amphetamine, methylphenidate resembles in many ways a more benign version of cocaine, yet with a much longer half-life. Methylphenidate blocks the reuptake of, but doesn't significantly release, the catecholamines noradrenaline and dopamine. If it is taken in sustained-release form or combined with an SSRI, all of which have anti-obsessive-compulsive properties too, then the likelihood of dose-escalation is minimised. In Europe and North America, students sometimes take Ritalin to gain a competitive edge in exams. However, its long-term effect on the developing brain is poorly understood.Chewing coca leaves with a dash of powdered lime is a nutritious and energising way to sustain healthy mood. Unfortunately, it's illicit and not very good for one's teeth.
A more cautious but still interesting option might be minaprine (Cantor). Minaprine blocks the reuptake of both dopamine and serotonin. It is also in some degree cholinomimetic. Thus it may exhibit both mood-brightening and nootropic properties. Much more research is needed. Unfortunately, minaprine is now obtainable only as a "research chemical".
Merital (nomifensine) showed great promise as a pleasantly stimulating dopaminergic that also potently inhibits the reuptake of noradrenaline and - to a much lesser extent - serotonin. It was marketed by its manufacturers Hoechst with the slogan "vive la difference!" Merital was withdrawn from licensed use after the discovery of its rare side-effect of precipitating a serious blood-disorder. For retarded melancholics, however, it was typically a very effective and well-tolerated mood-brightener with minimal side-effects. The risk/reward ratio of its carefully-monitored use may have been misjudged. Nomifensine is now obtainable only as a research chemical too.
And than there is amineptine that the US effectively had banned.
Dopamine is no diiferent than any of the other ads. For some depressed people raising serotonin may not be correct and the same may be true for norepinephrine.
It would seem to the most casual of observers that dopamine has to become part of the puzzle of creating a better ad. Why is ritalin part of your cocktail or at least was. It blocks reuptake of both ne and da.
I want more from my drug than being lifted out of depression and being a zombie than cannot feel pleaure because my med has depressed dopamine.
I don't understand how you can challenge people whose doctors with the patient symtoms present a picture of dopamine defeciency. Their clinical symtoms present that diagnosis. Your argument is studies that show how raising dopamine causes problems. Nobody is challening the fact that if dopamine is to high it can create problems.
The drug exctasy causes a massive release of serotonin. That causes people to feel touchy and feely and very sociable. Of course after the trip is over there can be massive depression. So you single out dopamine.
I can't really argue this with you anymore. Those of us who are dopamine responders understand the truth. For some of us this is our reality. Our minds are complex and we need a precise interactions of neurotransmitters. If one is titrated incorrectly the result will be bad.
Now if blocking dopamine for certain mental illness produces a good result does it not make sense that some may need a boost?
Posted by conundrum on February 22, 2010, at 1:21:00
In reply to Re: where the idea comes from + a small link » floatingbridge, posted by conundrum on February 6, 2010, at 18:24:16
This article shows that NE is needed for reward. Drugs and chocolate increase NE and if you block any the rats in the study don't know that they prefer it or dislike lithium.
http://www.pnas.org/content/104/12/5181.full
Posted by linkadge on February 22, 2010, at 1:21:01
In reply to Re: where the idea comes from...one view » floatingbridge, posted by conundrum on February 6, 2010, at 17:35:12
>My psychiatrist said that about 80 percent of >patients respond to SSRIs and then a portion of >those need NE boosted, and a smaller portion of >those need dopamine. In his experience if >someone needs dopamine he does a test with >ritalin and says they should feel something.
Thats not really a definitive test though as ritalin is not selective to dopamine. It has strong effect on NE too and its metabolite is primarily a NRI with 5-ht1a agonist activity. This could augment antidepressants in a manner like buspar.
Linkadge
Posted by linkadge on February 22, 2010, at 1:21:01
In reply to Re: where the idea comes from...one view » linkadge, posted by floatingbridge on February 6, 2010, at 17:44:44
I'm not shouting. If my ideas are too loud for you, skip my posts.
Linkadge
Posted by emmanuel98 on February 22, 2010, at 1:21:01
In reply to To make it more complicated., posted by conundrum on February 6, 2010, at 18:38:14
MAOIs raise norepinephrine, serotonin and dopamine. Also melatonin. And they seem to work better than selective inhibitors. At least for me.
Posted by floatingbridge on February 22, 2010, at 1:21:01
In reply to Re: where the idea comes from + a small link » floatingbridge, posted by conundrum on February 6, 2010, at 18:24:16
Thanks Conundrum--! Interesting. Muscled through it best I could. Good question, I think, regarding NET antagonist. Hmmm.
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Posted by linkadge on February 22, 2010, at 1:21:02
In reply to Re: Did you actually read the studies you posted?? » linkadge, posted by bulldog2 on February 6, 2010, at 18:34:38
>Of course I read all the studies. It is not >valid to cherry pick when the study actually >backs up the dopamine theory.
You obviously have no idea what that first study is suggesting. The *whole* idea behind the first study is that increasing dopamine levels in mice leads to depresive like behaviors. If you are unable to realize that I think you need to read it again. This is not cherry picking - it is the *entire* point of that first study.
>Many of us are dopamine responders and that is a >fact for us even if you believe it is not true.
What does a "dopamine responder" mean? You can call yourself whatever you want. Provide me with logical, conclusive evidence that your depression responds to dopamine. As I have said, response to a stimulant does not mean you are low on dopamine.
>You always complain how horrible the current >drugs are yet you deny that dopamine may be a >player in depression.
I am just going in circles here. I did not say that dopamine is absolutely not involved in depression, I just said we have no proof that dopamine is low in depression. Response to a stimulant is not proof that your dopamine levels are low. Sorry - try again.
>Read And Enjoy from "The Good Drug Guide"
>THE DOPAMINE CONNECTION
>What's missing, crucially, is the therapeutic >enrichment of hedonic tone via a combination of >mu opioid pathway enhancement and prolonged >stimulation of meso(cortico-)limbic dopamine >function.The cover page to the "Good drug guide" is *not a scientific journal*. It is an opinion piece - basing its ideas on theories about the involvement of dopamine in depression. This is not evidence. Sorry try again.
Linkadge
Posted by Metafunj on February 22, 2010, at 1:21:02
In reply to Re: where the idea comes from...one view, posted by linkadge on February 6, 2010, at 19:48:34
Also short acting atoms have a different effect from ones requiring down regulation.
Posted by floatingbridge on February 22, 2010, at 1:21:02
In reply to Re: where the idea comes from...one view » floatingbridge, posted by linkadge on February 6, 2010, at 19:50:41
> I'm not shouting. If my ideas are too loud for you, skip my posts.
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> LinkadgeHey Link, glad you clarified that for me. The capitalized WFT in your post are what threw me.
Ideas are fine w/ me-- I feel no need to skip your posts. As a babble participant, I'm aware that avoiding posts is always an option.
No harm, no foul?
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Posted by floatingbridge on February 22, 2010, at 1:21:02
In reply to To make it more complicated., posted by conundrum on February 6, 2010, at 18:38:14
Thanks--another informative link. Interesting, the release of NE in reaction to both positive and negative stimulation. How easy it is to mess somebody up, or one's self up, with that two way system. Coming from the view of stress-induced illness that is. Humans are a complex web.
Their must be some sort of electrical
term for the double work of NE
(But the poor mice...!)Thanks for complicating the thread!
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Posted by Mikez on February 22, 2010, at 1:21:03
In reply to Re: To make it more complicated. » conundrum, posted by floatingbridge on February 6, 2010, at 23:29:33
Linkadge , when you say if one responds to stimulants they are not necessarily a dopamine responder is that because stimulants work on other transmitters (ie Nora) as you said earlier? Just wanting to confirm because it helps me rule out certain drugs in my 'dopamine' trial. I want a drug that has minimal or no effect on nora compared to dopa. What do you think about L-dopa as a trial? The other one I can think of is low dose seligiline
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Dr. Bob is Robert Hsiung, MD,
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