Talk:Dopamine/Archive 1

Dihydroxyphenylalanine
Dihydroxyphenylalanine is not a synonym for Dopamine, as the article quoted. I've removed it. Dihydroxyphenylalanine can be converted to Dopamine, in the brain, though. It is an amino acid:  Malbi

Could somebody clarify what dopamine does in plain speak. The excess of medical terms make the definition as accessible as only a dopamine and an abject lack of simile could. 67.161.74.241 08:51, 27 November 2006 (UTC)anithinks

ADD
ADD and its medication have a lot to do with this stuff. When Psychosis is mentioned, couldn't that also be included somehow? I bet it would be of interest to many people (including me). 134.106.199.58


 * Methylphenidate, the medication commonly prescribed for ADD under the name "Ritalin," is both a dopamine and norepinephrine reuptake inhibitor, isolating the neurotransmitters in the synaptic cleft, causing them to continuously stimulate receptor sites on the post-synaptic neuron. However, dopamine has a tendency to simply diffuse from the synaptic cleft and interact with exogenous dopamine receptor cites in order to help regulate blood pressure. For this reason, it is fairly rare that a patient will receive a dose of methylphenidate high enough to incur psychosis. You will notice that on the methylphenidate page, psychosis is linked to Ritalin only as far as abuse of the drug. If we were to list all neuropsychopharmacological medications which may cause psychosis through abuse and thus over-exposure to dopamine, we would need a lot more space! Additionally, I believe the most common, modern variants of ADD medications go the way of modern antipsychotic medications and block D2 dopamine receptor sites as well, the one commonly linked to psychotic episodes. --24.4.45.246 (talk) 05:53, 23 May 2008 (UTC)

Restless Leg Syndrome
It is currently believed that Restless Leg Syndrome is caused by a deficiency of dopamine. A medication called REPREVE (or Ropinirole) works by having a similar effect as dopamine. Making up for the deficiency, therfore relieving the discomfort of RSL

Lucinda Grindrod 06:29, 10 November 2006 (UTC)

More on addiction needed?
This report of a paper in Archives of Neurology leaves the article somewhat lacking. It didn't answer my questions on the different receptors. Are the genes for these receptors known? Where are they located? How common are variations on those genes? And what other interreactions are there, with hormones for example?--Bluegreen 10:56, 12 July 2005 (UTC)

Parasites
I think the recent addition that suggested that "certain parasites can affect dopamine levels in the brain" was refering to toxoplasmosis, and particularly a recent paper that suggested a mechanism by which it has a behavioural effect on the host. (details here). It's still very speculative at the moment though, so I think it's probably best left out for the time being - Vaughan 12:09, 4 September 2005 (UTC)


 * Oh clearly. The mechanism is likely to be anatomical, with the propensity for Toxoplasma gondii to home in to areas rich in dopaminergic neurons. JFW | T@lk  13:33, 4 September 2005 (UTC)

Phenethylamines?

 * Appears as if someone has edited the lower part of this page to show "fucks" instead of "Phenethylamines" where can I revert this change? (I assume it is the result of vandalism)


 * WP:RV JFW | T@lk  00:12, 14 October 2005 (UTC)


 * The introduction refers to dopamine as "this phenethylamine" (PEA), suggesting that "phenethylamines" are a class of related chemicals. However, the article on PEA seems to describe PEA as a specific chemical. I think this needs to be clarified. Attys (talk) 06:12, 7 December 2010 (UTC)
 * I added the word "substituted". Does that help? (Or make it worse?) --Tryptofish (talk) 19:12, 7 December 2010 (UTC)
 * There's an article on substituted phenethylamines, I've linked directly to that. Does it seem better? Although I have just noticed that sPEA is AfD... Keepstherainoff (talk) 09:20, 8 December 2010 (UTC)
 * Good catch on that link. I didn't realize we had that page. But it looks to me like the AfD is over with a decision to keep. --Tryptofish (talk) 19:27, 8 December 2010 (UTC)

Dopamine Gating hypothesis ?
i think the end of the pleasure and motivation section is weak- notably, here:

"the above theories [viewing dopamine as the mediator of 'desire/wanting,' 'predicting pleasurable activity,' 'noticeableness' or "decision making] are based on correlational, rather than causal, experimental evidence. Importantly, the available experimental evidence which examined causal, rather than corrleational, relationships between dopamine and motivation, does not seem to agree with any of above theories."

first, there's no mention of a "decision making" theory anywhere else in the article. second, the statement seems baseless- are there any citations to back up that the so-called causal studies didn't agree with ANY of these theories? and how come there's no mention of activity-dependent gating- ie., interactions between glutamatergic and dopaminergic neruons?

sorry- i added this some time ago, and never signed. maybe some day i'll get around to doing the research to confidently add to this article. Amutepiggy 23:04, 30 December 2005 (UTC)

Substrate
Go look at the page for substrate. For me, there is what appears to be a disambig page for dopamine at the bottom, that does not show up on the edit page or links to dopamine. Is this true for everyone, or am i jus going crazy? 66.41.59.162 03:19, 5 February 2006 (UTC)

Featured Article
This looks like an article that could easily become featured later on with some expansion on certain areas and adding information about the influence of say, drugs on levels of dopamine and how specific levels of dopamine create different types of variables. I'll work on it when I get the chance. Strongfaithin1 17:42, 7 June 2006 (UTC)strongfaithin1

After reading this much more closely, this article needs major overhauling. One section especially is filled with several problems and this entire page could use the help of an expert! Strongfaithin1 01:09, 8 June 2006 (UTC)strongfaithin1

I think it is an excellent article one of the best ive ever read. The section that might be merged should be left where it is also! DONT MOVE IT! —Preceding unsigned comment added by 86.158.130.170 (talk) 16:08, 21 September 2007 (UTC)

Additions to the article
As a chemical substance, this article needs:
 * Use in treatment, and dosage.--Connection 11:21, 16 June 2006 (UTC)


 * Preparation (Lab).--Connection 11:21, 16 June 2006 (UTC)


 * Industrial Preparation.--Connection 11:21, 16 June 2006 (UTC)


 * Trade, major producers.--Connection 11:21, 16 June 2006 (UTC)


 * Legal issues.--Connection 11:21, 16 June 2006 (UTC)

We need something on (natural / alternative health) methods of increasing dopamine levels. It seems startlingly absent from the article. Any added edits much appreciated. Spanglej (talk) 13:44, 8 April 2009 (UTC)

To mention a very different addition, I believe articles like these are incomplete when they do not provide an evolutionary history of the substance in question. I think it is extremely important that we understand the given chemical's role in (brain) evolution, and I strongly suggest that this aspect be added as a subsection, both in this and other articles about brain chemicals. Tue Sorensen (talk) 02:37, 13 April 2010 (UTC)

Copyedit refs
I've had a major go at improving the citations given:
 * Whilst there is no policy on whether to use fn/note or cite.php (the existing stye should becontinued), an article can not have both systems running simultaneously with two sets of link numbers !
 * Given that fn5 was out of sequence of the other fn/notes, I opted to use the cite.php as it automatically numbers the footnotes in sequence. I used as the ref name the previous fn numbers to make transparent my relocation of the citation markups.
 * I changed all the references over to an apprpriate citation template to give a consistant styling to the references.
 * Dates of accessing websites are done with the accessdate=2006-07-06 parameter not date=URL accessed 2006-07-06 as the date parameter applies to when a web page was originaly written (not when the ability to access the website was checked)
 * I've adjusted a request for the therapeutic section to be expanded from the 'article expand' to 'section expand' request tags.
 * WP articles should not self-refer to wikipedia. Hence in the 'Dopamine and psychosis' section, the reader should not be instructed to read another wikipedia article on a topic. Instead the standard approach is to add at the start of teh section a 'Main article' tag.David Ruben Talk 01:24, 13 July 2006 (UTC)

Schizophrenia
The information this articles supplies on dopamine in connection with schizophrenia is both narrow and dated. It seems odd that its first reference is to reduced dopamine in schizophrenics, as the received wisdom in the 1970s was that elevated dopamine played a part in the onset of schizophrenia. However, even this hypothesis is now somewhat dated; there is a body of literature that suggests that it may not be elevated dopamine levels per se, but hyper-activity of dopamine receptors that links to schizophrenia. Given the rather narrow coverage of this subject, I would be against this becoming a featured article. ACEO 18:49, 7 August 2006 (UTC)

schizophrenia is not related to dopamine, and the reason why is: when you are diagnosed with a mental disease, nobody does any brain tests on you beforehand, so how do they know what's happening in your brain anyway? and the only brain tests I see done of schizophrenics (having read quite a lot of papers) is when they are already medicated in comparison to healthy patients non medicated or recently medicated (just for tests). So the only thing that affects dopamine is the medication that is specifically targetted to shut down your nervous system and frontal lobe, therefore artificially inducing a frontal lobe disorder with associated flattened emotions and decreased intelligence and increased compliance. — Preceding unsigned comment added by Booklaunch (talk • contribs) 15:39, 11 May 2013 (UTC)
 * You are overstating the case. The association between schizophrenia and dopamine is not proven, but the lack of an association is also not proven, so your flat assertion that "schizophrenia is not related to dopamine" goes well beyond what the literature can support.  I think our article on the Dopamine hypothesis of schizophrenia summarizes the evidence pretty well. Looie496 (talk) 15:47, 11 May 2013 (UTC)

I agree with you article regarding evidence in cocaine/other drugs and psychotic symptoms. However those were the days when people diagnosed with schizophrenia had real psychotic symptoms. Nowadays that doesn't happen, all patients that show an "erratic" or socially inconvenient behaviour are labelled no matter whats happening in their brains. Nobody does any tests about dopamine. And how about children being given antipsychotics for ADD? Or suicidal? Where are the psychotic delusional symptoms in suicidal people? There aren't, they are just trying to end suffering, still they still get drugs to balance their "dopamine excess" when in fact, dopamine is responsible for feelings of pleasure, so you're basically supressing pleasure to people already feeling suicidal (???). The reality is, dopamine antagonist drugs are being prescribed because they pay pretty well and shut people down. (Booklaunch (talk) 09:11, 12 May 2013 (UTC))

Another example of the money driven schizphrenia theory is depot injections. Now everyone is on depot injections after being diagnosed. this is because some antipsychotic patents expired years ago, and generics dont pay big pharmaceuticals. So they came up with this long term effect idea, developed by Alkermes, with the excuse people would be forced to take medication for longer and saved money to psychiatric hospital. They got new patents and now every cat and dog takes the depot even though effects are pretty much horrifying. http://www.in-pharmatechnologist.com/Ingredients/New-Risperdal-fends-off-patent-impact (Booklaunch (talk) 09:49, 12 May 2013 (UTC))


 * Talk pages should be directed to improving articles and not discussing the article topics by themselves or conspiracy theories.--Garrondo (talk) 14:59, 12 May 2013 (UTC)

As someone with Schizophrenia I'd be deeply worried if Booklaunch was in any way qualified on mental health as they sound like a Crank. It's apparent they don't know what a Control group is for methodology, or that psychotic depression exists as does various Mood-Psychotic disorders like Schizoaffective. Also Dopamine is the neurotransmitter for the brain's reward system, it's a key mechanism for addiction and recurring behaviours such as Self-Harm, and drug & alcohol misuse, there is a degree of sense in prescribing such medication. I'd be really keen to here what alternatives they'd propose, provided it doesn't involve ten steps and invoke Jebuz. (Sorry to blaspheme) Also I know this is just from experience but the Depot is at a Higher dosage but is designed for a slower release; and the side-effects I've had (and talked with others) have been milder with the pills. Also not everyone is on the depot as it's voluntary; I started on pills, went onto the depot and then went back on pills after I found out the local clinic didn't have a trained nurse to deliver it. 188.29.115.214 (talk) 19:17, 17 February 2014 (UTC)

Role In Movement
"...in which a person loses the ability to execute smooth, controlled movements." This is an ambiguous and in a purest sense an incorrect statement when referring to Parkinson's Disease (PD). The hallmark physical symptom of PD we are going after here is a resting tremor. The aforementioned statement implies that PD involves an intention tremor... that would be Huntington's Disease/choreaform movements caused by an atretic striatum/distended lateral ventricles among other pathophysiologic observations. Oligodendrocyte 16:30, 9 August 2006 (UTC)
 * I agree with the phrasing as written in the article. In PD, rigidity and bradikinesia leads to loss of smoothness and control, even without any obvious tremor. Resting tremor may be mentioned as a separate sign, but this is not an article on PD. --Seejyb 19:19, 19 August 2006 (UTC)

Increased Blood pressure?
The article says:

"Dopamine can be supplied as a medication that acts on the sympathetic nervous system, producing effects such as increased heart rate and blood pressure"

However, in the Levodopa article, it says:

"Possible adverse drug reactions include: Hypotension, especially if the dosage is too high."

Levodopa is converted to dopamine in the brain, so more levodopa = more dopamine, however, why does levodopa decrease blood pressure while dopamine increases blood pressure?

Also, Fenoldopam, "a dopamine D1 receptor agonist", "lowers blood pressure through arteriolar vasodilation". It seems to me that dopamine decreases B.P rather than increasing it. Can anyone verify this with me? --Mark PEA 22:06, 17 August 2006 (UTC)


 * There is this apparent contradiction because


 * 1) Dopamine (DA) has a direct peripheral effect on the heart and blood vessels, when you give DA by an infusion. This is not always the same effect on blood pressure (BP), but depends on how much you are giving the person. DA in all doses tends to increase the heart's contraction rate and strength, i.e. the heart can pump more blood. The fact that at low doses you do not see an increase in BP, is because the blood vessels relax at the low doses. The relaxed blood vessels counteracts the rise in BP that the increased blood flow would be expected to cause. If you give more DA, it starts causing constriction of the arterioles, and then the BP increases. Note that when given this way (intravenously) DA does not effect the brain, because the DA molecule cannot get to the brain (cannot cross the blood-brain barrier).
 * 2) DA has a different indirect effect on the circulation when it acts on centers in the brain. If you give a substance that has little direct effect on the heart and blood vessels, but can cross the blood-brain barrier to have a DA-like effect on the brain itself, then that DA effect in brain causes the brain to let the blood vessels in the body relax, which you observe as a drop in BP.
 * So DA outside of the brain (DA infusion) would tend to increase blood flow and BP, by a direct effect on the heart and blood vessels, while DA inside the brain (Levodopa) would tend to drop the BP indirectly, by inducing the autonomic nervous system to relax the blood vessels. --Seejyb 21:31, 19 August 2006 (UTC)
 * Thanks, that cleared it up for me. --Mark PEA 15:54, 20 August 2006 (UTC)

Further to this point:

The introduction to the article says: "it inhibits norepinephrine release and acts as a vasodilator" This is technically impossible, were it true one would never have Norepinephrine release since Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase in the secretory granules of the medullary chromaffin cells. Dopamine would thus be inhibiting the substance produced from it. Secondly if there is high dopamine and low Noradrenalin that may simply indicate that vasodilation is caused by lowered vaso-constriction due to lack of NorEp. A source is needed for this material, or it needs to be corrected. --Leopardtail (talk) 23:14, 10 May 2014 (UTC)

Dopamine agonists in fibromyaliga
A March 2005 book (The Fibromyalgia Cure, I think, but look it up) by Dr. David Dryland, MD (www.drdryland.com) discusses dopamine agonists (Mirapex, Requip) as helpful for fibromyalgia. This article makes no mention of that, yet in fibromyalgia circles Mirapex is a big deal. (See Dr. Andrew Holman, Pacific Rheumatology Associates, Seattle, WA) I don't know enough about dopamine to write this up, but I was surprised that it wasn't mentioned. Also, Wellbutrin works on dopamine as well and this isn't mentioned either. Just seems like an omission (sp?) to me. --Aunt Amanda 06:00, 24 October 2006 (UTC)

Agreed. Mirapex is used to treat fibromyalgia, though it's not FDA approved for that yet. The Neupro (rotigotine) patch is also being studied currently. Some mention should be made. AliaGemma 04:09, 3 December 2007 (UTC)

Why Freedom of Thought in "Related Articles"
Freedom of Thought has got to be the most unrelated to this page (Dopamine) possible. I am removing it because if this is valid why not add a link to George Orwell's works or something. Then we can link the pages of the motor areas of the brain to sport's psychology and let this site become like YTMND. —The preceding Kintaro 20:26, 11 December 2006 (UTC)

Sneaky vandal?
I can't figure out if this edit is correct or sneaky vandalism. Could someone with experience check? Thanks, delldot | talk 20:57, 19 December 2006 (UTC)


 * It looks like a genuine attempt at a correction, however I believe it is actually incorrect. The research in the linked section seems to be from the early stages of the move from the reward theory to the salience theory.  I don't know enough about it to make the necessary changes, but I've added a discussion section about it. Elplatt 22:59, 20 January 2007 (UTC)

Reward vs. Salience
As is, the page seems confused on whether dopamine is related to the reward system (positive feedback) or salience (both positive and negative feedback). I'm not an expert on the subject, but as I understand it, the salience theory is an extension of the reward theory. If there is a debate on the subject, someone should summarize the debate, otherwise the language should be changed to reflect one theory or the other. Elplatt 22:47, 20 January 2007 (UTC)

Non-human dopamine
Which animals other than the human use dopamine as a neurotransmitter? What is the role of dopamine in these animals (if it is different from the human)? 193.171.121.30 10:28, 27 January 2007 (UTC)

Lack of dopamine in a specific area of the brain leads to Parkinson's disease. So in simple terms, the symptoms of Parkinson's are normally not present due to normal dopamine expression. —The preceding unsigned comment was added by 138.38.26.160 (talk) 15:33, 20 April 2007 (UTC).

In which animals does this occur? When in evolution did dopamine acquire this role? 193.171.121.30 10:48, 22 April 2007 (UTC)
 * I was interested in this same question. A quick google search showed that it is also present in reptiles, and in molluscs. I've rewritten the first sentence of the lead to reflect this. It would be nice if someone with more knowledge could do a little more clarification about, e.g., whether it occurs in *all* invertebrates. AFAICT, insects and molluscs have both dopamine and octopamine...? There's also a note in the article that it occurs in bananas! So maybe the relevant question is whether it's a neurotransmitter in all animals that have a central nervous system, or...?--76.81.180.3 16:25, 1 September 2007 (UTC)


 * You are correct in your assumption that mollusks have dopamine. At least partially. L-dopa appears in the bindings agent which mollusks produce in order to secure themselves to rock faces, docks, etc. As far as other animals, the only other discussion on dopamine I remember, featuring an animal, was on the subject of extracting dopamine (or perhaps it was, again, L-dopa) from a rare species of ray. --24.4.45.246 (talk) 05:52, 23 May 2008 (UTC)

Dopaminergic Neuron should be merged with this article
Absolutely, with out a doubt, Dopaminergic neuron should get merged with dopamine. In the distant future, when every little piece of knowledge is on wikipedia, perhaps it should get made it's own article, where there will be discussion of the significant biophysical and molecular differences between dopaminergic neurons and other neurons. But as it stands, this is adding nothing. Bilz0r 22:49, 22 August 2007 (UTC)


 * I agree. Feel free to do the merge... MisterSheik 23:14, 22 August 2007 (UTC)

excellent work!
to all of you guys who helped write this article! the section that might be moved is great and shouldnt be touched! im going to remove that banner because i havent seen any talk on it being moved here. —Preceding unsigned comment added by 86.158.130.170 (talk) 16:12, 21 September 2007 (UTC)

Copied from article
commentary / editorial stuff See below - Alis o n  ❤ 03:38, 17 October 2007 (UTC)

One piece of research showed that it is the want chemical, not the 'pleasure' chemical, which doesn't contradict the evidence of schizophrenics the way the normal interpretation does: dopamine-knockout rodents won't move 5 inches to get food ( they'll starve-to-death, instead -- but if it were pleasure that were missing, that wouldn't make any sense ), but if it's put in their mouth, they'll eat, and give the grimace of their-kind's smile.

I'm sorry I can't find the specific article this want-not-pleasure-bit is from, I'm looking, and will get the citation in, as soon as I can ( if someone finds it before me, update please! ).

Here's one supporting article http://www.sciencedaily.com/releases/1999/03/990304052313.htm but not the one with the knockout rodents.

dopamine disambiguation
The disambiguation page refers to dopamine receptor, dopamine transporter etc, yet there are other pages on dopamine neurotransmitters, neuromodulator, dopamine pathways. As a main article, this article needs to do justice for various aspects of dopamine research and point to other useful resources. Perhaps a rewrite consolidating the existing wiki pages and identifying where the gaps needs to be filled in is necessary Kpmiyapuram (talk) 16:34, 2 April 2008 (UTC)

edit 'Salience'
The section regarding the effects of dopamine on salience and paranoia reads like a second-rate dissertation. It's an interesting thesis, yes, but it cites nothing but two primary sources, both anecdotal accounts by schizophrenic people. I'm sure this has been written about to at least some extent in at least one peer-reviewed journal. If this section can be buffered up by an expert, great, but as it stands, it is someone's original research. —Preceding unsigned comment added by Dlainhart (talk • contribs) 09:29, 10 February 2009 (UTC)

I agree. The whole salience section has been dropped in from an essay and makes no sense with the rest of the article. Can someone pull out just the salient points and leave the rest.Spanglej (talk) 13:40, 8 April 2009 (UTC)


 * For documentation purposes, except for the first paragraph, the material in that section was added on 26-27 Sept 2008 by, who has not edited since 12 October 2008. So it's unlikely that he's around to help justify or explain the material, but in any case I've added a note to his talk page asking him to come here. Looie496 (talk) 17:04, 8 April 2009 (UTC)

This is DrTonyFlagg speaking. My contribution to the Salience article is not "original research" and does not really advance a thesis. The purpose of my contribution was simply to make clear some of the philosophical issues attendant to salience and its relation to suspicion, including paranoid ideation. I don't believe that presenting philosophical issues constitutes research, original or otherwise. I simply meant to provide a way to begin reasoning about rather tricky phenomena, showing a way to think critically about paranoid ideation and its relation to salience (or lack thereof). Anyone who disagrees with my findings does not really disagree with me, insofar as philosophy as I practice it is analytic and not synthetic. DrTonyFlagg —Preceding unsigned comment added by Drtonyflagg (talk • contribs) 06:14, 9 April 2009 (UTC)
 * DrTonyFlagg, thank you for your contribution to Wikipedia. There is much to be done here. However, I also agree that this section is distracting (and does not flow) with the rest of the article. Also, it appears poorly sourced, as it does not have many citations to reliable secondary sources to verify and establish the notability of your section. I am going to be bold and cut a lot, if not all, out. -Tunocca (talk) 01:02, 29 July 2009 (UTC)
 * DrTonyFlagg, I couldn't help myself but to remove the entire section, because it looked inappropriate. Please feel free to add back some material. Your philosophical approach regarding dopamine is interesting, but we need citations to secondary sources for those philosophical thoughts regarding dopamine. Thanks. -Tunocca (talk) 01:22, 29 July 2009 (UTC)
 * Just want to say that I agree with the removal at this point. Looie496 (talk) 15:30, 29 July 2009 (UTC)
 * I largely agree, in that after the first paragraph it was clearly not encyclopedic. However, I have restored the first paragraph, and also rewritten it to make it less colloquial, because the cited work by Schulze really is very important in the dopamine field, and has been extensively replicated by others. --Tryptofish (talk) 20:01, 29 July 2009 (UTC)

Dopamine Defficiency.
There's way too much information in this article, but no sub article on the effects of a difficiency of Dopanine on the body & mind. —Preceding unsigned comment added by 24.17.118.100 (talk) 07:57, 8 July 2009 (UTC)


 * You might want to look here. If, on the other hand, you're talking about one of those "chemical imbalance" things, feel free to add on a section and back it up with appropriate citations. dlainhart (talk) 15:58, 8 July 2009 (UTC)

Under "Behavior disorders" (Sec 1.12) which is under "Functions in the brain" it says: "Deficient dopamine neurotransmission is implicated in attention-deficit hyperactivity disorder, and stimulant medications that are used to treat its symptoms increase dopamine neurotransmission."

I think this is a mistake. Wouldn't increased dopimamine increase hyperactivity, not decrease it. This seams to be indicated in the source below.

"a hypofunctioning mesolimbic dopamine branch produces altered reinforcement of behavior and deficient extinction of previously reinforced behavior. this gives rise to delay aversion, development of hyperactivity in novel situations, impulsiveness, deficient sustained attention, increased behavioral variability, and failure to “inhibit” responses (“disinhibition”)." Source: [38] Cambridge Journals Online - Behavioral and Brain Sciences - Abstract - a dynamic developmental theory of attention-deficit/hyperactivity disorder (adhd) predominantly hyperactive/impulsive and combined subtypes: Jacob81 (talk) 15:57, 22 May 2013 (UTC)


 * It isn't a mistake, it's a paradox. Dopamine and dopaminergic drugs seem to have opposite effects in people with ADHD from their effects in most people.  That's very strange, but there is a lot of evidence to support it.  The quote you cite is consistent with that.  I'm not sure what message you are getting from it -- are you aware that "hypofunctioning" means "deficient"? Looie496 (talk) 16:39, 22 May 2013 (UTC)
 * I just jumped in and changed "Deficient" to "Altered". Although it's certainly true that stimulants of dopaminergic transmission paradoxically improve ADHD symptoms (think tonic versus phasic stimulation of dopamine receptors), ADHD obviously is not a deficiency of dopamine, per se, because that would be Parkinson's disease. --Tryptofish (talk) 18:27, 22 May 2013 (UTC)
 * I was not aware that "hypofunctioning" means "deficient", I took it to mean the opeset because of the "hypo" prefix, I must have been mistaken. Your reply to my comment clears things up about the effects of dopamine and hyperactivity. Thanks. Jacob81 (talk) 13:56, 3 August 2013 (UTC)
 * "Hypo" means low; "hyper" means high. Looie496 (talk) 21:47, 3 August 2013 (UTC)

Model Clarification
I can't find any definitive article explaining the difference in writing OH or HO. This seems to change depending on the source. I have dopamine with: (HO HO), (HO OH), and (OH OH). I have a feeling that all are correct, so is this just a matter of preference? There are even differing images here.





Halld84 (talk) 12:05, 8 January 2010 (UTC)


 * Both of those images are correct. As long as the bond to the OH connects to the oxygen atom, it doesn't matter which side the H is on.  -- Ed (Edgar181) 12:24, 8 January 2010 (UTC)
 * Yes, I agree that either is correct, and I think it's the lower one that is at the top of the page now. --Tryptofish (talk) 18:20, 8 January 2010 (UTC)
 * I know that the HO/OH (hydroxyl?) distinction doesn't matter, but aren't they on different carbon atoms on the ring compared to the chain, does that make any difference?Keepstherainoff (talk) 10:10, 16 July 2010 (UTC)
 * About different ring carbons, no. You can visualize it by mentally rotating the aromatic ring around the single bond connecting the ring to the closer carbon on the chain. --Tryptofish (talk) 18:12, 16 July 2010 (UTC)
 * Doh, I didn't spot that! But if the two hydroxyls weren't on adjacent carbon atoms, that would make a difference, yes? —Preceding unsigned comment added by Keepstherainoff (talk • contribs) 22:40, 17 July 2010 (UTC)
 * No, not necessarily. If free rotation around the bond lets them superimpose, then they're the same structure. They would have to be different carbons, not simply non-adjacent. See also any textbook on organic chemistry. --Tryptofish (talk) 22:47, 17 July 2010 (UTC)
 * Sorry, I was a little unclear there. I meant if rather than being on adjacent carbon atoms, the hydroxyls were on non-adjacent atoms, then that would no longer be dopamine would it? Looking at this on benzene derivatives, p-xylene and m-xylene seems to answer my question.Keepstherainoff (talk) 09:50, 18 July 2010 (UTC)
 * Ah, yes, see also benzenediol. --Tryptofish (talk) 18:37, 18 July 2010 (UTC)

Tonic and phasic dopamine
We need to implement a detailed comparison of tonic and phasic dopamine effects. —  C M B J  08:29, 18 June 2010 (UTC)
 * Having a section about that (not too technical for a general readership) would be a good idea. --Tryptofish (talk) 18:52, 18 June 2010 (UTC)
 * I'm just redrafting the dopamine neuron activity section of my thesis. I can try and write something about the pacemaker/bursting activity of dopamine neurons and the supradditive release of dopamine, is that what you had in mind for 'effects'? I think it might be to complex to get into the different downstream effects of tonic/phasic dopamine on target structures. Would it go in after the anatomy section? Keepstherainoff (talk) 10:16, 16 July 2010 (UTC)
 * That would be great, if you would do that. A big part of keeping it simple is to keep it brief. Yes, that would be a good location to put it. --Tryptofish (talk) 18:15, 16 July 2010 (UTC)
 * I'd just written the following-
 * === Tonic and phasic activity ===


 * The activity of dopamine-containing cells is characterized by irregular "pacemaking" activity of single spikes, and rapid bursts of typically 2-6 spikes in quick succession. These two patterns of activity modulate the level of extracellular dopamine by what is referred to as tonic and phasic dopamine release. Tonic dopamine transmission occurs when small amounts of dopamine are released by the neurons, and is regulated by the activity of other neurons, and neurotransmitter reuptake, maintaining a stable level of extracellular dopamine. Phasic dopamine transmission results in a greater increase of extracellular dopamine levels than would be expected in the same time period, in response to a burst of action potentials in the cell. The respective functional roles of phasic and tonic dopamine levels are still unclear.
 * Which was my current understanding of what tonic and phasic dopamine were, but I've just read Grace (1991) Phasic versus tonic dopamine release and the modulation of dopamine system responsivity: a hypothesis for the etiology of schizophrenia which describes tonic dopamine release as being spike independant, and the result of presynaptic glutamate release from the prefrontal cortex. It's new to me, but it should only take a little bit of tinkering to correct what I've written. I just don't have the time/brainpower to do it right now, and I'm loathe to put in some half truth. Keepstherainoff (talk) 22:38, 17 July 2010 (UTC)
 * Thanks for working on this! I copyedited your passage above, just as I would have done if it were already on the page. In part, I edited for content and clarity: please check if you are satisfied that I got the facts right. In part (and less obviously), I also edited it to comply with WP:MOS, and you may want to look closely to see things like capitalization and punctuation. Please feel free to overrule anything that I did, and to go ahead and put it on the page yourself. --Tryptofish (talk) 23:03, 17 July 2010 (UTC)

I've redrafted the section to include my new understanding of tonic DA transmission and added it to the article. I'd like the last sentance to be a little clearer, but I can't word it concisely. Basically, when I say "the functional roles aren't understood", some functions related to dopamine are known to rely (possibly exclusively) on either tonic or phasic dopamine release, but other functions are less well understood, and are just known to involve dopamine in some way. Also, there is an interaction between the two mechanisms of dopamine transmission that as far as I know isn't totally understood. Keepstherainoff (talk) 15:01, 18 July 2010 (UTC)
 * It looks good, thanks for your work on it! With respect to the last sentence, I think maybe a solution for the time being would be to simply omit the sentence entirely, at least temporarily. I'm also making a few other cleanups to it. --Tryptofish (talk) 18:42, 18 July 2010 (UTC)

Reinforcement
The second paragraph about drug addiction gives three sources. The fist has no link. The other 2 have nothing to do with drug addiction. They are about sexual dysfunction. The claim "dopamine pathway is pathologically altered in addicted persons" definitely needs documented so someone, like me for instance, could find out just what the mean by "pathologically altered". I found the article for the first source (20) but I'm not fixing it because it also has nothing to do with drug addiction. I'm not removing the paragraph only because this page was written by people a couple of pay grades above mine about the topic, but I do think it should be removed. Jackhammer111 (talk) 20:50, 24 February 2011 (UTC)
 * Yes, you are right. It looks to me like those three sources are perfectly good sources for citing dopamine's role in sexual excitation, but not for what that paragraph is saying. I have a hunch that they got attached to that place on the page during some long-ago revision. They can always be brought back from the edit history, but for now I've deleted them and replaced them with a cite needed tag. There's a ton of sourcing for what the paragraph does say, but (at my pay grade!) I don't have time to look for them now. Thanks! --Tryptofish (talk) 21:39, 24 February 2011 (UTC)

Effects of drugs that reduce dopamine activity

This is a VERY poor section. It is totally biased and does not list any of the positive effects (of which there are many) of neuroleptics/antipsychotics.

This section should either be heavily amended so that it is more balanced, or removed. — Preceding unsigned comment added by GeneSGoodsell (talk • contribs) 06:16, 26 January 2012 (UTC)

Flag for section: Functions in the brain
Can someone who knows take a look at a strange addition placed in this section please?

". a research showed that a couple really loving each other shows a good amount of dopamine in the brain there brain automatically responds to the person through an unreasonable love and affection to his/her mate.--Sandeep.bejjam (talk) 03:59, 5 May 2012 " — Preceding unsigned comment added by Rob.weitemeyer (talk • contribs)

never mind, that was a quick edit. thank you. — Preceding unsigned comment added by Rob.weitemeyer (talk • contribs) 15:39, 5 May 2012 (UTC)

Animal models
I developed this section to explain dopamine's role in foraging. All the separate functions of dopamine make an obvious whole when you understand that dopamine manages foraging - the act of scanning the environment for evidence of new resources, moving toward those resources, and remembering cues necessary to finding them again.--Lbreuning (talk) 18:00, 1 November 2012 (UTC)Lbreuning

More on foraging
The role of dopamine in foraging seems intuitively obvious, across every species. Why see it as lots of separate, unrelated effects when the unifying explanation is so clear?--Lbreuning (talk) 18:23, 1 November 2012 (UTC)
 * Hello, please let me try to explain several things here. First, before I get to the main issues at hand, please understand that one should never sign content in the article itself, the way one signs comments here on a talk page. On a talk page, every section is put in chronological order, so new comments come at the bottom rather than at the top, and it's important not to delete older comments on the talk page. I've fixed each of those things for you now, so that's why these discussion comments are here, at the bottom.


 * About the foraging material, it's important to understand Wikipedia's policies of WP:NOR and WP:UNDUE. I appreciate and thank you for being interested in this article, and I hope that you don't feel badly about my disagreeing with some of what you did, but I'm following these editing policies. If you look at the Animal studies section, the second paragraph, you will see that I have retained a short version of what you added, so foraging is addressed on the page. However, I have obviously shortened it a lot. That's because we really do not have secondary sources that say that understanding foraging is the key to understanding dopamine's behavioral actions, and the preponderance of source material emphasizes reward and so forth, but not specifically foraging. Although it may be "intuitively obvious" and "so clear" to you, WP:NOR does not allow us to make editorial decisions that way. Instead, we can only present what sources say, in proportion to due weight, and without editor interpretation. --Tryptofish (talk) 18:44, 1 November 2012 (UTC)

psychosis
needs updating with the latest research ie mirror neurons firing at +20% and related to level of psychosis, dispite patients being on dopamine blockers. could also mention that clozapine (I can't spell) any how the best anti psychotic doesn't actually effect the dopamine system that much, i think it's more serotonin. esp as you mention pcp and ketamine, not serotine so much, naughty naughty. also I've never had a mdma psychosis, I have had a proper psychosis (thought psychosis is an umbrealla term) and it sorted itself out when I took amphetamines, citation you can have a hair sample and my medical records if you have a PhD and can actually analyse the sample. also I've had psudohallucinations from dopamine supersensitivity and antipsychotic withdrawl and my psychosis was nothing like that either, though it was seeded by the antipsychotic withdrawl so that says something, even if it's just my emotions where backed up and I'd forgotten how to cope with them and become too impulsive on the antipsychotics. also I've taken lots of ketamine, it was nothing like that either. no I don't have schizophrenia it was seeded by antipsychotic withdrawl almost a year before. yes I did have a psychosis, for several months and was hospitalized yes I| did cure it with speed (I had serious memory issues, took speed, almost instantly sorted those issues, psychosis gone)  — Preceding unsigned comment added by 92.40.254.78 (talk) 06:48, 5 February 2013 (UTC)

actually I just read something on hallucinations in schizophrenia (inadvertanttly, I was looking for ego!) and it says that schizophrenics have animated hallucinations with no affect, though I suppose schizo-affectie disorder has to be taken into account. I'd say my dopamine supersensitivity pusohallucinations where animated, e.g. coke bugs, glass apparing to be full of sparking contents, glowing fluffy slipper feet, 'ghosts' etc.. they did however always have quite a strong affective element.

maybe psychosis should be split so that the distinction betwee hallucination and say paranoia of delusion, other types  of psychosis is a bit clearer. also could reference things like coke bugs and how schizophrenic halluciations are animated without affect/ ketaminn psudohallucinations are absolutly nothing like that. — Preceding unsigned comment added by 92.40.254.78 (talk) 08:11, 5 February 2013 (UTC)

laboratory synthesis and other issues with Chemistry section
The "Chemistry" section currently contains this: " In the laboratory, dopamine may be synthesized by demethylation of 3,4-dimethoxyphenethylamine using hydrogen bromide:  ".

I am unable to find anything that matches the first reference, and I can't make anything out of the second, since (a) it is in German, (b) I don't have access to the journal, and (c) the abstract gives no indication that the article explains how to synthesize dopamine.

I also couldn't find any other source to validate the statement. (I'm not a chemist, so that doesn't necessarily mean much.) Pending verification, I am going to remove that statement. When I also remove everything else that does not belong in this article, there is only one thing left, the statement that dopamine belongs to the catecholamine and phenethylamine classes.

More material that would be appropriate for the level of this article would be welcome. Looie496 (talk) 17:32, 18 May 2013 (UTC)
 * Are you saying merely that you cannot read the cited articles, or that they actually do not appear to exist? If it's only the former, I'm uncomfortable with the amount of deletion, because the chemistry seemed to me to be non-dubious. I'd like to see a little more explanation for all of the things, not all of which were about laboratory synthesis, that were removed. --Tryptofish (talk) 19:38, 18 May 2013 (UTC)
 * For the first ref listed there, I can't locate anything that matches the information given, or even parts of it. I don't even know what journal "Ann. Chem." is supposed to be.  The second ref is the one I can find but can't check.  Regarding the remainder of the section, if you see anything I took out that you think belongs there, please by all means put it back. Looie496 (talk) 20:24, 18 May 2013 (UTC)

Cell groups
In the course of reorganizing, I added a paragraph to the bottom of the Anatomy section about the names of the various dopamine cell groups. I hope I got it right, but the sources that I could find don't make very clear statements, so I might have botched it in some way. If anybody is in a position to check, I would be grateful. Looie496 (talk) 21:40, 20 May 2013 (UTC)
 * Given that you are making a series of revisions, I figure I'll stay out of your way until you are done, and then I'll jump in. --Tryptofish (talk) 21:37, 21 May 2013 (UTC)
 * That's fine, but I know this is more an area of expertise for you than for me, so I won't be annoyed at all if you jump in. I'm only working on this because it's consistently one of the most widely viewed neuroscience articles and ought to be better, not because I have especially deep knowledge of the topic.  Regards, Looie496 (talk) 22:38, 21 May 2013 (UTC)

Drug addiction section
It mentions that chronic drug use cause the dopamine sensativity to "down-regulate". I'm pretty sure this is incorrect. I believe that there is actually up-regulation, that is an increase in the ammount of dopaminergic receptors. This would cause a need for more and more DA to satisfy the addiction through those hungry receptors. Having a down-regulation would mean fewer DA receptors and therefore less DA to satisfy. It is true that they undergo desensitization, but the ammount of receptors will actually increase... unless I'm completely wrong on this. Thanks guys. Superbuttons (talk) 13:20, 2 July 2013 (UTC)
 * Yes, I'm afraid you're completely wrong. The basic error is the idea that each receptor has its own individual "need" for dopamine.  The need for dopamine arises at the cell level, not the receptor level.  When there are fewer receptors, or the receptors are less sensitive, each individual receptor needs to be more highly activated in order to meet the cell's needs, so a higher concentration of dopamine is required.  (I'm trying to get an intuition across here, not to give a precise explanation of the cellular process.) Looie496 (talk) 13:50, 2 July 2013 (UTC)
 * Although it's true that chronic dopamine receptor blockers, such as neuroleptics, cause an increase in the numbers of receptors, the cocaine-like and amphetamine-like stimulants tend to decrease the numbers of receptors. However, the result of that decrease in receptor number is actually that the addicted person will want more and more drug, because, with fewer receptors, it becomes "harder" (loosely speaking) to achieve the same level of receptor stimulation. --Tryptofish (talk) 18:38, 2 July 2013 (UTC)


 * Well thanks for clearing that up. Sorry about that.  Superbuttons (talk) 21:19, 2 July 2013 (UTC)
 * No problem! I think it was a good question. --Tryptofish (talk) 23:12, 2 July 2013 (UTC)

Important content worth adding
I noticed the article makes no mention of the phenylalanine->phenethylamine->N-methylphenethylamine(endogenous amphetamine isomer) pathway or TAAR1. It may be worth adding this content, since drugs like phenethylamine, its monomethylated derivatives (includes amphetamine), methamphetamine, and many other phenethylamines derive their dopamine reuptake inhibitory effects by acting as agonists at that receptor - in a nutshell, TAAR1 inactivates DAT.

The TAAR1 section TAAR1 has information/citations on this that may be worth using, depending on how it's incorporated. I'd strongly suggest adding a reference to this receptor, as TAAR1 agonists are arguably the most potent neuromodulators of the dopamine system.

As for the phenylalanine pathway, figure 2 shows the complete phenylalanine pathways. The article is a recent review, although it's unfortunately not free. That said, I'm hosting the article in pdf format at https://sites.google.com/site/seppilurvespancakes/home/wikicontent for 24 hours to allow an interested, active editor of this article to download and use to update the article content. Seppi333 (talk) 05:13, 17 September 2013 (UTC)


 * The complexity of the neurochemistry here is beyond my ability to comprehend, but if the pathway is really that important, I'm surprised that it hasn't received more attention. Looie496 (talk) 05:37, 17 September 2013 (UTC)


 * It's effects on cAMP and protein kinase probably aren't as relevant to this article as the effect it has on the dopamine transporter, so it's probably not necessary to go into any technical detail. That said, there have keen a plethora of papers written about trace amine receptors and trace amines since the discovery of that neurotransmitter system a decade ago.  Nearly every endogenous trace amine in the phenylalanine pathways is a TAAR1 agonist.
 * There's some more background information on that receptor and its significance if you care to read it.Seppi333 (talk) 16:34, 17 September 2013 (UTC)


 * Figured I'd offer links on the neuropharmacology as well. These two papers discuss the effects TAAR1 activation has on DAT, NET, SERT and monoamine efflux: (primary source) and  (secondary source that cites that primary source).  Both are free articles.  — Preceding unsigned comment added by Seppi333 (talk • contribs) 22:51, 17 September 2013 (UTC)
 * Rather late follow up, but I added this pathway (and more) in a recent edit. Seppi 333  (Insert 2¢ &#124; Maintained) 20:57, 1 February 2014 (UTC)

Content imbalance
Any leading endocrinology textbook discusses Dopamine as an endocrine hormone and its production in the adrenal medulla, the article makes no mention of this. It is also one of the hormone released during hypoglycaemia, again this is not mentioned.

Too much of the Neurospychiatry material references primary sources. — Preceding unsigned comment added by Leopardtail (talk • contribs) 01:07, 5 June 2014 (UTC)


 * If you could provide good recent secondary sources to back up the statements in the first paragraph, it would be very helpful. I have not been able to.


 * Also, I have moved the medref tag you added into the section it applies to. I can't see justification for disfiguring the entire article because of such a minor issue.  Regards, Looie496 (talk) 14:57, 5 June 2014 (UTC)

Narcotics/Opioids
Shouldn't they take a more prominent role in this article, especially the sections that deal with drugs? The opioids are the main class of dopamine agonist drugs that exist, yet things that that only are slightly related seem to get more coverage. -- Dougie WII (talk) 22:31, 5 August 2014 (UTC)
 * Opioids are opioid receptor agonists; they only indirectly affect dopamine neurotransmission. Seppi 333  (Insert 2¢ &#124; Maintained) 06:18, 6 August 2014 (UTC)