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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: [1] 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 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
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)
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)
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)
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)
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)
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)
As a chemical substance, this article needs:
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)
I've had a major go at improving the citations given:
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)
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))
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)
"...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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
commentary / editorial stuff See below - Alison ❤ 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.
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)
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)
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)
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)
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)
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)
We need to implement a detailed comparison of tonic and phasic dopamine effects. — C M B J 08:29, 18 June 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)
References
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)
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)
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)
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
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)
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)
The "Chemistry" section currently contains this: "In the laboratory, dopamine may be synthesized by [[demethylation]] of [[3,4-dimethoxyphenethylamine]] using [[hydrogen bromide]]:<ref>J. S. Bayeler, Ann. Chem., 513, 196 (1934).</ref><ref>G. Hahn, K. Stiehl, Chem. Ber., 69, 2640 (1936).</ref>".
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)
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)
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)
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#Monoaminergic_systems 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,
PMID
19948186 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)
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)
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)
![]() | This page is an archive of past discussions. Do not edit the contents of this page. If you wish to start a new discussion or revive an old one, please do so on the current talk page. |
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: [1] 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 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
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)
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)
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)
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)
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)
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)
As a chemical substance, this article needs:
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)
I've had a major go at improving the citations given:
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)
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))
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)
"...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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
commentary / editorial stuff See below - Alison ❤ 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.
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)
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)
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)
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)
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)
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)
We need to implement a detailed comparison of tonic and phasic dopamine effects. — C M B J 08:29, 18 June 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)
References
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)
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)
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)
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
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)
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)
The "Chemistry" section currently contains this: "In the laboratory, dopamine may be synthesized by [[demethylation]] of [[3,4-dimethoxyphenethylamine]] using [[hydrogen bromide]]:<ref>J. S. Bayeler, Ann. Chem., 513, 196 (1934).</ref><ref>G. Hahn, K. Stiehl, Chem. Ber., 69, 2640 (1936).</ref>".
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)
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)
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)
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#Monoaminergic_systems 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,
PMID
19948186 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)
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)
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)