Talk:Dopamine

Template:Wikiproject MCB 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

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)

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

Additions

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)

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)

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)

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)

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.