View source for Dopamine

{{Other uses}}
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|ImageSize=200px
|ImageFile2=Dopamine-3d-CPK.png
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|IUPACName=4-(2-aminoethyl)benzene-1,2-diol
|OtherNames=2-(3,4-dihydroxyphenyl)ethylamine;<br/> 3,4-dihydroxyphenethylamine;<br/> 3-hydroxytyramine; DA; Intropin; Revivan; Oxytyramine
|Section1= {{Chembox Identifiers
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| InChIKey = VYFYYTLLBUKUHU-UHFFFAOYAA
| CASNo=51-61-6
|   CASNo_Ref = {{cascite}}
|  CASOther=<br/>62-31-7 (hydrochloride) <!-- Also CAS verified -->
|  PubChem=681
|  ChemSpiderID = 661
|  SMILES = Oc1ccc(cc1O)CCN
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|Section2= {{Chembox Properties
|  Formula=C<sub>8</sub>H<sub>11</sub>NO<sub>2</sub>
|  MolarMass=153.18 g/mol
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|  MeltingPtC=128
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|  Solubility=60.0 g/100 ml
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|Section3= {{Chembox Hazards
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'''Dopamine''' is a [[catecholamine]] [[neurotransmitter]] present in a wide variety of animals, including both vertebrates and invertebrates. In the [[human brain|brain]], this [[phenethylamine]] functions as a [[neurotransmitter]], activating the five types of [[dopamine receptor]]s—[[Dopamine D1 receptor|D<sub>1</sub>]], [[Dopamine D2 receptor|D<sub>2</sub>]], [[Dopamine D3 receptor|D<sub>3</sub>]], [[Dopamine D4 receptor|D<sub>4</sub>]], and [[Dopamine D5 receptor|D<sub>5</sub>]]—and their variants. Dopamine is produced in several areas of the brain, including the [[substantia nigra]] and the [[ventral tegmental area]].<ref>http://www.encyclopedia.com/doc/1O87-ventraltegmentalarea.html Reference for VTA.</ref> Dopamine is also a [[neurohormone]] released by the [[hypothalamus]]. Its main function as a hormone is to inhibit the release of [[prolactin]] from the anterior lobe of the [[pituitary]].

Dopamine is available as an intravenous [[medication]] acting on the [[sympathetic nervous system|sympathetic]] [[nervous system]], producing effects such as increased [[heart rate]] and [[blood pressure]]. However, because dopamine cannot cross the [[blood-brain barrier]], dopamine given as a drug does not directly affect the [[central nervous system]]. To increase the amount of dopamine in the brains of patients with diseases such as [[Parkinson's disease]] and dopa-responsive [[dystonia]], [[L-DOPA]], which is the precursor of dopamine, can be given because it can cross the [[blood-brain barrier]].

== History ==
Dopamine was first synthesized in 1910 by George Barger and James Ewens at Wellcome Laboratories in London, England.<ref>[http://movementdisorders.org/education/onlinecme/levodopa/print.pdf Fahn, Stanley, "The History of Levodopa as it Pertains to Parkinson's disease," Movement Disorder Society’s 10th International Congress of Parkinson's Disease and Movement Disorders on November 1, 2006, in Kyoto, Japan.]</ref> It was named dopamine because it was a [[monoamine]], and its synthetic precursor was 3,4-''d''ihydr''o''xy''p''henyl''a''lanine ([[L-DOPA]]). Dopamine's function as a neurotransmitter was first recognized in 1958 by [[Arvid Carlsson]] and Nils-Åke Hillarp  at the Laboratory for Chemical Pharmacology of the National Heart Institute of [[Sweden]].<ref>Benes, F.M. Carlsson and the discovery of dopamine.'' Trends in Pharmacological Sciences'', Volume 22, Issue 1, 1 January 2001, Pages 46-47.</ref> Carlsson was awarded the 2000 [[Nobel Prize in Physiology or Medicine]] for showing that dopamine is not just a precursor of [[norepinephrine]] (noradrenaline) and [[epinephrine]] (adrenaline), but a neurotransmitter as well.

== Biochemistry ==
[[Image:Catecholamines biosynthesis.svg|thumb|right|Biosynthesis of dopamine]]
=== Name and family ===

Dopamine has the chemical formula C<sub>6</sub>H<sub>3</sub>(OH)<sub>2</sub>-CH<sub>2</sub>-CH<sub>2</sub>-NH<sub>2</sub>. Its chemical name is "4-(2-aminoethyl)benzene-1,2-diol" and its abbreviation is "DA."

As a member of the [[catecholamine]] family, dopamine is a precursor to [[norepinephrine]] (noradrenaline) and then [[epinephrine]] (adrenaline) in the biosynthetic pathways for these neurotransmitters.

=== Biosynthesis ===

Dopamine is biosynthesized in the body (mainly by nervous tissue and the [[adrenal medulla|medulla]] of the [[adrenal gland]]s) first by the hydroxylation of the amino acid [[L-tyrosine]] to L-DOPA via the enzyme tyrosine 3-monooxygenase, also known as [[tyrosine hydroxylase]], and then by the [[decarboxylation]] of [[L-DOPA]] by [[aromatic L-amino acid decarboxylase]] (which is often referred to as dopa decarboxylase). In some neurons, dopamine is further processed into [[norepinephrine]] by [[dopamine beta-hydroxylase]].

In [[neuron]]s, dopamine is packaged after synthesis into [[Vesicle (biology)|vesicles]], which are then released into the [[synapse]] in response to a presynaptic [[action potential]].
{{clear}}
[[Image:Dopamine degradation.svg|thumb|right|Biodegradation of dopamine]]
=== Inactivation and degradation ===
Two major degradation pathways for dopamine exist.  In most areas of the brain, including the [[striatum]] and [[basal ganglia]], dopamine is inactivated by [[reuptake]] via the [[dopamine transporter]] (DAT1), then enzymatic breakdown by [[monoamine oxidase]] ([[MAOA]] and [[MAOB]]) into [[3,4-dihydroxyphenylacetic acid]]. In the prefrontal cortex, however, there are very few dopamine transporter proteins, and dopamine is instead inactivated by reuptake via the [[norepinephrine transporter]] (NET), presumably on neighboring norepinephrine neurons, then enzymatic breakdown by [[catechol-O-methyl transferase|catechol-''O''-methyl transferase]] (COMT) into [[3-methoxytyramine]].<ref>[http://www.jneurosci.org/cgi/content/abstract/22/2/389]</ref>  The DAT1 pathway is roughly an order of magnitude faster than the NET pathway: in mice, dopamine concentrations decay with a half-life of 200 ms in the caudate nucleus (which uses the DAT1 pathway) versus 2,000 ms in the prefrontal cortex.<ref>[http://www.jneurosci.org/cgi/content/abstract/27/38/10196]</ref>  Dopamine that is not broken down by enzymes is repackaged into vesicles for reuse by [[VMAT2]].
{{clear}}

==Functions in the brain== <!-- Neurotransmitter systems has a link to here -->
Dopamine has many functions in the brain, including important roles in behavior and [[cognition]], [[animal locomotion|voluntary movement]], [[motivation]], [[punishment]] and [[reward system|reward]], inhibition of [[prolactin]] production (involved in [[lactation]] and [[prolactin#Effects|sexual gratification]]), [[sleep]], [[Mood (psychology)|mood]], [[attention]], [[working memory]], and [[learning]]. Dopaminergic neurons (i.e., neurons whose primary neurotransmitter is dopamine) are present chiefly in the [[ventral tegmental area]] (VTA) of the [[midbrain]], the [[substantia nigra|substantia nigra pars compacta]], and the [[arcuate nucleus]] of the hypothalamus.

It has been hypothesized that dopamine transmits reward prediction error, although this has been questioned.<ref name="dopamine function">{{cite journal | author=Peter Redgrave, Kevin Gurney|title=The short-latency dopamine signal: a role in discovering novel actions? |journal=Nature Reviews Neuroscience |volume=7 |pages=967–975 |year=2006 |doi=10.1038/nrn2022 | pmid=17115078 | issue=12}}</ref> According to this hypothesis, the phasic responses of dopamine neurons are observed when an unexpected reward is presented. These responses transfer to the onset of a [[Classical conditioning|conditioned stimulus]] after repeated pairings with the reward. Further, dopamine neurons are depressed when the expected reward is omitted. Thus, dopamine neurons seem to [[Neural encoding|encode]] the prediction error of rewarding outcomes. In nature, we learn to repeat behaviors that lead to maximizing rewards. Dopamine is therefore believed to provide a teaching signal to parts of the brain responsible for acquiring new behavior. [[Temporal difference learning]] provides a computational model describing how the prediction error of dopamine neurons is used as a teaching signal.

The reward system in insects uses [[octopamine]], which is the presumed arthropod homolog of [[norepinephrine]],<ref name="octopamine-honeybee">{{cite journal |author=Barron AB, Maleszka R, Vander Meer RK, Robinson GE |title=Octopamine modulates honey bee dance behavior |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=104 |issue=5 |pages=1703–7 |year=2007 |pmid=17237217 |doi=10.1073/pnas.0610506104 |pmc=1779631}}</ref> rather than dopamine. In insects, dopamine acts instead as a punishment signal and is necessary to form aversive memories.<ref name="pmid14627633">{{cite journal |author=Schwaerzel M, Monastirioti M, Scholz H, Friggi-Grelin F, Birman S, Heisenberg M |title=Dopamine and octopamine differentiate between aversive and appetitive olfactory memories in Drosophila |journal=J. Neurosci. |volume=23 |issue=33 |pages=10495–502 |year=2003 |month=November |pmid=14627633 |doi= |url=http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=14627633}}</ref><ref name="pmid19521527">{{cite journal |author=Selcho M, Pauls D, Han KA, Stocker RF, Thum AS |title=The role of dopamine in Drosophila larval classical olfactory conditioning |journal=PLoS ONE |volume=4 |issue=6 |pages=e5897 |year=2009 |pmid=19521527 |pmc=2690826 |doi=10.1371/journal.pone.0005897 |url=http://dx.plos.org/10.1371/journal.pone.0005897}}</ref>

=== Anatomy ===
{{Main|Dopaminergic pathways}}
[[Dopaminergic]] neurons form a [[neurotransmitter system]] which originates in [[substantia nigra pars compacta]], [[ventral tegmental area]] (VTA), and [[hypothalamus]]. These project [[axon]]s to large areas of the brain which are typically divided into four major pathways:

* [[Mesocortical pathway]] connects the ventral tegmental area to the frontal lobe of the [[pre-frontal cortex]]. Neurons with [[Soma (biology)|somas]] in the ventral tegmental area project axons into the pre-frontal cortex.
* [[Mesolimbic pathway]] carries dopamine from the ventral tegmental area to the [[nucleus accumbens]] via the [[amygdala]] and [[hippocampus]].  The somas of the projecting neurons are in the ventral tegmental area.
* [[Nigrostriatal pathway]] runs from the substantia nigra to the [[neostriatum]].  Somas in the substantia nigra project axons into the [[caudate nucleus]] and [[putamen]].  The pathway is involved in the basal ganglia motor loop.
* [[Tuberoinfundibular pathway]] runs from the hypothalamus to the pituitary gland.

This innervation explains many of the effects of activating this dopamine system. For instance, the [[mesolimbic pathway]] connects the VTA and [[nucleus accumbens]]; both are central to the brain [[reward system]].<ref>[http://www.pdn.cam.ac.uk/staff/schultz/ Schultz, Cambridge university, UK]</ref>

Whilst the distinction between pathways is widely used, and is regarded as a “convenient heuristic when considering the dopamine system”, it is not absolute, and there is some overlap in the projection targets of each group of neurons.<ref>{{Cite journal |author=Bjorklund A, Dunnett SB |title=Dopamine neuron systems in the brain: an update |journal=Trends in Neurosciences |year=2007 |volume=20 |issue=5 |pages=194–202 |pmid=17408759 |doi=10.1016/j.tins.2007.03.006 }}</ref>

===Tonic and phasic activity===

The level of extracellular dopamine is modulated by two mechanisms, tonic and phasic dopamine transmission. Tonic dopamine transmission occurs when small amounts of dopamine are released independently of neuronal activity, and is regulated by the activity of other neurons and neurotransmitter reuptake.<ref>{{Cite journal |author=Grace AA, |title=Phasic versus tonic dopamine release and the modulation of dopamine system responsivity: A hypothesis for the eitiology of schizophrenia |url=http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0F-485YGDY-4&_user=128590&_coverDate=12%2F31%2F1991&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1403836309&_rerunOrigin=scholar.google&_acct=C000010619&_version=1&_urlVersion=0&_userid=128590&md5=1c4978d564d1aaa5afc501a3454d469c |format=pdf |journal=Neuroscience |volume=41 |issue=1 |pages=1–24 |year=1991 |pmid=1676137 |doi=10.1016/0306-4522(91)90196-U }}</ref> Phasic dopamine release results from the activity of the dopamine-containing cells themselves. This activity is characterized by irregular [[Pacemaker action potential|pacemaking]] activity of single spikes, and rapid bursts of typically 2-6 spikes in quick succession.<ref>{{Cite journal |author=Grace AA, Bunney BS |title=The control of firing pattern in nigral dopamine neurons: single spike firing |url=http://www.jneurosci.org/cgi/reprint/4/11/2866 |format=pdf |journal=Journal of Neuroscience |volume=4 |issue=11 |pages=2866–2876 |year=1984 |pmid=6150070 }}</ref><ref>{{Cite journal |author=Grace AA, Bunney BS |title=The control of firing pattern in nigral dopamine neurons: burst firing |url=http://www.jneurosci.org/cgi/reprint/4/11/2877 |format=pdf |journal=Journal of Neuroscience |volume=4 |issue=11 |pages=28677–2890 |year=1984 |pmid=6150071 }}</ref> Concentrated bursts of activity result in a greater increase of extracellular dopamine levels than would be expected from the same number of spikes distributed over a longer period of time.<ref>{{Cite journal |author=Gonon FG |title=Nonlinear relationship between impulse flow and dopamine released by rat midbrain dopaminergic neurons as studied by in vivo electrochemistry |url=http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0F-485P3C0-5Y&_user=128590&_coverDate=01%2F31%2F1988&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1403496208&_rerunOrigin=scholar.google&_acct=C000010619&_version=1&_urlVersion=0&_userid=128590&md5=366f22be3c8d212a7bf26bf7630eeb93 |format=pdf |journal=Neuroscience |volume=24 |issue=1 |pages=19–28 |year=1988 |pmid=3368048  |doi=10.1016/0306-4522(88)90307-7 }}</ref>

=== Movement ===

Via the [[dopamine receptor]]s, D<sub>1-5</sub>, dopamine reduces the influence of the indirect pathway, and increases the actions of the direct pathway within the [[basal ganglia]]. Insufficient dopamine [[biosynthesis]] in the dopaminergic neurons can cause [[Parkinson's disease]], in which a person loses the ability to execute smooth, controlled movements.

=== Cognition and frontal cortex ===

In the [[frontal lobe]]s, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in [[neurocognitive]] functions, especially [[memory]], [[attention]], and [[problem-solving]]. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to [[attention deficit disorder]]. It has been found that D1 receptors<ref name="Inhibitorydopamine">{{cite journal |author=Heijtz RD, Kolb B, Forssberg H |title=Motor inhibitory role of dopamine D1 receptors: implications for ADHD |url=http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T0P-4NTB97R-Y-1&_cdi=4868&_user=308069&_orig=search&_coverDate=09%2F30%2F2007&_sk=999079998&view=c&wchp=dGLbVzz-zSkzV&md5=c49d721e7e713190c2ac6fab7a491093&ie=/sdarticle.pdf |format=PDF|journal=Physiol Behav |volume=92 |issue=1-2 |pages=155–160 |year=2007 |pmid=17585966 |doi=10.1016/j.physbeh.2007.05.024 }}</ref> as well as D4 receptors<ref>Browman KE, Curzon P, Pan JB, Molesky AL, Komater VA, Decker MW, Brioni JD, Moreland RB, Fox GB. A-412997, a selective dopamine D4 agonist, improves cognitive performance in rats. ''Pharmacology, Biochemistry and Behaviour''. 2005 Sep;82(1):148-55. PMID 16154186</ref> are responsible for the cognitive-enhancing effects of dopamine.

=== Regulating prolactin secretion ===

Dopamine is the primary [[neuroendocrine]] inhibitor of the secretion of [[prolactin]] from the [[anterior pituitary]] gland.<ref name="prolactininhibition">{{cite journal |author=Ben-Jonathan N, Hnasko R  |title=Dopamine as a Prolactin (PRL) Inhibitor|journal=Endocrine Reviews |volume=22 |issue=6 |pages=724–763 |year=2001| doi = 10.1210/er.22.6.724|url=http://edrv.endojournals.org/cgi/reprint/22/6/724.pdf|format=PDF |pmid=11739329}}</ref> Dopamine produced by neurons in the [[arcuate nucleus]] of the hypothalamus is secreted into the hypothalamo-hypophysial blood vessels of the [[median eminence]], which supply the [[pituitary gland]]. The lactotrope cells that produce [[prolactin]], in the absence of dopamine, secrete prolactin continuously; dopamine inhibits this secretion. Thus, in the context of regulating prolactin secretion, dopamine is occasionally called '''prolactin-inhibiting factor''' ('''PIF'''), '''prolactin-inhibiting hormone''' ('''PIH'''), or '''prolactostatin'''.

=== Motivation and pleasure ===
[[File:Dopamine Pathways.png|thumb|Dopamine Pathways. In the brain, dopamine plays an important role in the regulation of reward and movement. As part of the reward pathway, dopamine is manufactured in nerve cell bodies located within the ventral tegmental area (VTA) and is released in the nucleus accumbens and the prefrontal cortex. Its motor functions are linked to a separate pathway, with cell bodies in the substantia nigra that manufacture and release dopamine into the striatum.]]
{{See|Motivation}}
==== Reinforcement ====
Dopamine is commonly associated with the [[reward system]] of the brain, providing feelings of enjoyment and [[reinforcement]] to motivate a person proactively to perform certain activities. Dopamine is released (particularly in areas such as the [[nucleus accumbens]] and [[prefrontal cortex]]) by [[reward system|rewarding]] experiences such as [[food]], [[Human sexual behaviour|sex]], [[drugs]], and [[neutral stimulus|neutral stimuli]] that become [[Classical conditioning|associated]] with them. Recent studies indicate that [[aggression]] may also stimulate the release of dopamine in this way.<ref>[http://www.medicalnewstoday.com/articles/94023.php ''Dopamine Involved In Aggression - Medical News Today'']</ref>

This theory is often discussed in terms of drugs such as [[cocaine]], [[nicotine]], and [[amphetamine]]s, which directly or indirectly lead to an increase of dopamine in the [[mesolimbic pathway|mesolimbic reward pathway]] of the brain, and in relation to [[neurobiology|neurobiological]] theories of [[physical dependence|chemical addiction]] (not to be confused with [[Substance dependence|psychological dependence]]), arguing that this [[dopaminergic pathways|dopamine pathway]] is pathologically altered in addicted persons.<ref>Vanderbilt University (2008, January 15). Aggression As Rewarding As Sex, Food And Drugs, New Research Shows. ScienceDaily.</ref><ref name="PMID11805404">{{cite journal|last=Giuliano|first=F.|coauthors=Allard J.|year=2001|title=Dopamine and male sexual function|url=|journal=Eur Urol|volume=40|issue=6|pages=601–608|pmid=11805404|doi=10.1159/000049844}}</ref><ref name="PMID11477488">{{cite journal|last=Giuliano|first=F.|coauthors=Allard J. |year=2001|title=Dopamine and sexual function|url=http://www.nature.com/ijir/journal/v13/n3s/index.html|journal=Int J Impot Res|volume=13|issue=Suppl 3|pages=S18–S28|doi=10.1038/sj.ijir.3900719|pmid=11477488}}</ref>

==== Reuptake inhibition, expulsion ====

Cocaine and amphetamines inhibit the [[re-uptake]] of dopamine; however, they influence separate mechanisms of action. Cocaine is a [[dopamine transporter]] and [[norepinephrine transporter]] blocker that competitively inhibits dopamine uptake to increase the lifetime of dopamine and augments an overabundance of dopamine (an increase of up to 150 percent) within the parameters of the dopamine neurotransmitters. Like cocaine, amphetamines increase the concentration of dopamine in the [[synapse|synaptic]] gap, but by a different mechanism. Amphetamines and [[methamphetamine]] are similar in structure to dopamine, and so can enter the terminal bouton of the presynaptic neuron via its dopamine transporters as well as by diffusing through the neural membrane directly.{{Citation needed|date=April 2010}} By entering the presynaptic neuron, amphetamines force dopamine molecules out of their storage [[Synaptic vesicle|vesicles]] and expel them into the synaptic gap by making the dopamine transporters work in reverse.

==== Incentive salience ====
{{Main|Incentive salience}}
Dopamine's role in experiencing pleasure has been questioned by several researchers. It has been argued that dopamine is more associated with anticipatory desire and motivation (commonly referred to as "wanting") as opposed to actual consummatory pleasure (commonly referred to as "liking").

==== Dopamine, learning, and reward-seeking behavior ====
Dopaminergic neurons of the midbrain are the main source of dopamine in the brain.<!----><ref name="fn5">{{cite journal | author = Arias-Carrión O, Pöppel E | title = Dopamine, learning and reward-seeking behavior | journal = Act Neurobiol Exp | volume = 67 | issue = 4 | pages = 481–488 | year = 2007|url=http://www.ane.pl/pdfdownload.php?art=6738 }}</ref>  Dopamine has been shown to be involved in the control of movements, the signaling of error in prediction of reward, motivation, and cognition. Cerebral dopamine depletion is the hallmark of Parkinson's disease.<!----><ref name="fn5">{{cite journal | author = Arias-Carrión O, Freundlieb N, Oertel WH, Höglinger GU | title = Adult neurogenesis and Parkinson's disease | journal = CNS Neurol Disord Drug Targets. | volume = 6 | issue = 5 | pages = 326–335. | year = 2007 | pmid = 18045161 | doi = 10.2174/187152707783220875}}</ref> Other pathological states have also been associated with dopamine dysfunction, such as schizophrenia, autism, and attention deficit hyperactivity disorder, as well as drug abuse.

Dopamine is closely associated with reward-seeking behaviors, such as approach, consumption, and addiction.<!----><ref name="fn5">{{cite journal | author = Arias-Carrión O, Pöppel E | title = Dopamine, learning and reward-seeking behavior | journal = Act Neurobiol Exp | volume = 67 | issue = 4 | pages = 481–488 | year = 2007 | pmid = }}</ref> Recent researches suggest that the firing of dopaminergic neurons is a motivational substance as a consequence of reward-anticipation. This hypothesis is based on the evidence that, when a reward is greater than expected, the firing of certain dopaminergic neurons increases, which consequently increases desire or motivation towards the reward.<!----><ref name="fn5"/> However, recent research finds that while some dopaminergic neurons react in the way expected of reward neurons, others do not and seem to respond in regard to unpredictability.<ref name="Matsumoto">Matsumoto M, Hikosaka O. (2009). Two types of dopamine neuron distinctly convey positive and negative motivational signals. Nature. 459: 837-41. PMID 19448610 {{doi|10.1038/nature08028}}</ref> This research finds the reward neurons predominate in the ventromedial region in the [[substantia nigra pars compacta]] as well as the [[ventral tegmental area]]. Neurons in these areas project mainly to the [[ventral striatum]] and thus might transmit value-related information in regard to reward values.<ref name="Matsumoto"/> The nonreward neurons are predominate in the dorsolateral area of the substantia nigra pars compacta which projects to the [[dorsal striatum]] and may relate to orienting behaviour.<ref name="Matsumoto"/> It has been suggested that the difference between these two types of dopaminergic neurons arises from their input: reward-linked ones have input from the [[basal forebrain]] while the nonreward-related ones from the [[Habenula#Lateral_habenula|lateral habenula]].<ref name="Matsumoto"/>

==== Animal studies ====

Clues to dopamine's role in motivation, desire, and pleasure have come from studies performed on animals. In one such study, rats were depleted of dopamine by up to 99 percent in the [[nucleus accumbens]] and [[neostriatum]] using 6-hydroxydopamine.<!--
--><ref name="fn5">{{cite journal | author = Berridge K, Robinson T | title = What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? | journal = Brain Res Brain Res Rev | volume = 28 | issue = 3 | pages = 309–69 | year = 1998 | pmid = 9858756 | doi = 10.1016/S0165-0173(98)00019-8}}</ref>
With this large reduction in dopamine, the rats would no longer eat by their own volition. The researchers then force-fed the rats food and noted whether they had the proper facial expressions indicating whether they liked or disliked it. The researchers of this study concluded that the reduction in dopamine did not reduce the rat's consummatory pleasure, only the desire to actually eat. In another study, mutant hyperdopaminergic (increased dopamine) mice show higher "wanting" but not "liking" of sweet rewards.<!--
--><ref name="fn1">{{cite journal | author = Peciña S, Cagniard B, Berridge K, Aldridge J, Zhuang X | title = Hyperdopaminergic mutant mice have higher "wanting" but not "liking" for sweet rewards | journal = J Neurosci | volume = 23 | issue = 28 | pages = 9395–402 | year = 2003 | pmid = 14561867}}</ref>

==== The effects of drugs that reduce dopamine activity ====

In humans, drugs that reduce dopamine activity ([[neuroleptic]]s, e.g. [[antipsychotic]]s) have been shown to reduce motivation, cause [[anhedonia]] (inability to experience pleasure), and long-term use has been associated with the irreversible movement disorder, [[tardive dyskinesia]].<!--
--><ref name="fn2">{{cite journal | author = Lambert M, Schimmelmann B, Karow A, Naber D | title = Subjective well-being and initial dysphoric reaction under antipsychotic drugs - concepts, measurement and clinical relevance | journal = Pharmacopsychiatry | volume = 36 | issue = Suppl 3| pages = S181–90 | year = 2003 | pmid = 14677077 | doi = 10.1055/s-2003-45128}}</ref> Furthermore, antipsychotic drugs are associated with [[weight gain]], [[diabetes]], [[lactation]], [[gynecomastia]], [[drooling]], [[dysphoria]], [[fatigue]], [[sexual dysfunction]], and [[heart rhythm]] problems.
Selective D2/D3 agonists [[pramipexole]] and [[ropinirole]], used to treat [[restless legs syndrome]] (RLS), have limited anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale (SHAPS).<!--
--><ref name="fn3">{{cite journal | author = Lemke M, Brecht H, Koester J, Kraus P, Reichmann H | title = Anhedonia, depression, and motor functioning in Parkinson's disease during treatment with pramipexole | journal = J Neuropsychiatry Clin Neurosci | volume = 17 | issue = 2 | pages = 214–20 | year = 2005 | pmid = 15939976 | url=http://neuro.psychiatryonline.org/cgi/content/full/17/2/214 | doi = 10.1176/appi.neuropsych.17.2.214}}</ref>

==== Opioid and cannabinoid transmission ====

[[Opioid]] and [[cannabinoid]] transmission instead of dopamine may modulate consummatory pleasure and food palatability (liking).<!--
--><ref name="fn4">{{cite journal | author = Peciña S, Berridge K | title = Hedonic hot spot in nucleus accumbens shell: where do mu-opioids cause increased hedonic impact of sweetness? | journal = J Neurosci | volume = 25 | issue = 50 | pages = 11777–86 | year = 2005 | pmid = 16354936 | url=http://www.jneurosci.org/cgi/content/full/jneuro;25/50/11777 | doi = 10.1523/JNEUROSCI.2329-05.2005}}</ref>
This could explain why animals' "liking" of food is independent of brain dopamine concentration. Other consummatory pleasures, however, may be more associated with dopamine. One study found that both anticipatory and consummatory measures of sexual behavior (male rats) were disrupted by DA receptor antagonists.<!--
--><ref name="fn6">{{cite journal | author = Pfaus J, Phillips A | title = Role of dopamine in anticipatory and consummatory aspects of sexual behavior in the male rat | journal = Behav Neurosci | volume = 105 | issue = 5 | pages = 727–43 | year = 1991 | pmid = 1840012 | doi = 10.1037/0735-7044.105.5.727}}</ref>
Libido can be increased by drugs that affect dopamine, but not by drugs that affect opioid peptides or other neurotransmitters.

==== Sociability ====

Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor-binding is found in people with [[social anxiety]]. Traits common to negative [[schizophrenia]] ([[social withdrawal]], [[apathy]], [[anhedonia]]) are thought to be related to a hypodopaminergic state in certain areas of the brain. In instances of [[bipolar disorder]], [[manic]] subjects can become hypersocial, as well as [[hypersexual]].{{Citation needed|date=May 2010}} This is credited to an increase in dopamine, because mania can be reduced by dopamine-blocking anti-psychotics.<ref>http://bipolar.about.com/cs/menu_treat/a/0312_treatmania_3.htm</ref>

==== Processing of pain ====

Dopamine has been demonstrated to play a role in [[pain]] processing in multiple levels of the [[central nervous system]] including the [[spinal cord]],<ref>Jensen TS, Yaksh TL.Effects of an intrathecal dopamine agonist, apomorphine, on thermal and chemical evoked noxious responses in rats.Brain Res. 1984 Apr 2;296(2):285-93</ref> [[periaqueductal gray]] (PAG),<ref>Flores JA, El Banoua F, Galán-Rodríguez B, Fernandez-Espejo E.Opiate anti-nociception is attenuated following lesion of large dopamine neurons of the periaqueductal grey: critical role for D1 (not D2) dopamine receptors.Pain. 2004 Jul;110(1-2):205-14.</ref> [[thalamus]],<ref>Shyu BC, Kiritsy-Roy JA, Morrow TJ, Casey KL.Neurophysiological, pharmacological and behavioral evidence for medial thalamic mediation of cocaine-induced dopaminergic analgesia.Brain Res. 1992 Feb 14;572(1-2):216-23.</ref> [[basal ganglia]],<ref>Chudler EH, Dong WK.The role of the basal ganglia in nociception and pain.Pain. 1995 Jan;60(1):3-38</ref><ref>Altier N, Stewart J.The role of dopamine in the nucleus accumbens in analgesia.Life Sci. 1999;65(22):2269-87</ref> [[insular cortex]],<ref>Burkey AR, Carstens E, Jasmin L.Dopamine reuptake inhibition in the rostral agranular insular cortex produces antinociception.J Neurosci. 1999 May 15;19(10):4169-79.</ref><ref>Coffeen U, López-Avila A, Ortega-Legaspi JM, del Angel R, López-Muñoz FJ, Pellicer F.Dopamine receptors in the anterior insular cortex modulate long-term nociception in the rat.Eur J Pain. 2008 Jul;12(5):535-43.</ref> and [[cingulate cortex]].<ref>López-Avila A, Coffeen U, Ortega-Legaspi JM, del Angel R, Pellicer F.Dopamine and NMDA systems modulate long-term nociception in the rat anterior cingulate cortex.Pain. 2004 Sep;111(1-2):136-43.</ref><!--
-->  Accordingly, decreased levels of dopamine have been associated with painful symptoms that frequently occur in [[Parkinson's disease]].<ref>Brefel-Courbon C, Payoux P, Thalamas C, Ory F, Quelven I, Chollet F, Montastruc JL, Rascol O.Effect of levodopa on pain threshold in Parkinson's disease: a clinical and positron emission tomography study.Mov Disord. 2005 Dec;20(12):1557-63.</ref> Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including [[burning mouth syndrome]],<ref>Jääskeläinen SK, Rinne JO, Forssell H, Tenovuo O, Kaasinen V, Sonninen P, Bergman J.Role of the dopaminergic system in chronic pain -- a fluorodopa-PET study.Pain. 2001 Feb 15;90(3):257-60.</ref> [[fibromyalgia]],<ref>Wood PB, Patterson JC 2nd, Sunderland JJ, Tainter KH, Glabus MF, Lilien DL.Reduced presynaptic dopamine activity in fibromyalgia syndrome demonstrated with positron emission tomography: a pilot study.J Pain. 2007 Jan;8(1):51-8.</ref><ref>Wood PB, Schweinhardt P, Jaeger E, Dagher A, Hakyemez H, Rabiner EA, Bushnell MC, Chizh BA.Fibromyalgia patients show an abnormal dopamine response to pain.Eur J Neurosci. 2007 Jun;25(12):3576-82.</ref> and [[restless legs syndrome]].<ref>Cervenka S, Pålhagen SE, Comley RA, Panagiotidis G, Cselényi Z, Matthews JC, Lai RY, Halldin C, Farde L.Support for dopaminergic hypoactivity in restless legs syndrome: a PET study on D2-receptor binding.Brain. 2006 Aug;129(Pt 8):2017-28.</ref>  In general, the analgesic capacity of dopamine occurs as a result of dopamine D2 receptor activation; however, exceptions to this exist in the PAG, in which dopamine D1 receptor activation attenuates pain presumably ''via'' activation of neurons involved in descending inhibition.<ref>Wood PB.Role of central dopamine in pain and analgesia.Expert Rev Neurother. 2008 May;8(5):781-97.</ref>  In addition, D1 receptor activation in the insular cortex appears to attenuate subsequent pain-related behavior.

==== Salience ====

Dopamine may also have a role in the [[Salience (neuroscience)|salience]] of potentially important stimuli, such as sources of reward or of danger.<ref>{{cite journal | author = Schultz W | title = Getting formal with dopamine and reward | journal = Neuron | volume = 36 | issue = 2 | pages = 241–263 | year = 2002 | pmid = 12383780 | doi = 10.1016/S0896-6273(02)00967-4}}</ref> This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.

==== Behavior disorders ====

Deficient dopamine neurotransmission is implicated in [[attention-deficit hyperactivity disorder]], and stimulant medications used to successfully treat the disorder increase dopamine neurotransmission, leading to decreased symptoms.<ref>{{cite web |publisher=Cambridge Journals |title=A dynamic developmental theory of attention-deficit/hyperactivity disorder (ADHD) predominantly hyperactive/impulsive and combined subtypes | accessdate=2009-04-20 | url=http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=332927}}</ref> Consistent with this hypothesis, dopaminergic pathways have a role in inhibitory action control and the inhibition of the tendency to make unwanted actions.<ref>Colzato LS, van den Wildenberg WP, van Wouwe NC, Pannebakker MM, Hommel B. (2009). [http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2700244&blobtype=pdf Dopamine and inhibitory action control: evidence from spontaneous eye blink rates.] Exp Brain Res. 196(3):467-74. PMID 19484465 {{DOI|10.1007/s00221-009-1862-x}}</ref>

The long term use of [[levodopa]] in [[Parkinson's disease]] has been linked to [[dopamine dysregulation syndrome]].<ref name="pmid17988927">{{cite journal
|author=Merims D, Giladi N
|title=Dopamine dysregulation syndrome, addiction and behavioral changes in Parkinson's disease
|journal=Parkinsonism Relat. Disord.
|volume=14
|issue=4
|pages=273–80
|year=2008
|pmid=17988927
|doi=10.1016/j.parkreldis.2007.09.007
|url=
}}</ref>

=== Latent inhibition and creative drive ===

Dopamine in the [[mesolimbic pathway]] increases general [[arousal]] and goal directed behaviors and decreases [[latent inhibition]]; all three effects increase the creative drive of idea generation. This has led to a three-factor model of [[creativity]] involving the [[frontal lobe]]s, the [[temporal lobe]]s, and mesolimbic dopamine.<ref>{{cite journal | author= Flaherty, A.W, | year = 2005 | journal = Journal of Comparative Neurology | title = Frontotemporal and dopaminergic control of idea generation and creative drive | volume = 493 | issue = 1 | pages = 147–153 | pmid = 16254989 | doi = 10.1002/cne.20768 | pmc= 2571074}}</ref>

=== Chemoreceptor trigger zone ===
Dopamine is one of the neurotransmitters implicated in the control of [[nausea]] and [[vomit]]ing via interactions in the [[chemoreceptor trigger zone]].  [[Metoclopramide]] is a D2-receptor antagonist that functions as a [[prokinetic]]/[[antiemetic]].

=== Dopaminergic mind hypothesis ===

The dopaminergic mind hypothesis seeks to explain the differences between modern humans and their hominid relatives by focusing on changes in dopamine.<ref name=Previc>Previc F (2009). ''The Dopaminergic Mind in Human Evolution and History'' Cambridge University Press. ISBN 978-0-521-51699-0.</ref> It theorizes that increased levels of dopamine were part of a general physiological adaptation due to an increased consumption of meat around two million years ago in ''[[Homo habilis]]'', and later enhanced by changes in diet and other environmental and social factors beginning approximately 80,000 years ago. Under this theory, the "high-dopamine" personality is characterized by high intelligence, a sense of personal destiny, a religious/cosmic preoccupation, an obsession with achieving goals and conquests, an emotional detachment that in many cases leads to ruthlessness, and a risk-taking mentality. High levels of dopamine are proposed to underlie increased psychological disorders in industrialized societies. According to this hypothesis, a "dopaminergic society" is an extremely goal-oriented, fast-paced, and even manic society, "given that dopamine is known to increase activity levels, speed up our internal clocks and create a preference for novel over unchanging environments."<ref name=Previc/> In the same way that high-dopamine individuals lack empathy and exhibit a more masculine behavioral style, dopaminergic societies are "typified by more conquest, competition, and aggression than nurturance and communality."<ref name=Previc/> Although behavioral evidence and some indirect anatomical evidence (e.g., enlargement of the dopamine-rich striatum in humans)<ref>Rapoport, S. I. (1990). Integrated phylogeny of the primate brain, with special reference to humans and their diseases. ''Brain Research Reviews'', 15, 267-294.</ref> support a dopaminergic expansion in humans, there is still no direct evidence that dopamine levels are markedly higher in humans relative to other apes.<ref>Raghanti,  M. A., Stimpson,  C. D., Marcinkiewicz, J. L., Erwin, J. M., Hof, P. R., & Sherwood,  C. C. (2008a).  Cortical dopaminergic innervation among humans, chimpanzees, and macaque monkeys: A comparative study. ''Neuroscience'',  155, 203-20</ref> However, recent discoveries about the sea-side settlements of early man may provide evidence of dietary changes consistent with this hypothesis.<ref>http://www.scientificamerican.com/article.cfm?id=interactive-seas-saved-humanity</ref>

== Links to psychosis ==
{{Main|Dopamine hypothesis of schizophrenia}}

Abnormally high dopaminergic transmission has been linked to [[psychosis]] and [[schizophrenia]]<!--
-->.<ref>{{cite web |publisher=St. Jude Children's Research Hospital |title=Disruption of gene interaction linked to schizophrenia | accessdate=2006-07-06 | url=http://www.innovations-report.com/html/reports/life_sciences/report-52499.html}}</ref> Increased dopaminergic functional activity, specifically in the [[mesolimbic pathway]], is found in schizophrenic individuals. [[Anti-psychotic]] [[medication]]s act largely as dopamine antagonists, inhibiting dopamine at the [[dopamine receptor|receptor]] level, and thereby blocking the effects of the neurochemical in a dose-dependant manner. The older, so-called [[typical antipsychotics]] most commonly act on D2 receptors,<ref>http://www.williams.edu/imput/synapse/pages/IIIB5.htm</ref> while the [[Atypical antipsychotic|atypical drugs]] also act on D1, D3 and D4 receptors.<ref>http://bjp.rcpsych.org/cgi/content/full/181/4/271</ref><ref>http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T99-3YYTH6C-3P&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=7fda10d8dad0b9937580f6371eebb2d5</ref> The finding that drugs such as amphetamines, methamphetamine and cocaine, which can increase dopamine levels by more than tenfold,<ref>[http://74.125.153.132/search?q=cache:b3pkrTPLeT0J:www.stopmethinflorida.org/documents/Methamphetamine101.ppt+www.stopmethinflorida.org/documents/Methamphetamine101.ppt&cd=1&hl=en&ct=clnk&gl ''Methamphetamine 101'']</ref> can temporarily cause psychosis, provides further evidence for this link.<ref>{{cite journal | last = Lieberman | first = J.A. | coauthors = JM Kane, J. Alvir | title = Provocative tests with psychostimulant drugs in schizophrenia | journal = Psychopharmacology (Berl). | volume = 91 | issue = 4 | pages = 415–433 | publisher = | year = 1997 | doi = 10.1007/BF00216006| pmid = 2884687 | accessdate = 2007-10-16 }}</ref>

== Therapeutic use ==
{{Main|L-DOPA}}

[[L-DOPA|Levodopa]] is a dopamine precursor used in various forms to treat [[Parkinson's disease]] and dopa-responsive [[dystonia]]. It is typically co-administered with an inhibitor of peripheral decarboxylation (DDC, [[Aromatic-L-amino-acid decarboxylase|dopa decarboxylase]]), such as [[carbidopa]] or [[benserazide]]. Inhibitors of alternative metabolic route for dopamine by [[catechol-O-methyl transferase]] are also used. These include [[entacapone]] and [[tolcapone]].

==Nonneural functions==
===Immunoregulatory===

Dopamine acts upon receptors present on immune cells, with all subtypes of dopamine receptors found on [[leukocyte]]s. There is low expression of receptors on [[T lymphocyte]]s and [[monocyte]]s, moderate expression on [[neutrophil]]s and [[eosinophil]]s, and high expression on [[B cell]]s and [[natural killer cell]]s.<ref>McKenna F, McLaughlin PJ, Lewis BJ, Sibbring GC, Cummerson JA, Bowen-Jones D, Moots RJ. (2002). Dopamine receptor expression on human T- and B-lymphocytes, monocytes, neutrophils, eosinophils and NK cells: a flow cytometric study. J Neuroimmunol.  132(1-2):34-40. PMID 12417431</ref> The [[Sympathetic  nervous system|sympathetic innervation]] of [[lymphoid tissue]]s is dopaminergic, and increases during stress.<ref>Mignini F, Streccioni V, Amenta F. (2003). Autonomic innervation of immune organs and neuroimmune modulation. Auton Autacoid Pharmacol.  23(1):1-25.  PMID 14565534 </ref> Dopamine can also affect immune cells in the [[spleen]], [[bone marrow]], and [[blood circulation]].<ref>Basu S, Dasgupta PS. (2000). Dopamine, a neurotransmitter, influences the immune system. J Neuroimmunol.  102(2):113-24. PMID 10636479</ref> In addition, dopamine can be synthesized and released by the immune cells themselves.<ref>Bergquist J, Tarkowski A, Ekman R, Ewing A. (1994). [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC45550/pdf/pnas01477-0567.pdf Discovery of endogenous catecholamines in lymphocytes and evidence for catecholamine regulation of lymphocyte function via an autocrine loop]. Proc Natl Acad Sci U S A.   91(26):12912-6. PMID  7809145 </ref><ref>Cosentino M, Fietta AM, Ferrari M, Rasini E, Bombelli R, Carcano E, Saporiti F, Meloni F, Marino F, Lecchini S. (2007). [http://bloodjournal.hematologylibrary.org/cgi/reprint/109/2/632 Human CD4+CD25+ regulatory T cells selectively express tyrosine hydroxylase and contain endogenous catecholamines subserving an autocrine/paracrine inhibitory functional loop.] Blood.   109(2):632-42.  PMID 16985181</ref>

The effects of dopamine on immune cells depend upon their physiological state. While dopamine activates resting [[T cell]]s, it inhibits them when they are activated. Disorders such as [[schizophrenia]] and [[Parkinson's disease]], in which there are changes in brain dopamine receptors and dopamine signaling pathways, are also associated with altered immune functioning.<ref>Sarkar C, Basu B, Chakroborty D, Dasgupta PS, Basu S. (2010). The immunoregulatory role of dopamine: an update. Brain Behav Immun. 24(4):525-8. {{doi|10.1016/j.bbi.2009.10.015}} PMID 19896530 </ref>

=== Peripheral effects ===

Dopamine also has effects when administered through an [[Intravenous therapy|IV]] line outside the central nervous system. The brand name of this preparation is known as [[Intropin]]. The effects in this form are dose dependent.

* Dosages from 2 to 5 μg/kg/min are considered the "renal dose."<ref>{{cite web |publisher=Circulation. 2008;117:200-205 |title=Renal Vasodilatory Action of Dopamine in Patients With Heart Failure: Magnitude of Effect and Site of Action  | accessdate=2009-04-20 | url=http://www.circ.ahajournals.org/cgi/content/full/117/2/200}}</ref> At this low dosage, dopamine binds [[Dopamine receptor D1|D<sub>1</sub>]] receptors, dilating blood vessels, increasing blood flow to [[renal artery|renal]], [[mesenteric artery|mesenteric]], and [[coronary artery|coronary]] arteries; and increasing overall renal perfusion.<ref name=pharmnemonics>{{Cite book | author=Shen, Howard | title=Illustrated Pharmacology Memory Cards: PharMnemonics | year=2008 | publisher=Minireview | isbn=1-59541-101-1 | pages=8}}</ref> Dopamine therefore has a diuretic effect, potentially increasing urine output from 5 ml/kg/hr to 10 ml/kg/hr.{{Citation needed|date=August 2008}}

* Intermediate dosages from 5 to 10 μg/kg/min additionally have a positive [[inotropic]] and [[chronotropic]] effect through increased [[Beta-1 adrenergic receptor|β<sub>1</sub> receptor]] activation. It is used in patients with [[shock (circulatory)|shock]] or [[heart failure]] to increase [[cardiac output]] and [[blood pressure]].<ref name=pharmnemonics /> Dopamine begins to affect the heart at the lower doses, from about 3 μg/kg/min IV.<ref>{{cite web |publisher=Drugs.com |title=Dopamine and Dextrose  | accessdate=2009-04-20 | url=http://www.drugs.com/pro/dopamine-and-dextrose.html}}</ref>

* High doses from 10 to 20 μg/kg/min is the "pressor" dose.{{Citation needed|date=August 2008}} This dose causes vasoconstriction, increases [[systemic vascular resistance]], and increases blood pressure through [[alpha 1 receptor|α<sub>1</sub> receptor]] activation;<ref name=pharmnemonics /> but can cause the vessels in the kidneys to constrict to the point where they will become non-functional.{{Citation needed|date=August 2008}}

=== Renal effects ===
Dopamine induces [[natriuresis]] (sodium loss) in the [[kidney]]s.<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847451/?tool=pmcentrez&report=abstract]</ref><ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576148/?tool=pmcentrez&report=abstract]</ref>

== Dopamine and fruit browning ==

[[Polyphenol oxidase]]s (PPOs) are a family of enzymes responsible for the [[Browning (chemical process)|browning]] of fresh fruits and vegetables when they are cut or bruised. These enzymes use molecular [[oxygen]] (O<sub>2</sub>) to [[redox|oxidise]] various [[diphenol|1,2-diphenols]] to their corresponding [[quinone]]s. The natural substrate for PPOs in [[banana]]s is dopamine. The product of their oxidation, dopamine quinone, spontaneously oxidises to other quinones. The quinones then [[polymerisation|polymerise]] and [[condense]] with [[amino acid]]s and [[protein]]s to form brown [[biological pigment|pigments]] known as [[melanin]]s. The quinones and melanins derived from dopamine may help protect damaged fruit and vegetables against growth of [[bacteria]] and [[fungi]].<ref name="mayer">{{cite journal | author = Mayer, AM | title = Polyphenol oxidases in plants and fungi: Going places? A review | journal = [[Phytochemistry (journal)|Phytochemistry]] | year=2006 | volume=67 | pages=2318–2331 | pmid = 16973188 | doi = 10.1016/j.phytochem.2006.08.006 | issue = 21}}</ref>

== See also ==

<div style="-moz-column-count:3; column-count: 3;">
* [[Substance use disorder|Addiction]]
* [[Amphetamine]]
* [[Antipsychotic]]
* [[Catecholamine]]
* [[Catechol-O-methyl transferase]]
* [[Classical conditioning]]
* [[Operant conditioning]]
* [[Cocaine]]
* [[Depression (mood)|Depression]]
* [[Dopamine hypothesis of schizophrenia]]
* [[Dopamine reuptake inhibitor]]s
* [[Dopaminergic]]
* [[Methylphenidate]]
* [[Neurotransmitter]]
* [[Parkinson's disease]]
* [[Prolactinoma]]
* [[Schizophrenia]]
* [[Selegiline]]
* [[Serotonin]]</div>

== References ==

{{Reflist|2}}

== External links ==
{{Wiktionary|Dopamine}}
* {{DrugBank|APRD00085}}
* [http://druginfo.nlm.nih.gov/drugportal/dpdirect.jsp?name=Dopamine U.S. National Library of Medicine: Drug Information Portal - Dopamine]

{{Dopaminergics}}
{{Phenethylamines}}
{{Cardiac stimulants excluding cardiac glycosides}}
{{Neurotransmitters}}

[[Category:Catecholamines]]
[[Category:Hormones of the hypothalamus]]
[[Category:Inotropic agents]]
[[Category:Motivation]]
[[Category:Neurotransmitters]]
[[Category:Biology of bipolar disorder]]
[[Category:World Health Organization essential medicines]]

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