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Dopamine

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Dopamine is a <a title="Catecholamine" href="/wiki/Catecholamine">catecholamine</a> <a title="Neurotransmitter" href="/wiki/Neurotransmitter">neurotransmitter</a> present in a wide variety of animals, including both vertebrates and invertebrates. In the <a title="Human brain" href="/wiki/Human_brain">brain</a>, this <a title="Phenethylamine" href="/wiki/Phenethylamine">phenethylamine</a> functions as a <a title="Neurotransmitter" href="/wiki/Neurotransmitter">neurotransmitter</a>, activating the five types of <a title="Dopamine receptor" href="/wiki/Dopamine_receptor">dopamine receptors</a>—<a class="mw-redirect" title="Dopamine D1 receptor" href="/wiki/Dopamine_D1_receptor">D1</a>, <a class="mw-redirect" title="Dopamine D2 receptor" href="/wiki/Dopamine_D2_receptor">D2</a>, <a class="mw-redirect" title="Dopamine D3 receptor" href="/wiki/Dopamine_D3_receptor">D3</a>, <a class="mw-redirect" title="Dopamine D4 receptor" href="/wiki/Dopamine_D4_receptor">D4</a>, and <a class="mw-redirect" title="Dopamine D5 receptor" href="/wiki/Dopamine_D5_receptor">D5</a>—and their variants. Dopamine is produced in several areas of the brain, including the <a title="Substantia nigra" href="/wiki/Substantia_nigra">substantia nigra</a> and the <a title="Ventral tegmental area" href="/wiki/Ventral_tegmental_area">ventral tegmental area</a>.<a href="#cite_note-0">[1]</a> Dopamine is also a <a title="Neurohormone" href="/wiki/Neurohormone">neurohormone</a> released by the <a title="Hypothalamus" href="/wiki/Hypothalamus">hypothalamus</a>. Its main function as a hormone is to inhibit the release of <a title="Prolactin" href="/wiki/Prolactin">prolactin</a> from the anterior lobe of the <a class="mw-redirect" title="Pituitary" href="/wiki/Pituitary">pituitary</a>.

Dopamine is available as an intravenous <a class="mw-redirect" title="Medication" href="/wiki/Medication">medication</a> acting on the <a title="Sympathetic nervous system" href="/wiki/Sympathetic_nervous_system">sympathetic</a> <a title="Nervous system" href="/wiki/Nervous_system">nervous system</a>, producing effects such as increased <a title="Heart rate" href="/wiki/Heart_rate">heart rate</a> and <a title="Blood pressure" href="/wiki/Blood_pressure">blood pressure</a>. However, because dopamine cannot cross the <a title="Blood-brain barrier" href="/wiki/Blood-brain_barrier">blood-brain barrier</a>, dopamine given as a drug does not directly affect the <a title="Central nervous system" href="/wiki/Central_nervous_system">central nervous system</a>. To increase the amount of dopamine in the brains of patients with diseases such as <a title="Parkinson's disease" href="/wiki/Parkinson%27s_disease">Parkinson's disease</a> and dopa-responsive <a title="Dystonia" href="/wiki/Dystonia">dystonia</a>, <a title="L-DOPA" href="/wiki/L-DOPA">L-DOPA</a>, which is the precursor of dopamine, can be given because it can cross the <a title="Blood-brain barrier" href="/wiki/Blood-brain_barrier">blood-brain barrier</a>.

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<h2>Contents</h2>

[<a id="togglelink" class="internal" href="#">hide</a>]</div>

<ul>

<li class="toclevel-1 tocsection-1"><a href="#History">1 History</a></li>

<li class="toclevel-1 tocsection-2"><a href="#Biochemistry">2 Biochemistry</a>

<ul>

<li class="toclevel-2 tocsection-3"><a href="#Name_and_family">2.1 Name and family</a></li>

<li class="toclevel-2 tocsection-4"><a href="#Biosynthesis">2.2 Biosynthesis</a></li>

<li class="toclevel-2 tocsection-5"><a href="#Inactivation_and_degradation">2.3 Inactivation and degradation</a></li>

</ul>

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<li class="toclevel-1 tocsection-6"><a href="#Functions_in_the_brain">3 Functions in the brain</a>

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<li class="toclevel-2 tocsection-7"><a href="#Anatomy">3.1 Anatomy</a></li>

<li class="toclevel-2 tocsection-8"><a href="#Tonic_and_phasic_activity">3.2 Tonic and phasic activity</a></li>

<li class="toclevel-2 tocsection-9"><a href="#Movement">3.3 Movement</a></li>

<li class="toclevel-2 tocsection-10"><a href="#Cognition_and_frontal_cortex">3.4 Cognition and frontal cortex</a></li>

<li class="toclevel-2 tocsection-11"><a href="#Regulating_prolactin_secretion">3.5 Regulating prolactin secretion</a></li>

<li class="toclevel-2 tocsection-12"><a href="#Motivation_and_pleasure">3.6 Motivation and pleasure</a>

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<li class="toclevel-3 tocsection-13"><a href="#Reinforcement">3.6.1 Reinforcement</a></li>

<li class="toclevel-3 tocsection-14"><a href="#Reuptake_inhibition.2C_expulsion">3.6.2 Reuptake inhibition, expulsion</a></li>

<li class="toclevel-3 tocsection-15"><a href="#Incentive_salience">3.6.3 Incentive salience</a></li>

<li class="toclevel-3 tocsection-16"><a href="#Dopamine.2C_learning.2C_and_reward-seeking_behavior">3.6.4 Dopamine, learning, and reward-seeking behavior</a></li>

<li class="toclevel-3 tocsection-17"><a href="#Animal_studies">3.6.5 Animal studies</a></li>

<li class="toclevel-3 tocsection-18"><a href="#The_effects_of_drugs_that_reduce_dopamine_activity">3.6.6 The effects of drugs that reduce dopamine activity</a></li>

<li class="toclevel-3 tocsection-19"><a href="#Opioid_and_cannabinoid_transmission">3.6.7 Opioid and cannabinoid transmission</a></li>

<li class="toclevel-3 tocsection-20"><a href="#Sociability">3.6.8 Sociability</a></li>

<li class="toclevel-3 tocsection-21"><a href="#Processing_of_pain">3.6.9 Processing of pain</a></li>

<li class="toclevel-3 tocsection-22"><a href="#Salience">3.6.10 Salience</a></li>

<li class="toclevel-3 tocsection-23"><a href="#Behavior_disorders">3.6.11 Behavior disorders</a></li>

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<li class="toclevel-2 tocsection-24"><a href="#Latent_inhibition_and_creative_drive">3.7 Latent inhibition and creative drive</a></li>

<li class="toclevel-2 tocsection-25"><a href="#Chemoreceptor_trigger_zone">3.8 Chemoreceptor trigger zone</a></li>

<li class="toclevel-2 tocsection-26"><a href="#Dopaminergic_mind_hypothesis">3.9 Dopaminergic mind hypothesis</a></li>

</ul>

</li>

<li class="toclevel-1 tocsection-27"><a href="#Links_to_psychosis">4 Links to psychosis</a></li>

<li class="toclevel-1 tocsection-28"><a href="#Therapeutic_use">5 Therapeutic use</a></li>

<li class="toclevel-1 tocsection-29"><a href="#Nonneural_functions">6 Nonneural functions</a>

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<li class="toclevel-2 tocsection-30"><a href="#Immunoregulatory">6.1 Immunoregulatory</a></li>

<li class="toclevel-2 tocsection-31"><a href="#Peripheral_effects">6.2 Peripheral effects</a></li>

<li class="toclevel-2 tocsection-32"><a href="#Renal_effects">6.3 Renal effects</a></li>

</ul>

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<li class="toclevel-1 tocsection-33"><a href="#Dopamine_and_fruit_browning">7 Dopamine and fruit browning</a></li>

<li class="toclevel-1 tocsection-35"><a href="#References">9 References</a></li>

<li class="toclevel-1 tocsection-36"><a href="#External_links">10 External links</a></li>

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<h2>[<a title="Edit section: History" href="/w/index.php?title=Dopamine&action=edit&section=1">edit</a>] History</h2>

Dopamine was first synthesized in 1910 by George Barger and James Ewens at Wellcome Laboratories in London, England.<a href="#cite_note-1">[2]</a> It was named dopamine because it was a <a class="mw-redirect" title="Monoamine" href="/wiki/Monoamine">monoamine</a>, and its synthetic precursor was 3,4-dihydroxyphenylalanine (<a title="L-DOPA" href="/wiki/L-DOPA">L-DOPA</a>). Dopamine's function as a neurotransmitter was first recognized in 1958 by <a title="Arvid Carlsson" href="/wiki/Arvid_Carlsson">Arvid Carlsson</a> and Nils-Åke Hillarp at the Laboratory for Chemical Pharmacology of the National Heart Institute of <a title="Sweden" href="/wiki/Sweden">Sweden</a>.<a href="#cite_note-2">[3]</a> Carlsson was awarded the 2000 <a title="Nobel Prize in Physiology or Medicine" href="/wiki/Nobel_Prize_in_Physiology_or_Medicine">Nobel Prize in Physiology or Medicine</a> for showing that dopamine is not just a precursor of <a title="Norepinephrine" href="/wiki/Norepinephrine">norepinephrine</a> (noradrenaline) and <a title="Epinephrine" href="/wiki/Epinephrine">epinephrine</a> (adrenaline), but a neurotransmitter as well.

<h2>[<a title="Edit section: Biochemistry" href="/w/index.php?title=Dopamine&action=edit&section=2">edit</a>] Biochemistry</h2>

Biosynthesis of dopamine</div>

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<h3>[<a title="Edit section: Name and family" href="/w/index.php?title=Dopamine&action=edit&section=3">edit</a>] Name and family</h3>

Dopamine has the chemical formula C6H3(OH)2-CH2-CH2-NH2. Its chemical name is "4-(2-aminoethyl)benzene-1,2-diol" and its abbreviation is "DA."

As a member of the <a title="Catecholamine" href="/wiki/Catecholamine">catecholamine</a> family, dopamine is a precursor to <a title="Norepinephrine" href="/wiki/Norepinephrine">norepinephrine</a> (noradrenaline) and then <a title="Epinephrine" href="/wiki/Epinephrine">epinephrine</a> (adrenaline) in the biosynthetic pathways for these neurotransmitters.

<h3>[<a title="Edit section: Biosynthesis" href="/w/index.php?title=Dopamine&action=edit&section=4">edit</a>] Biosynthesis</h3>

Dopamine is biosynthesized in the body (mainly by nervous tissue and the <a title="Adrenal medulla" href="/wiki/Adrenal_medulla">medulla</a> of the <a title="Adrenal gland" href="/wiki/Adrenal_gland">adrenal glands</a>) first by the hydroxylation of the amino acid <a class="mw-redirect" title="L-tyrosine" href="/wiki/L-tyrosine">L-tyrosine</a> to L-DOPA via the enzyme tyrosine 3-monooxygenase, also known as <a title="Tyrosine hydroxylase" href="/wiki/Tyrosine_hydroxylase">tyrosine hydroxylase</a>, and then by the <a title="Decarboxylation" href="/wiki/Decarboxylation">decarboxylation</a> of <a title="L-DOPA" href="/wiki/L-DOPA">L-DOPA</a> by <a title="Aromatic L-amino acid decarboxylase" href="/wiki/Aromatic_L-amino_acid_decarboxylase">aromatic L-amino acid decarboxylase</a> (which is often referred to as dopa decarboxylase). In some neurons, dopamine is further processed into <a title="Norepinephrine" href="/wiki/Norepinephrine">norepinephrine</a> by <a class="mw-redirect" title="Dopamine beta-hydroxylase" href="/wiki/Dopamine_beta-hydroxylase">dopamine beta-hydroxylase</a>.

In <a title="Neuron" href="/wiki/Neuron">neurons</a>, dopamine is packaged after synthesis into <a class="mw-redirect" title="Vesicle (biology)" href="/wiki/Vesicle_(biology)">vesicles</a>, which are then released into the <a title="Synapse" href="/wiki/Synapse">synapse</a> in response to a presynaptic <a title="Action potential" href="/wiki/Action_potential">action potential</a>.

Biodegradation of dopamine</div>

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<h3>[<a title="Edit section: Inactivation and degradation" href="/w/index.php?title=Dopamine&action=edit&section=5">edit</a>] Inactivation and degradation</h3>

Two major degradation pathways for dopamine exist. In most areas of the brain, including the <a title="Striatum" href="/wiki/Striatum">striatum</a> and <a title="Basal ganglia" href="/wiki/Basal_ganglia">basal ganglia</a>, dopamine is inactivated by <a title="Reuptake" href="/wiki/Reuptake">reuptake</a> via the <a title="Dopamine transporter" href="/wiki/Dopamine_transporter">dopamine transporter</a> (DAT1), then enzymatic breakdown by <a title="Monoamine oxidase" href="/wiki/Monoamine_oxidase">monoamine oxidase</a> (<a class="mw-redirect" title="MAOA" href="/wiki/MAOA">MAOA</a> and <a class="mw-redirect" title="MAOB" href="/wiki/MAOB">MAOB</a>) into <a class="mw-redirect" title="3,4-dihydroxyphenylacetic acid" href="/wiki/3,4-dihydroxyphenylacetic_acid">3,4-dihydroxyphenylacetic acid</a>. In the prefrontal cortex, however, there are very few dopamine transporter proteins, and dopamine is instead inactivated by reuptake via the <a title="Norepinephrine transporter" href="/wiki/Norepinephrine_transporter">norepinephrine transporter</a> (NET), presumably on neighboring norepinephrine neurons, then enzymatic breakdown by <a title="Catechol-O-methyl transferase" href="/wiki/Catechol-O-methyl_transferase">catechol-O-methyl transferase</a> (COMT) into <a class="mw-redirect" title="3-methoxytyramine" href="/wiki/3-methoxytyramine">3-methoxytyramine</a>.<a href="#cite_note-3">[4]</a> 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.<a href="#cite_note-4">[5]</a> Dopamine that is not broken down by enzymes is repackaged into vesicles for reuse by <a class="mw-redirect" title="VMAT2" href="/wiki/VMAT2">VMAT2</a>.

<h2>[<a title="Edit section: Functions in the brain" href="/w/index.php?title=Dopamine&action=edit&section=6">edit</a>] Functions in the brain</h2>

Dopamine has many functions in the brain, including important roles in behavior and <a title="Cognition" href="/wiki/Cognition">cognition</a>, <a title="Animal locomotion" href="/wiki/Animal_locomotion">voluntary movement</a>, <a title="Motivation" href="/wiki/Motivation">motivation</a>, <a title="Punishment" href="/wiki/Punishment">punishment</a> and <a title="Reward system" href="/wiki/Reward_system">reward</a>, inhibition of <a title="Prolactin" href="/wiki/Prolactin">prolactin</a> production (involved in <a title="Lactation" href="/wiki/Lactation">lactation</a> and <a title="Prolactin" href="/wiki/Prolactin#Effects">sexual gratification</a>), <a title="Sleep" href="/wiki/Sleep">sleep</a>, <a title="Mood (psychology)" href="/wiki/Mood_(psychology)">mood</a>, <a title="Attention" href="/wiki/Attention">attention</a>, <a title="Working memory" href="/wiki/Working_memory">working memory</a>, and <a title="Learning" href="/wiki/Learning">learning</a>. Dopaminergic neurons (i.e., neurons whose primary neurotransmitter is dopamine) are present chiefly in the <a title="Ventral tegmental area" href="/wiki/Ventral_tegmental_area">ventral tegmental area</a> (VTA) of the <a title="Midbrain" href="/wiki/Midbrain">midbrain</a>, the <a title="Substantia nigra" href="/wiki/Substantia_nigra">substantia nigra pars compacta</a>, and the <a title="Arcuate nucleus" href="/wiki/Arcuate_nucleus">arcuate nucleus</a> of the hypothalamus.

It has been hypothesized that dopamine transmits reward prediction error, although this has been questioned.<a href="#cite_note-dopamine_function-5">[6]</a> 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 <a title="Classical conditioning" href="/wiki/Classical_conditioning">conditioned stimulus</a> after repeated pairings with the reward. Further, dopamine neurons are depressed when the expected reward is omitted. Thus, dopamine neurons seem to <a class="mw-redirect" title="Neural encoding" href="/wiki/Neural_encoding">encode</a> 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. <a title="Temporal difference learning" href="/wiki/Temporal_difference_learning">Temporal difference learning</a> provides a computational model describing how the prediction error of dopamine neurons is used as a teaching signal.

The reward system in insects uses <a title="Octopamine" href="/wiki/Octopamine">octopamine</a>, which is the presumed arthropod homolog of <a title="Norepinephrine" href="/wiki/Norepinephrine">norepinephrine</a>,<a href="#cite_note-octopamine-honeybee-6">[7]</a> rather than dopamine. In insects, dopamine acts instead as a punishment signal and is necessary to form aversive memories.<a href="#cite_note-pmid14627633-7">[8]</a><a href="#cite_note-pmid19521527-8">[9]</a>

<h3>[<a title="Edit section: Anatomy" href="/w/index.php?title=Dopamine&action=edit&section=7">edit</a>] Anatomy</h3>

<div class="rellink relarticle mainarticle">Main article: <a title="Dopaminergic pathways" href="/wiki/Dopaminergic_pathways">Dopaminergic pathways</a></div>

<a title="Dopaminergic" href="/wiki/Dopaminergic">Dopaminergic</a> neurons form a <a class="mw-redirect" title="Neurotransmitter system" href="/wiki/Neurotransmitter_system">neurotransmitter system</a> which originates in <a class="mw-redirect" title="Substantia nigra pars compacta" href="/wiki/Substantia_nigra_pars_compacta">substantia nigra pars compacta</a>, <a title="Ventral tegmental area" href="/wiki/Ventral_tegmental_area">ventral tegmental area</a> (VTA), and <a title="Hypothalamus" href="/wiki/Hypothalamus">hypothalamus</a>. These project <a title="Axon" href="/wiki/Axon">axons</a> to large areas of the brain which are typically divided into four major pathways:

<ul>

<li><a title="Mesocortical pathway" href="/wiki/Mesocortical_pathway">Mesocortical pathway</a> connects the ventral tegmental area to the frontal lobe of the <a class="mw-redirect" title="Pre-frontal cortex" href="/wiki/Pre-frontal_cortex">pre-frontal cortex</a>. Neurons with <a title="Soma (biology)" href="/wiki/Soma_(biology)">somas</a> in the ventral tegmental area project axons into the pre-frontal cortex.</li> <li><a title="Mesolimbic pathway" href="/wiki/Mesolimbic_pathway">Mesolimbic pathway</a> carries dopamine from the ventral tegmental area to the <a title="Nucleus accumbens" href="/wiki/Nucleus_accumbens">nucleus accumbens</a> via the <a title="Amygdala" href="/wiki/Amygdala">amygdala</a> and <a title="Hippocampus" href="/wiki/Hippocampus">hippocampus</a>. The somas of the projecting neurons are in the ventral tegmental area.</li> <li><a title="Nigrostriatal pathway" href="/wiki/Nigrostriatal_pathway">Nigrostriatal pathway</a> runs from the substantia nigra to the <a class="mw-redirect" title="Neostriatum" href="/wiki/Neostriatum">neostriatum</a>. Somas in the substantia nigra project axons into the <a title="Caudate nucleus" href="/wiki/Caudate_nucleus">caudate nucleus</a> and <a title="Putamen" href="/wiki/Putamen">putamen</a>. The pathway is involved in the basal ganglia motor loop.</li> <li><a title="Tuberoinfundibular pathway" href="/wiki/Tuberoinfundibular_pathway">Tuberoinfundibular pathway</a> runs from the hypothalamus to the pituitary gland.</li></ul>This innervation explains many of the effects of activating this dopamine system. For instance, the <a title="Mesolimbic pathway" href="/wiki/Mesolimbic_pathway">mesolimbic pathway</a> connects the VTA and <a title="Nucleus accumbens" href="/wiki/Nucleus_accumbens">nucleus accumbens</a>; both are central to the brain <a title="Reward system" href="/wiki/Reward_system">reward system</a>.<a href="#cite_note-9">[10]</a>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.<a href="#cite_note-10">[11]</a><h3>[<a title="Edit section: Tonic and phasic activity" href="/w/index.php?title=Dopamine&action=edit&section=8">edit</a>] Tonic and phasic activity</h3>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.<a href="#cite_note-11">[12]</a> Phasic dopamine release results from the activity of the dopamine-containing cells themselves. This activity is characterized by irregular <a title="Pacemaker action potential" href="/wiki/Pacemaker_action_potential">pacemaking</a> activity of single spikes, and rapid bursts of typically 2-6 spikes in quick succession.<a href="#cite_note-12">[13]</a><a href="#cite_note-13">[14]</a> 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.<a href="#cite_note-14">[15]</a><h3>[<a title="Edit section: Movement" href="/w/index.php?title=Dopamine&action=edit&section=9">edit</a>] Movement</h3>Via the <a title="Dopamine receptor" href="/wiki/Dopamine_receptor">dopamine receptors</a>, D1-5, dopamine reduces the influence of the indirect pathway, and increases the actions of the direct pathway within the <a title="Basal ganglia" href="/wiki/Basal_ganglia">basal ganglia</a>. Insufficient dopamine <a title="Biosynthesis" href="/wiki/Biosynthesis">biosynthesis</a> in the dopaminergic neurons can cause <a title="Parkinson's disease" href="/wiki/Parkinson%27s_disease">Parkinson's disease</a>, in which a person loses the ability to execute smooth, controlled movements.<h3>[<a title="Edit section: Cognition and frontal cortex" href="/w/index.php?title=Dopamine&action=edit&section=10">edit</a>] Cognition and frontal cortex</h3>In the <a title="Frontal lobe" href="/wiki/Frontal_lobe">frontal lobes</a>, 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 <a title="Neurocognitive" href="/wiki/Neurocognitive">neurocognitive</a> functions, especially <a title="Memory" href="/wiki/Memory">memory</a>, <a title="Attention" href="/wiki/Attention">attention</a>, and <a class="mw-redirect" title="Problem-solving" href="/wiki/Problem-solving">problem-solving</a>. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to <a class="mw-redirect" title="Attention deficit disorder" href="/wiki/Attention_deficit_disorder">attention deficit disorder</a>. It has been found that D1 receptors<a href="#cite_note-Inhibitorydopamine-15">[16]</a> as well as D4 receptors<a href="#cite_note-16">[17]</a> are responsible for the cognitive-enhancing effects of dopamine.<h3>[<a title="Edit section: Regulating prolactin secretion" href="/w/index.php?title=Dopamine&action=edit&section=11">edit</a>] Regulating prolactin secretion</h3>Dopamine is the primary <a class="mw-redirect" title="Neuroendocrine" href="/wiki/Neuroendocrine">neuroendocrine</a> inhibitor of the secretion of <a title="Prolactin" href="/wiki/Prolactin">prolactin</a> from the <a title="Anterior pituitary" href="/wiki/Anterior_pituitary">anterior pituitary</a> gland.<a href="#cite_note-prolactininhibition-17">[18]</a> Dopamine produced by neurons in the <a title="Arcuate nucleus" href="/wiki/Arcuate_nucleus">arcuate nucleus</a> of the hypothalamus is secreted into the hypothalamo-hypophysial blood vessels of the <a title="Median eminence" href="/wiki/Median_eminence">median eminence</a>, which supply the <a title="Pituitary gland" href="/wiki/Pituitary_gland">pituitary gland</a>. The lactotrope cells that produce <a title="Prolactin" href="/wiki/Prolactin">prolactin</a>, 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.<h3>[<a title="Edit section: Motivation and pleasure" href="/w/index.php?title=Dopamine&action=edit&section=12">edit</a>] Motivation and pleasure</h3><div class="thumb tright"><div style="WIDTH: 222px" class="thumbinner"><a class="image" href="/wiki/File:Dopamine_Pathways.png"><img class="thumbimage" alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/5/51/Dopamine_Pathways.png/220px-Dopamine_Pathways.png" width="220" height="163" /></a><div class="thumbcaption"><div class="magnify"><a class="internal" title="Enlarge" href="/wiki/File:Dopamine_Pathways.png"><img alt="" src="http://bits.wikimedia.org/skins-1.5/common/images/magnify-clip.png" width="15" height="11" /></a></div>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.</div></div></div><div class="rellink">Further information: <a title="Motivation" href="/wiki/Motivation">Motivation</a></div><h4>[<a title="Edit section: Reinforcement" href="/w/index.php?title=Dopamine&action=edit&section=13">edit</a>] Reinforcement</h4>Dopamine is commonly associated with the <a title="Reward system" href="/wiki/Reward_system">reward system</a> of the brain, providing feelings of enjoyment and <a title="Reinforcement" href="/wiki/Reinforcement">reinforcement</a> to motivate a person proactively to perform certain activities. Dopamine is released (particularly in areas such as the <a title="Nucleus accumbens" href="/wiki/Nucleus_accumbens">nucleus accumbens</a> and <a title="Prefrontal cortex" href="/wiki/Prefrontal_cortex">prefrontal cortex</a>) by <a title="Reward system" href="/wiki/Reward_system">rewarding</a> experiences such as <a title="Food" href="/wiki/Food">food</a>, <a class="mw-redirect" title="Human sexual behaviour" href="/wiki/Human_sexual_behaviour">sex</a>, <a class="mw-redirect" title="Drugs" href="/wiki/Drugs">drugs</a>, and <a title="Neutral stimulus" href="/wiki/Neutral_stimulus">neutral stimuli</a> that become <a title="Classical conditioning" href="/wiki/Classical_conditioning">associated</a> with them. Recent studies indicate that <a title="Aggression" href="/wiki/Aggression">aggression</a> may also stimulate the release of dopamine in this way.<a href="#cite_note-18">[19]</a>This theory is often discussed in terms of drugs such as <a title="Cocaine" href="/wiki/Cocaine">cocaine</a>, <a title="Nicotine" href="/wiki/Nicotine">nicotine</a>, and <a title="Amphetamine" href="/wiki/Amphetamine">amphetamines</a>, which directly or indirectly lead to an increase of dopamine in the <a title="Mesolimbic pathway" href="/wiki/Mesolimbic_pathway">mesolimbic reward pathway</a> of the brain, and in relation to <a class="mw-redirect" title="Neurobiology" href="/wiki/Neurobiology">neurobiological</a> theories of <a title="Physical dependence" href="/wiki/Physical_dependence">chemical addiction</a> (not to be confused with <a title="Substance dependence" href="/wiki/Substance_dependence">psychological dependence</a>), arguing that this <a title="Dopaminergic pathways" href="/wiki/Dopaminergic_pathways">dopamine pathway</a> is pathologically altered in addicted persons.<a href="#cite_note-19">[20]</a><a href="#cite_note-PMID11805404-20">[21]</a><a href="#cite_note-PMID11477488-21">[22]</a><h4>[<a title="Edit section: Reuptake inhibition, expulsion" href="/w/index.php?title=Dopamine&action=edit&section=14">edit</a>] Reuptake inhibition, expulsion</h4>Cocaine and amphetamines inhibit the <a class="mw-redirect" title="Re-uptake" href="/wiki/Re-uptake">re-uptake</a> of dopamine; however, they influence separate mechanisms of action. Cocaine is a <a title="Dopamine transporter" href="/wiki/Dopamine_transporter">dopamine transporter</a> and <a title="Norepinephrine transporter" href="/wiki/Norepinephrine_transporter">norepinephrine transporter</a> 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 <a title="Synapse" href="/wiki/Synapse">synaptic</a> gap, but by a different mechanism. Amphetamines and <a title="Methamphetamine" href="/wiki/Methamphetamine">methamphetamine</a> 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.[<a title="Wikipedia:Citation needed" href="/wiki/Wikipedia:Citation_needed">citation needed</a>] By entering the presynaptic neuron, amphetamines force dopamine molecules out of their storage <a title="Synaptic vesicle" href="/wiki/Synaptic_vesicle">vesicles</a> and expel them into the synaptic gap by making the dopamine transporters work in reverse.<h4>[<a title="Edit section: Incentive salience" href="/w/index.php?title=Dopamine&action=edit&section=15">edit</a>] Incentive salience</h4><div class="rellink relarticle mainarticle">Main article: <a title="Incentive salience" href="/wiki/Incentive_salience">Incentive salience</a></div>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").<h4>[<a title="Edit section: Dopamine, learning, and reward-seeking behavior" href="/w/index.php?title=Dopamine&action=edit&section=16">edit</a>] Dopamine, learning, and reward-seeking behavior</h4>Dopaminergic neurons of the midbrain are the main source of dopamine in the brain.<a href="#cite_note-fn5-22">[23]</a> 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.<a href="#cite_note-fn5-22">[23]</a> 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.<a href="#cite_note-fn5-22">[23]</a> 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.<a href="#cite_note-fn5-22">[23]</a> 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.<a href="#cite_note-Matsumoto-23">[24]</a> This research finds the reward neurons predominate in the ventromedial region in the <a class="mw-redirect" title="Substantia nigra pars compacta" href="/wiki/Substantia_nigra_pars_compacta">substantia nigra pars compacta</a> as well as the <a title="Ventral tegmental area" href="/wiki/Ventral_tegmental_area">ventral tegmental area</a>. Neurons in these areas project mainly to the <a title="Ventral striatum" href="/wiki/Ventral_striatum">ventral striatum</a> and thus might transmit value-related information in regard to reward values.<a href="#cite_note-Matsumoto-23">[24]</a> The nonreward neurons are predominate in the dorsolateral area of the substantia nigra pars compacta which projects to the <a class="mw-redirect" title="Dorsal striatum" href="/wiki/Dorsal_striatum">dorsal striatum</a> and may relate to orienting behaviour.<a href="#cite_note-Matsumoto-23">[24]</a> 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 <a title="Basal forebrain" href="/wiki/Basal_forebrain">basal forebrain</a> while the nonreward-related ones from the <a title="Habenula" href="/wiki/Habenula#Lateral_habenula">lateral habenula</a>.<a href="#cite_note-Matsumoto-23">[24]</a><h4>[<a title="Edit section: Animal studies" href="/w/index.php?title=Dopamine&action=edit&section=17">edit</a>] Animal studies</h4>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 <a title="Nucleus accumbens" href="/wiki/Nucleus_accumbens">nucleus accumbens</a> and <a class="mw-redirect" title="Neostriatum" href="/wiki/Neostriatum">neostriatum</a> using 6-hydroxydopamine.<a href="#cite_note-fn5-22">[23]</a> 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.<a href="#cite_note-fn1-24">[25]</a><h4>[<a title="Edit section: The effects of drugs that reduce dopamine activity" href="/w/index.php?title=Dopamine&action=edit&section=18">edit</a>] The effects of drugs that reduce dopamine activity</h4>In humans, drugs that reduce dopamine activity (<a class="mw-redirect" title="Neuroleptic" href="/wiki/Neuroleptic">neuroleptics</a>, e.g. <a title="Antipsychotic" href="/wiki/Antipsychotic">antipsychotics</a>) have been shown to reduce motivation, cause <a title="Anhedonia" href="/wiki/Anhedonia">anhedonia</a> (inability to experience pleasure), and long-term use has been associated with the irreversible movement disorder, <a title="Tardive dyskinesia" href="/wiki/Tardive_dyskinesia">tardive dyskinesia</a>.<a href="#cite_note-fn2-25">[26]</a> Furthermore, antipsychotic drugs are associated with <a title="Weight gain" href="/wiki/Weight_gain">weight gain</a>, <a class="mw-redirect" title="Diabetes" href="/wiki/Diabetes">diabetes</a>, <a title="Lactation" href="/wiki/Lactation">lactation</a>, <a title="Gynecomastia" href="/wiki/Gynecomastia">gynecomastia</a>, <a title="Drooling" href="/wiki/Drooling">drooling</a>, <a title="Dysphoria" href="/wiki/Dysphoria">dysphoria</a>, <a title="Fatigue (medical)" href="/wiki/Fatigue_(medical)">fatigue</a>, <a title="Sexual dysfunction" href="/wiki/Sexual_dysfunction">sexual dysfunction</a>, and <a class="mw-redirect" title="Heart rhythm" href="/wiki/Heart_rhythm">heart rhythm</a> problems. Selective D2/D3 agonists <a title="Pramipexole" href="/wiki/Pramipexole">pramipexole</a> and <a title="Ropinirole" href="/wiki/Ropinirole">ropinirole</a>, used to treat <a title="Restless legs syndrome" href="/wiki/Restless_legs_syndrome">restless legs syndrome</a> (RLS), have limited anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale (SHAPS).<a href="#cite_note-fn3-26">[27]</a><h4>[<a title="Edit section: Opioid and cannabinoid transmission" href="/w/index.php?title=Dopamine&action=edit&section=19">edit</a>] Opioid and cannabinoid transmission</h4><a title="Opioid" href="/wiki/Opioid">Opioid</a> and <a title="Cannabinoid" href="/wiki/Cannabinoid">cannabinoid</a> transmission instead of dopamine may modulate consummatory pleasure and food palatability (liking).<a href="#cite_note-fn4-27">[28]</a> 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.<a href="#cite_note-fn6-28">[29]</a> Libido can be increased by drugs that affect dopamine, but not by drugs that affect opioid peptides or other neurotransmitters.<h4>[<a title="Edit section: Sociability" href="/w/index.php?title=Dopamine&action=edit&section=20">edit</a>] Sociability</h4>Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor-binding is found in people with <a title="Social anxiety" href="/wiki/Social_anxiety">social anxiety</a>. Traits common to negative <a title="Schizophrenia" href="/wiki/Schizophrenia">schizophrenia</a> (<a class="mw-redirect" title="Social withdrawal" href="/wiki/Social_withdrawal">social withdrawal</a>, <a title="Apathy" href="/wiki/Apathy">apathy</a>, <a title="Anhedonia" href="/wiki/Anhedonia">anhedonia</a>) are thought to be related to a hypodopaminergic state in certain areas of the brain. In instances of <a title="Bipolar disorder" href="/wiki/Bipolar_disorder">bipolar disorder</a>, <a title="Manic" href="/wiki/Manic">manic</a> subjects can become hypersocial, as well as <a class="mw-redirect" title="Hypersexual" href="/wiki/Hypersexual">hypersexual</a>.[<a title="Wikipedia:Citation needed" href="/wiki/Wikipedia:Citation_needed">citation needed</a>] This is credited to an increase in dopamine, because mania can be reduced by dopamine-blocking anti-psychotics.<a href="#cite_note-29">[30]</a><h4>[<a title="Edit section: Processing of pain" href="/w/index.php?title=Dopamine&action=edit&section=21">edit</a>] Processing of pain</h4>Dopamine has been demonstrated to play a role in <a title="Pain" href="/wiki/Pain">pain</a> processing in multiple levels of the <a title="Central nervous system" href="/wiki/Central_nervous_system">central nervous system</a> including the <a title="Spinal cord" href="/wiki/Spinal_cord">spinal cord</a>,<a href="#cite_note-30">[31]</a> <a title="Periaqueductal gray" href="/wiki/Periaqueductal_gray">periaqueductal gray</a> (PAG),<a href="#cite_note-31">[32]</a> <a title="Thalamus" href="/wiki/Thalamus">thalamus</a>,<a href="#cite_note-32">[33]</a> <a title="Basal ganglia" href="/wiki/Basal_ganglia">basal ganglia</a>,<a href="#cite_note-33">[34]</a><a href="#cite_note-34">[35]</a> <a title="Insular cortex" href="/wiki/Insular_cortex">insular cortex</a>,<a href="#cite_note-35">[36]</a><a href="#cite_note-36">[37]</a> and <a title="Cingulate cortex" href="/wiki/Cingulate_cortex">cingulate cortex</a>.<a href="#cite_note-37">[38]</a> Accordingly, decreased levels of dopamine have been associated with painful symptoms that frequently occur in <a title="Parkinson's disease" href="/wiki/Parkinson%27s_disease">Parkinson's disease</a>.<a href="#cite_note-38">[39]</a> Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including <a class="mw-redirect" title="Burning mouth syndrome" href="/wiki/Burning_mouth_syndrome">burning mouth syndrome</a>,<a href="#cite_note-39">[40]</a> <a title="Fibromyalgia" href="/wiki/Fibromyalgia">fibromyalgia</a>,<a href="#cite_note-40">[41]</a><a href="#cite_note-41">[42]</a> and <a title="Restless legs syndrome" href="/wiki/Restless_legs_syndrome">restless legs syndrome</a>.<a href="#cite_note-42">[43]</a> 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.<a href="#cite_note-43">[44]</a> In addition, D1 receptor activation in the insular cortex appears to attenuate subsequent pain-related behavior.<h4>[<a title="Edit section: Salience" href="/w/index.php?title=Dopamine&action=edit&section=22">edit</a>] Salience</h4>Dopamine may also have a role in the <a title="Salience (neuroscience)" href="/wiki/Salience_(neuroscience)">salience</a> of potentially important stimuli, such as sources of reward or of danger.<a href="#cite_note-44">[45]</a> This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.<h4>[<a title="Edit section: Behavior disorders" href="/w/index.php?title=Dopamine&action=edit&section=23">edit</a>] Behavior disorders</h4>Deficient dopamine neurotransmission is implicated in <a class="mw-redirect" title="Attention-deficit hyperactivity disorder" href="/wiki/Attention-deficit_hyperactivity_disorder">attention-deficit hyperactivity disorder</a>, and stimulant medications used to successfully treat the disorder increase dopamine neurotransmission, leading to decreased symptoms.<a href="#cite_note-45">[46]</a> Consistent with this hypothesis, dopaminergic pathways have a role in inhibitory action control and the inhibition of the tendency to make unwanted actions.<a href="#cite_note-46">[47]</a>The long term use of <a class="mw-redirect" title="Levodopa" href="/wiki/Levodopa">levodopa</a> in <a title="Parkinson's disease" href="/wiki/Parkinson%27s_disease">Parkinson's disease</a> has been linked to <a title="Dopamine dysregulation syndrome" href="/wiki/Dopamine_dysregulation_syndrome">dopamine dysregulation syndrome</a>.<a href="#cite_note-pmid17988927-47">[48]</a><h3>[<a title="Edit section: Latent inhibition and creative drive" href="/w/index.php?title=Dopamine&action=edit&section=24">edit</a>] Latent inhibition and creative drive</h3>Dopamine in the <a title="Mesolimbic pathway" href="/wiki/Mesolimbic_pathway">mesolimbic pathway</a> increases general <a title="Arousal" href="/wiki/Arousal">arousal</a> and goal directed behaviors and decreases <a title="Latent inhibition" href="/wiki/Latent_inhibition">latent inhibition</a>; all three effects increase the creative drive of idea generation. This has led to a three-factor model of <a title="Creativity" href="/wiki/Creativity">creativity</a> involving the <a title="Frontal lobe" href="/wiki/Frontal_lobe">frontal lobes</a>, the <a title="Temporal lobe" href="/wiki/Temporal_lobe">temporal lobes</a>, and mesolimbic dopamine.<a href="#cite_note-48">[49]</a><h3>[<a title="Edit section: Chemoreceptor trigger zone" href="/w/index.php?title=Dopamine&action=edit&section=25">edit</a>]Chemoreceptor trigger zone</h3>Dopamine is one of the neurotransmitters implicated in the control of <a title="Nausea" href="/wiki/Nausea">nausea</a> and <a class="mw-redirect" title="Vomit" href="/wiki/Vomit">vomiting</a> via interactions in the <a title="Chemoreceptor trigger zone" href="/wiki/Chemoreceptor_trigger_zone">chemoreceptor trigger zone</a>. <a title="Metoclopramide" href="/wiki/Metoclopramide">Metoclopramide</a> is a D2-receptor antagonist that functions as a <a class="mw-redirect" title="Prokinetic" href="/wiki/Prokinetic">prokinetic</a>/<a title="Antiemetic" href="/wiki/Antiemetic">antiemetic</a>.<h3>[<a title="Edit section: Dopaminergic mind hypothesis" href="/w/index.php?title=Dopamine&action=edit&section=26">edit</a>] Dopaminergic mind hypothesis</h3>The dopaminergic mind hypothesis seeks to explain the differences between modern humans and their hominid relatives by focusing on changes in dopamine.<a href="#cite_note-Previc-49">[50]</a> 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 <a title="Homo habilis" href="/wiki/Homo_habilis">Homo habilis</a>, 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."<a href="#cite_note-Previc-49">[50]</a> 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."<a href="#cite_note-Previc-49">[50]</a> Although behavioral evidence and some indirect anatomical evidence (e.g., enlargement of the dopamine-rich striatum in humans)<a href="#cite_note-50">[51]</a> support a dopaminergic expansion in humans, there is still no direct evidence that dopamine levels are markedly higher in humans relative to other apes.<a href="#cite_note-51">[52]</a> However, recent discoveries about the sea-side settlements of early man may provide evidence of dietary changes consistent with this hypothesis.<a href="#cite_note-52">[53]</a><h2>[<a title="Edit section: Links to psychosis" href="/w/index.php?title=Dopamine&action=edit&section=27">edit</a>] Links to psychosis</h2><div class="rellink relarticle mainarticle">Main article: <a title="Dopamine hypothesis of schizophrenia" href="/wiki/Dopamine_hypothesis_of_schizophrenia">Dopamine hypothesis of schizophrenia</a></div>Abnormally high dopaminergic transmission has been linked to <a title="Psychosis" href="/wiki/Psychosis">psychosis</a> and <a title="Schizophrenia" href="/wiki/Schizophrenia">schizophrenia</a>.<a href="#cite_note-53">[54]</a> Increased dopaminergic functional activity, specifically in the <a title="Mesolimbic pathway" href="/wiki/Mesolimbic_pathway">mesolimbic pathway</a>, is found in schizophrenic individuals. <a class="mw-redirect" title="Anti-psychotic" href="/wiki/Anti-psychotic">Anti-psychotic</a> <a class="mw-redirect" title="Medication" href="/wiki/Medication">medications</a> act largely as dopamine antagonists, inhibiting dopamine at the <a title="Dopamine receptor" href="/wiki/Dopamine_receptor">receptor</a> level, and thereby blocking the effects of the neurochemical in a dose-dependant manner. The older, so-called <a class="mw-redirect" title="Typical antipsychotics" href="/wiki/Typical_antipsychotics">typical antipsychotics</a> most commonly act on D2 receptors,<a href="#cite_note-54">[55]</a> while the <a title="Atypical antipsychotic" href="/wiki/Atypical_antipsychotic">atypical drugs</a> also act on D1, D3 and D4 receptors.<a href="#cite_note-55">[56]</a><a href="#cite_note-56">[57]</a> The finding that drugs such as amphetamines, methamphetamine and cocaine, which can increase dopamine levels by more than tenfold,<a href="#cite_note-57">[58]</a> can temporarily cause psychosis, provides further evidence for this link.<a href="#cite_note-58">[59]</a><h2>[<a title="Edit section: Therapeutic use" href="/w/index.php?title=Dopamine&action=edit&section=28">edit</a>] Therapeutic use</h2><div class="rellink relarticle mainarticle">Main article: <a title="L-DOPA" href="/wiki/L-DOPA">L-DOPA</a></div><a title="L-DOPA" href="/wiki/L-DOPA">Levodopa</a> is a dopamine precursor used in various forms to treat <a title="Parkinson's disease" href="/wiki/Parkinson%27s_disease">Parkinson's disease</a> and dopa-responsive <a title="Dystonia" href="/wiki/Dystonia">dystonia</a>. It is typically co-administered with an inhibitor of peripheral decarboxylation (DDC, <a class="mw-redirect" title="Aromatic-L-amino-acid decarboxylase" href="/wiki/Aromatic-L-amino-acid_decarboxylase">dopa decarboxylase</a>), such as <a title="Carbidopa" href="/wiki/Carbidopa">carbidopa</a> or <a title="Benserazide" href="/wiki/Benserazide">benserazide</a>. Inhibitors of alternative metabolic route for dopamine by <a title="Catechol-O-methyl transferase" href="/wiki/Catechol-O-methyl_transferase">catechol-O-methyl transferase</a> are also used. These include <a title="Entacapone" href="/wiki/Entacapone">entacapone</a> and <a title="Tolcapone" href="/wiki/Tolcapone">tolcapone</a>.<h2>[<a title="Edit section: Nonneural functions" href="/w/index.php?title=Dopamine&action=edit&section=29">edit</a>] Nonneural functions</h2><h3>[<a title="Edit section: Immunoregulatory" href="/w/index.php?title=Dopamine&action=edit&section=30">edit</a>] Immunoregulatory</h3>Dopamine acts upon receptors present on immune cells, with all subtypes of dopamine receptors found on <a class="mw-redirect" title="Leukocyte" href="/wiki/Leukocyte">leukocytes</a>. There is low expression of receptors on <a class="mw-redirect" title="T lymphocyte" href="/wiki/T_lymphocyte">T lymphocytes</a> and <a title="Monocyte" href="/wiki/Monocyte">monocytes</a>, moderate expression on <a class="mw-redirect" title="Neutrophil" href="/wiki/Neutrophil">neutrophils</a> and <a class="mw-redirect" title="Eosinophil" href="/wiki/Eosinophil">eosinophils</a>, and high expression on <a title="B cell" href="/wiki/B_cell">B cells</a> and <a title="Natural killer cell" href="/wiki/Natural_killer_cell">natural killer cells</a>.<a href="#cite_note-59">[60]</a> The <a title="Sympathetic nervous system" href="/wiki/Sympathetic_nervous_system">sympathetic innervation</a> of <a class="mw-redirect" title="Lymphoid tissue" href="/wiki/Lymphoid_tissue">lymphoid tissues</a> is dopaminergic, and increases during stress.<a href="#cite_note-60">[61]</a> Dopamine can also affect immune cells in the <a title="Spleen" href="/wiki/Spleen">spleen</a>, <a title="Bone marrow" href="/wiki/Bone_marrow">bone marrow</a>, and <a class="mw-redirect" title="Blood circulation" href="/wiki/Blood_circulation">blood circulation</a>.<a href="#cite_note-61">[62]</a> In addition, dopamine can be synthesized and released by the immune cells themselves.<a href="#cite_note-62">[63]</a><a href="#cite_note-63">[64]</a>The effects of dopamine on immune cells depend upon their physiological state. While dopamine activates resting <a title="T cell" href="/wiki/T_cell">T cells</a>, it inhibits them when they are activated. Disorders such as <a title="Schizophrenia" href="/wiki/Schizophrenia">schizophrenia</a> and <a title="Parkinson's disease" href="/wiki/Parkinson%27s_disease">Parkinson's disease</a>, in which there are changes in brain dopamine receptors and dopamine signaling pathways, are also associated with altered immune functioning.<a href="#cite_note-64">[65]</a><h3>[<a title="Edit section: Peripheral effects" href="/w/index.php?title=Dopamine&action=edit&section=31">edit</a>] Peripheral effects</h3>Dopamine also has effects when administered through an <a title="Intravenous therapy" href="/wiki/Intravenous_therapy">IV</a> line outside the central nervous system. The brand name of this preparation is known as <a class="mw-redirect" title="Intropin" href="/wiki/Intropin">Intropin</a>. The effects in this form are dose dependent.<ul> <li>Dosages from 2 to 5 μg/kg/min are considered the "renal dose."<a href="#cite_note-65">[66]</a> At this low dosage, dopamine binds <a title="Dopamine receptor D1" href="/wiki/Dopamine_receptor_D1">D1</a> receptors, dilating blood vessels, increasing blood flow to <a title="Renal artery" href="/wiki/Renal_artery">renal</a>, <a class="mw-redirect" title="Mesenteric artery" href="/wiki/Mesenteric_artery">mesenteric</a>, and <a class="mw-redirect" title="Coronary artery" href="/wiki/Coronary_artery">coronary</a> arteries; and increasing overall renal perfusion.<a href="#cite_note-pharmnemonics-66">[67]</a> Dopamine therefore has a diuretic effect, potentially increasing urine output from 5 ml/kg/hr to 10 ml/kg/hr.[<a title="Wikipedia:Citation needed" href="/wiki/Wikipedia:Citation_needed">citation needed</a>]</li></ul><ul> <li>Intermediate dosages from 5 to 10 μg/kg/min additionally have a positive <a class="mw-redirect" title="Inotropic" href="/wiki/Inotropic">inotropic</a> and <a title="Chronotropic" href="/wiki/Chronotropic">chronotropic</a> effect through increased <a title="Beta-1 adrenergic receptor" href="/wiki/Beta-1_adrenergic_receptor">β1 receptor</a> activation. It is used in patients with <a title="Shock (circulatory)" href="/wiki/Shock_(circulatory)">shock</a> or <a title="Heart failure" href="/wiki/Heart_failure">heart failure</a> to increase <a title="Cardiac output" href="/wiki/Cardiac_output">cardiac output</a> and <a title="Blood pressure" href="/wiki/Blood_pressure">blood pressure</a>.<a href="#cite_note-pharmnemonics-66">[67]</a> Dopamine begins to affect the heart at the lower doses, from about 3 μg/kg/min IV.<a href="#cite_note-67">[68]</a></li></ul><ul> <li>High doses from 10 to 20 μg/kg/min is the "pressor" dose.[<a title="Wikipedia:Citation needed" href="/wiki/Wikipedia:Citation_needed">citation needed</a>] This dose causes vasoconstriction, increases <a class="mw-redirect" title="Systemic vascular resistance" href="/wiki/Systemic_vascular_resistance">systemic vascular resistance</a>, and increases blood pressure through <a class="mw-redirect" title="Alpha 1 receptor" href="/wiki/Alpha_1_receptor">α1 receptor</a> activation;<a href="#cite_note-pharmnemonics-66">[67]</a> but can cause the vessels in the kidneys to constrict to the point where they will become non-functional.[<a title="Wikipedia:Citation needed" href="/wiki/Wikipedia:Citation_needed">citation needed</a>]</li></ul><h3>[<a title="Edit section: Renal effects" href="/w/index.php?title=Dopamine&action=edit&section=32">edit</a>] Renal effects</h3>Dopamine induces <a title="Natriuresis" href="/wiki/Natriuresis">natriuresis</a> (sodium loss) in the <a title="Kidney" href="/wiki/Kidney">kidneys</a>.<a href="#cite_note-68">[69]</a><a href="#cite_note-69">[70]</a><h2>[<a title="Edit section: Dopamine and fruit browning" href="/w/index.php?title=Dopamine&action=edit&section=33">edit</a>] Dopamine and fruit browning</h2><a title="Polyphenol oxidase" href="/wiki/Polyphenol_oxidase">Polyphenol oxidases</a> (PPOs) are a family of enzymes responsible for the <a title="Browning (chemical process)" href="/wiki/Browning_(chemical_process)">browning</a> of fresh fruits and vegetables when they are cut or bruised. These enzymes use molecular <a title="Oxygen" href="/wiki/Oxygen">oxygen</a> (O2) to <a title="Redox" href="/wiki/Redox">oxidise</a> various <a class="mw-redirect" title="Diphenol" href="/wiki/Diphenol">1,2-diphenols</a> to their corresponding <a title="Quinone" href="/wiki/Quinone">quinones</a>. The natural substrate for PPOs in <a title="Banana" href="/wiki/Banana">bananas</a> is dopamine. The product of their oxidation, dopamine quinone, spontaneously oxidises to other quinones. The quinones then <a class="mw-redirect" title="Polymerisation" href="/wiki/Polymerisation">polymerise</a> and <a class="mw-redirect" title="Condense" href="/wiki/Condense">condense</a> with <a title="Amino acid" href="/wiki/Amino_acid">amino acids</a> and <a title="Protein" href="/wiki/Protein">proteins</a> to form brown <a title="Biological pigment" href="/wiki/Biological_pigment">pigments</a> known as <a title="Melanin" href="/wiki/Melanin">melanins</a>. The quinones and melanins derived from dopamine may help protect damaged fruit and vegetables against growth of <a title="Bacteria" href="/wiki/Bacteria">bacteria</a> and <a class="mw-redirect" title="Fungi" href="/wiki/Fungi">fungi</a>.<a href="#cite_note-mayer-70">[71]</a><h2>[<a title="Edit section: See also" href="/w/index.php?title=Dopamine&action=edit&section=34">edit</a>] See also</h2><div style="column-count: 3; -moz-column-count: 3"><ul> <li><a title="Substance use disorder" href="/wiki/Substance_use_disorder">Addiction</a></li> <li><a title="Amphetamine" href="/wiki/Amphetamine">Amphetamine</a></li> <li><a title="Antipsychotic" href="/wiki/Antipsychotic">Antipsychotic</a></li> <li><a title="Catecholamine" href="/wiki/Catecholamine">Catecholamine</a></li> <li><a title="Catechol-O-methyl transferase" href="/wiki/Catechol-O-methyl_transferase">Catechol-O-methyl transferase</a></li> <li><a title="Classical conditioning" href="/wiki/Classical_conditioning">Classical conditioning</a></li> <li><a title="Operant conditioning" href="/wiki/Operant_conditioning">Operant conditioning</a></li> <li><a title="Cocaine" href="/wiki/Cocaine">Cocaine</a></li> <li><a title="Depression (mood)" href="/wiki/Depression_(mood)">Depression</a></li> <li><a title="Dopamine hypothesis of schizophrenia" href="/wiki/Dopamine_hypothesis_of_schizophrenia">Dopamine hypothesis of schizophrenia</a></li> <li><a title="Dopamine reuptake inhibitor" href="/wiki/Dopamine_reuptake_inhibitor">Dopamine reuptake inhibitors</a></li> <li><a title="Dopaminergic" href="/wiki/Dopaminergic">Dopaminergic</a></li> <li><a title="Methylphenidate" href="/wiki/Methylphenidate">Methylphenidate</a></li> <li><a title="Neurotransmitter" href="/wiki/Neurotransmitter">Neurotransmitter</a></li> <li><a title="Parkinson's disease" href="/wiki/Parkinson%27s_disease">Parkinson's disease</a></li> <li><a title="Prolactinoma" href="/wiki/Prolactinoma">Prolactinoma</a></li> <li><a title="Schizophrenia" href="/wiki/Schizophrenia">Schizophrenia</a></li> <li><a title="Selegiline" href="/wiki/Selegiline">Selegiline</a></li> <li><a title="Serotonin" href="/wiki/Serotonin">Serotonin</a></li></ul></div><h2>[<a title="Edit section: References" href="/w/index.php?title=Dopamine&action=edit&section=35">edit</a>] References</h2><div style="column-count: 2; -moz-column-count: 2; -webkit-column-count: 2" class="references-small references-column-count references-column-count-2"><ol class="references"> <li id="cite_note-0"><a href="#cite_ref-0">^</a> <a class="external free" href="http://www.encyclopedia.com/doc/1O87-ventraltegmentalarea.html" rel="nofollow">http://www.encyclopedia.com/doc/1O87-ventraltegmentalarea.html</a> Reference for VTA.</li> <li id="cite_note-1"><a href="#cite_ref-1">^</a> <a class="external text" href="http://movementdisorders.org/education/onlinecme/levodopa/print.pdf" rel="nofollow">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.</a></li> <li id="cite_note-2"><a href="#cite_ref-2">^</a> Benes, F.M. Carlsson and the discovery of dopamine. Trends in Pharmacological Sciences, Volume 22, Issue 1, 1 January 2001, Pages 46-47.</li> <li id="cite_note-3"><a href="#cite_ref-3">^</a> <a class="external autonumber" href="http://www.jneurosci.org/cgi/content/abstract/22/2/389" rel="nofollow">[1]</a></li> <li id="cite_note-4"><a href="#cite_ref-4">^</a> <a class="external autonumber" href="http://www.jneurosci.org/cgi/content/abstract/27/38/10196" rel="nofollow">[2]</a></li> <li id="cite_note-dopamine_function-5"><a href="#cite_ref-dopamine_function_5-0">^</a> Peter Redgrave, Kevin Gurney (2006). "The short-latency dopamine signal: a role in discovering novel actions?". 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(2007). <a class="external text" href="http://bloodjournal.hematologylibrary.org/cgi/reprint/109/2/632" rel="nofollow">Human CD4+CD25+ regulatory T cells selectively express tyrosine hydroxylase and contain endogenous catecholamines subserving an autocrine/paracrine inhibitory functional loop.</a> Blood. 109(2):632-42. <a class="external mw-magiclink-pmid" href="http://www.ncbi.nlm.nih.gov/pubmed/16985181">PMID 16985181</a></li> <li id="cite_note-64"><a href="#cite_ref-64">^</a> 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. <a title="Digital object identifier" href="/wiki/Digital_object_identifier">doi</a>:<a class="external text" href="http://dx.doi.org/10.1016%2Fj.bbi.2009.10.015" rel="nofollow">10.1016/j.bbi.2009.10.015</a> <a class="external mw-magiclink-pmid" href="http://www.ncbi.nlm.nih.gov/pubmed/19896530">PMID 19896530</a></li> <li id="cite_note-65"><a href="#cite_ref-65">^</a> <a class="external text" href="http://www.circ.ahajournals.org/cgi/content/full/117/2/200" rel="nofollow">"Renal Vasodilatory Action of Dopamine in Patients With Heart Failure: Magnitude of Effect and Site of Action"</a>. Circulation. 2008;117:200-205. <a class="external free" href="http://www.circ.ahajournals.org/cgi/content/full/117/2/200" rel="nofollow">http://www.circ.ahajournals.org/cgi/content/full/117/2/200</a>. Retrieved 2009-04-20.<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=bookitem&rft.btitle=Renal+Vasodilatory+Action+of+Dopamine+in+Patients+With+Heart+Failure%3A+Magnitude+of+Effect+and+Site+of+Action&rft.atitle=&rft.pub=Circulation.+2008%3B117%3A200-205&rft_id=http%3A%2F%2Fwww.circ.ahajournals.org%2Fcgi%2Fcontent%2Ffull%2F117%2F2%2F200&rfr_id=info:sid/en.wikipedia.org:Dopamine"> </li> <li id="cite_note-pharmnemonics-66">^ <a href="#cite_ref-pharmnemonics_66-0">a</a> <a href="#cite_ref-pharmnemonics_66-1">정의b <a href="#cite_ref-pharmnemonics_66-~~히드록시티라민으로서 생리활성 아민~~2">c</a> Shen, Howard (2008). Illustrated Pharmacology Memory Cards: PharMnemonics. Minireview. pp.&~~middot~~nbsp;~~카테콜아민의 일종~~8. <a title="International Standard Book Number" href="/wiki/International_Standard_Book_Number"> ISBN</a> <a title="Special:BookSources/1-59541-101-1" href="/wiki/Special:BookSources/1-59541-101-1">1-59541-101-1</a>.<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Abook&rft.genre=book&rft.btitle=Illustrated+Pharmacology+Memory+Cards%3A+PharMnemonics&rft.aulast=Shen%2C+Howard&rft.au=Shen%2C+Howard&rft.date=2008&rft.pages=pp.%26nbsp%3B8&rft.pub=Minireview&rft.isbn=1-59541-101-1&rfr_id=info:sid/en.wikipedia.org:Dopamine">  </li> <liid="cite_note-67"><a href="#cite_ref-67">^</a> <a class="external text" href="http://www.drugs.com/pro/dopamine-and-dextrose.html" rel="nofollow">"Dopamine and Dextrose"</a>. Drugs.com. <a class="external free" href="http://www.drugs.com/pro/dopamine-and-dextrose.html" rel="nofollow">http://www.drugs.com/pro/dopamine-and-dextrose.html</a>. 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A review". <a title="Phytochemistry (journal)" href="/wiki/Phytochemistry_(journal)">Phytochemistry</a> 67 (21): 2318–2331. <a title="Digital object identifier" href="/wiki/Digital_object_identifier">doi</a>:<a class="external text" href="http://dx.doi.org/10.1016%2Fj.phytochem.2006.08.006" rel="nofollow">10.1016/j.phytochem.2006.08.006</a>. <a class="mw-redirect" title="PubMed Identifier" href="/wiki/PubMed_Identifier">PMID</a> <a class="external text" href="http://www.ncbi.nlm.nih.gov/pubmed/16973188" rel="nofollow">16973188</a>.<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Polyphenol+oxidases+in+plants+and+fungi%3A+Going+places%3F+A+review&rft.jtitle=%5B%5BPhytochemistry+%28journal%29%7CPhytochemistry%5D%5D&rft.aulast=Mayer%2C+AM&rft.au=Mayer%2C+AM&rft.date=2006&rft.volume=67&rft.issue=21&rft.pages=2318%E2%80%932331&rft_id=info:doi/10.1016%2Fj.phytochem.2006.08.006&rft_id=info:pmid/16973188&rfr_id=info:sid/en.wikipedia.org:Dopamine"> </li></ol></div><h2>External links</h2><table style="BORDER-BOTTOM: #aaa 1px solid; BORDER-LEFT: #aaa 1px solid; BACKGROUND-COLOR: #f9f9f9; BORDER-TOP: #aaa 1px solid; BORDER-RIGHT: #aaa 1px solid" class="metadata mbox-small plainlinks"> <tbody> <tr> <td class="mbox-image"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/f/f8/Wiktionary-logo-en.svg/37px-Wiktionary-logo-en.svg.png" width="37" height="40" /></td> <td class="mbox-text">Look up <a class="extiw" title="wiktionary:Dopamine" href="http://en.wiktionary.org/wiki/Dopamine">Dopamine</a> in <a title="Wiktionary" href="/wiki/Wiktionary">Wiktionary</a>, the free dictionary.</td> </tr> </tbody></table><ul> <li><a title="DrugBank" href="/wiki/DrugBank">내용DrugBank <a class="external text" href="http://redpoll.pharmacy.ualberta.ca/drugbank/cgi-~~호르몬이나~~bin/getCard.cgi?CARD=APRD00085.txt" rel="nofollow">APRD00085</a></li> <li><a class="external text" href="http://druginfo.nlm.nih.gov/drugportal/dpdirect.jsp?name=Dopamine" rel="nofollow"> ~~신경전달물질로서 중요한 노르에피네프린과 에피네프린 합성체의~~U.S. National Library of Medicine: Drug Information Portal - Dopamine ~~전구물질~~ </li></ul><ul> <li></li> <li></li> <li>[[도파민]] </li>

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