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{{short description|Organic chemical that functions both as a hormone and a neurotransmitter}}
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{{About|the neurotransmitter|medical uses|Dopamine (medication)|other uses}}
{{Good article}}
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| drug_name =
| IUPAC_name = 4-(2-Aminoethyl)benzene-1,2-diol
| synonyms = {{ubl|DA, |2-(3,4-Dihydroxyphenyl)ethylamine, |3,4-Dihydroxyphenethylamine, |3-Hydroxytyramine, |Oxytyramine,
| image = Dopamine.svg
| alt = Dopamine structure
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| target_tissues = System-wide
| receptors = [[Dopamine receptor D1|D<sub>1</sub>]], [[Dopamine receptor D2|D<sub>2</sub>]], [[Dopamine receptor D3|D<sub>3</sub>]], [[Dopamine receptor D4|D<sub>4</sub>]], [[Dopamine receptor D5|D<sub>5</sub>]], [[TAAR1]]<ref name="DA IUPHAR"/>
| agonists = Direct: [[apomorphine]], [[bromocriptine]]<br/>[[Indirect agonist|Indirect]]: [[cocaine]], [[amphetamine]],[[methylphenidate]]
| antagonists = [[Neuroleptic]]s, [[metoclopramide]], [[domperidone]]
| precursor = [[Phenylalanine]], [[tyrosine]], and [[L-DOPA]]
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'''Dopamine''' ('''DA''', a contraction of '''3,4-<u>d</u>ihydr<u>o</u>xy<u>p</u>henethyl<u>amine</u>''') is a [[neuromodulatory]] [[molecule]] that plays several important roles in cells. It is an [[organic compound|organic chemical]] of the [[catecholamine]] and [[phenethylamine]] families. Dopamine constitutes about 80% of the catecholamine content in the brain. It is an [[amine]] synthesized by removing a [[carboxyl group]] from a molecule of its [[precursor (chemistry)|precursor chemical]], [[L-DOPA]], which is [[biosynthesis|synthesized]] in the brain and kidneys. Dopamine is also synthesized in plants and most animals. In the brain, dopamine functions as a [[neurotransmitter]]—a chemical released by [[neuron]]s (nerve cells) to send signals to other nerve cells. Neurotransmitters are synthesized in specific regions of the brain, but affect many regions systemically. The brain includes several distinct [[dopaminergic pathway|dopamine pathways]], one of which plays a major role in the motivational component of [[reward system|reward-motivated behavior]]. The anticipation of most types of rewards increases the level of dopamine in the brain,<ref>{{cite journal |vauthors=Berridge KC |date=April 2007 |title=The debate over dopamine's role in reward: the case for incentive salience |journal=Psychopharmacology |language=en-US |volume=191 |issue=3 |pages=391–431 |doi=10.1007/s00213-006-0578-x |pmid=17072591 |s2cid=468204}}</ref> and many [[addiction|addictive]] [[Psychoactive drug|drugs]] increase dopamine release or block its [[reuptake]] into neurons following release.<ref name="Wise2020">{{cite journal |vauthors=Wise RA, Robble MA |date=January 2020 |title=Dopamine and Addiction |journal=Annual Review of Psychology |language=en-US |volume=71 |issue=1 |pages=79–106 |doi=10.1146/annurev-psych-010418-103337 |pmid=31905114 |s2cid=210043316 |doi-access=free}}</ref> Other brain dopamine pathways are involved in [[motor system|motor control]] and in controlling the release of various hormones. These pathways and [[dopaminergic cell groups|cell groups]] form a dopamine system which is [[neuromodulation|neuromodulatory]].<ref name="Wise2020"/>
In [[popular culture]] and media, dopamine is often portrayed as the main chemical of pleasure, but the current opinion in pharmacology is that dopamine instead confers [[motivational salience]];<ref name="NAcc function" /><ref name="pmid24107968">{{cite journal |vauthors=Baliki MN, Mansour A, Baria AT, Huang L, Berger SE, Fields HL, Apkarian AV |date=October 2013 |title=Parceling human accumbens into putative core and shell dissociates encoding of values for reward and pain |journal=The Journal of Neuroscience |language=en-US |volume=33 |issue=41 |pages=16383–93 |doi=10.1523/JNEUROSCI.1731-13.2013 |pmc=3792469 |pmid=24107968 |quote=<!--Recent evidence indicates that inactivation of D2 receptors, in the indirect striatopallidal pathway in rodents, is necessary for both acquisition and expression of aversive behavior, and direct pathway D1 receptor activation controls reward-based learning (Hikida et al., 2010; Hikida et al., 2013). It seems we can conclude that direct and indirect pathways of the NAc, via D1 and D2 receptors, subserve distinct anticipation and valuation roles in the shell and core of NAc, which is consistent with observations regarding spatial segregation and diversity of responses of midbrain dopaminergic neurons for rewarding and aversive conditions, some encoding motivational value, others motivational salience, each connected with distinct brain networks and having distinct roles in motivational control (Bromberg-Martin et al., 2010; Cohen et al., 2012; Lammel et al., 2013). ... Thus, the previous results, coupled with the current observations, imply that the NAc pshell response reflects a prediction/anticipation or salience signal, and the NAc pcore response is a valuation response (reward predictive signal) that signals the negative reinforcement value of cessation of pain (i.e., anticipated analgesia). -->}}</ref><ref name="Aversion neurons">{{cite journal |vauthors=Wenzel JM, Rauscher NA, Cheer JF, Oleson EB |date=January 2015 |title=A role for phasic dopamine release within the nucleus accumbens in encoding aversion: a review of the neurochemical literature |journal=ACS Chemical Neuroscience |language=en-US |volume=6 |issue=1 |pages=16–26 |doi=10.1021/cn500255p |pmc=5820768 |pmid=25491156 |quote=Thus, fear-evoking stimuli are capable of differentially altering phasic dopamine transmission across NAcc subregions. The authors propose that the observed enhancement in NAcc shell dopamine likely reflects general motivational salience, perhaps due to relief from a CS-induced fear state when the US (foot shock) is not delivered. This reasoning is supported by a report from Budygin and colleagues<sup>112</sup> showing that, in anesthetized rats, the termination of tail pinch results in augmented dopamine release in the shell.}}</ref> in other words, dopamine signals the perceived motivational prominence (i.e., the desirability or aversiveness) of an outcome, which in turn propels the organism's behavior toward or away from achieving that outcome.<ref name="Aversion neurons" /><ref name="Motivational salience">{{cite journal | vauthors = Puglisi-Allegra S, Ventura R | title = Prefrontal/accumbal catecholamine system processes high motivational salience | journal = Front. Behav. Neurosci. | volume = 6 | page = 31 | date = June 2012 | pmid = 22754514 | pmc = 3384081 | doi = 10.3389/fnbeh.2012.00031 | quote = <!--Motivational salience regulates the strength of goal seeking, the amount of risk taken, and the energy invested from mild to extreme. ... Motivation can be conceptually described as a continuum along which stimuli can either reinforce or punish responses to other stimuli. Behaviorally, stimuli that reinforce are called rewarding and those that punish aversive (Skinner, 1953). Reward and aversion describe the impact a stimulus has on behavior, and provided of motivational properties, thus able to induce attribution of motivational salience. ... Attribution of motivational salience is related to the salience of an UCS (Dallman et al., 2003; Pecina et al., 2006). Thus, the more salient an UCS the more likely a neutral (to-be-conditioned) stimulus will be associated with it through motivational salience attribution. Prior experience is a major determinant of the motivational impact of any given stimulus (Borsook et al., 2007) and emotional arousal induced by motivational stimuli increases the attention given to stimuli influencing both the initial perceptual encoding and the consolidation process (Anderson et al., 2006; McGaugh, 2006).-->| doi-access = free
Outside the central nervous system, dopamine functions primarily as a local [[paracrine]] messenger. In blood vessels, it inhibits [[norepinephrine]] release and acts as a [[vasodilator]]; in the kidneys, it increases sodium excretion and urine output; in the pancreas, it reduces insulin production; in the digestive system, it reduces [[Gastrointestinal physiology#Motility|gastrointestinal motility]] and protects [[intestinal mucosa]]; and in the immune system, it reduces the activity of [[lymphocytes]]. With the exception of the blood vessels, dopamine in each of these peripheral systems is synthesized locally and exerts its effects near the cells that release it.
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[[Dopaminergic]] neurons (dopamine-producing nerve cells) are comparatively few in number—a total of around 400,000 in the human brain<ref name=SchultzAnnRev>{{cite journal | vauthors = Schultz W | s2cid = 13503219 | title = Multiple dopamine functions at different time courses | journal = Annual Review of Neuroscience | volume = 30 | pages = 259–88 | year = 2007 | pmid = 17600522 | doi = 10.1146/annurev.neuro.28.061604.135722 }}</ref>—and their [[soma (biology)|cell bodies]] are confined in groups to a few relatively small brain areas.<ref name=Bjorklund/> However their [[axon]]s project to many other brain areas, and they exert powerful effects on their targets.<ref name=Bjorklund/> These dopaminergic cell groups were first mapped in 1964 by [[Annica Dahlström]] and Kjell Fuxe, who assigned them labels starting with the letter "A" (for "aminergic").<ref name=DahlstromFuxe>{{cite journal | vauthors = Dahlstroem A, Fuxe K | title = Evidence for the existence of monoamine-containing neurons in the central nervous system. I. Demonstration of monoamines in the cell bodies of brain stem neurons | journal = Acta Physiologica Scandinavica. Supplementum | volume = 232 | issue = Suppl | pages = 1–55 | year = 1964 | pmid = 14229500 }}</ref> In their scheme, areas A1 through A7 contain the neurotransmitter norepinephrine, whereas A8 through A14 contain dopamine. The dopaminergic areas they identified are the substantia nigra (groups 8 and 9); the [[ventral tegmental area]] (group 10); the posterior [[hypothalamus]] (group 11); the [[arcuate nucleus]] (group 12); the [[zona incerta]] (group 13) and the [[periventricular nucleus]] (group 14).<ref name=DahlstromFuxe/>
The substantia nigra is a small midbrain area that forms a component of the [[basal ganglia]]. This has two parts—an input area called the [[pars
The [[ventral tegmental area]] (VTA) is another midbrain area. The most prominent group of VTA dopaminergic neurons projects to the prefrontal cortex via the [[mesocortical pathway]] and another smaller group projects to the nucleus accumbens via the [[mesolimbic pathway]]. Together, these two pathways are collectively termed the ''[[mesocorticolimbic projection]]''.<ref name=Bjorklund/><ref name="Malenka pathways" /> The VTA also sends dopaminergic projections to the [[amygdala]], [[cingulate gyrus]], [[hippocampus]], and [[olfactory bulb]].<ref name=Bjorklund/><ref name="Malenka pathways">{{cite book | vauthors = Malenka RC, Nestler EJ, Hyman SE | veditors = Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | pages = 147–48, 154–57 | edition = 2nd | chapter = Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin }}</ref> Mesocorticolimbic neurons play a central role in reward and other aspects of motivation.<ref name="Malenka pathways" /> Accumulating literature shows that dopamine also plays a crucial role in aversive learning through its effects on a number of brain regions.<ref>{{cite journal | vauthors = Fadok JP, Dickerson TM, Palmiter RD | title = Dopamine is necessary for cue-dependent fear conditioning | journal = The Journal of Neuroscience | volume = 29 | issue = 36 | pages = 11089–97 | date = September 2009 | pmid = 19741115 | pmc = 2759996 | doi = 10.1523/JNEUROSCI.1616-09.2009 }}</ref><ref>{{cite journal | vauthors = Tang W, Kochubey O, Kintscher M, Schneggenburger R | title = A VTA to basal amygdala dopamine projection contributes to signal salient somatosensory events during fear learning | journal = The Journal of Neuroscience | pages = JN–RM–1796-19 | date = April 2020 | volume = 40 | issue = 20 | pmid = 32277045 | doi = 10.1523/JNEUROSCI.1796-19.2020 | pmc = 7219297 }}</ref><ref>{{cite journal | vauthors = Jo YS, Heymann G, Zweifel LS | title = Dopamine Neurons Reflect the Uncertainty in Fear Generalization | language = en | journal = Neuron | volume = 100 | issue = 4 | pages = 916–925.e3 | date = November 2018 | pmid = 30318411 | pmc = 6226002 | doi = 10.1016/j.neuron.2018.09.028 }}</ref>
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The posterior hypothalamus has dopamine neurons that project to the spinal cord, but their function is not well established.<ref name=Paulus/> There is some evidence that pathology in this area plays a role in restless legs syndrome, a condition in which people have difficulty sleeping due to an overwhelming compulsion to constantly move parts of the body, especially the legs.<ref name=Paulus>{{cite journal | vauthors = Paulus W, Schomburg ED | title = Dopamine and the spinal cord in restless legs syndrome: does spinal cord physiology reveal a basis for augmentation? | journal = Sleep Medicine Reviews | volume = 10 | issue = 3 | pages = 185–96 | date = June 2006 | pmid = 16762808 | doi = 10.1016/j.smrv.2006.01.004 }}</ref>
The arcuate nucleus and the periventricular nucleus of the hypothalamus have dopamine neurons that form an important projection—the ''[[tuberoinfundibular pathway]]'' which goes to the [[pituitary gland]], where it influences the secretion of the hormone [[prolactin]].<ref name=BenJonathan/> Dopamine is the primary [[neuroendocrine]] inhibitor of the secretion of [[prolactin]] from the [[anterior pituitary]] gland.<ref name=BenJonathan/> Dopamine produced by neurons in the arcuate nucleus is secreted into the [[hypophyseal portal system]] of the [[median eminence]], which supplies the [[pituitary gland]].<ref name=BenJonathan/> The [[prolactin cell]]s that produce prolactin, in the absence of dopamine, secrete prolactin continuously; dopamine inhibits this secretion
The zona incerta, grouped between the arcuate and periventricular nuclei, projects to several areas of the hypothalamus, and participates in the control of [[gonadotropin-releasing hormone]], which is necessary to activate the development of the [[male reproductive system|male]] and [[female reproductive system]]s, following puberty.<ref name=BenJonathan/>
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====Pleasure====
While dopamine has a central role in causing "wanting," associated with the appetitive or approach behavioral responses to rewarding stimuli, detailed studies have shown that dopamine cannot simply be equated with hedonic "liking" or pleasure, as reflected in the consummatory behavioral response.<ref name=Robinson/> Dopamine neurotransmission is involved in some but not all aspects of pleasure-related cognition, since [[pleasure center]]s have been identified both within the dopamine system (i.e., nucleus accumbens shell) and outside the dopamine system (i.e., [[ventral pallidum]] and [[parabrachial nucleus]]).<ref name=Robinson/><ref name=Berridge2/><ref name="Pleasure system">{{cite journal | vauthors = Berridge KC, Kringelbach ML | title = Pleasure systems in the brain | journal = Neuron | volume = 86 | issue = 3 | pages = 646–64 | date = May 2015 | pmid = 25950633 | pmc = 4425246 | doi = 10.1016/j.neuron.2015.02.018 }}</ref> For example, [[Brain stimulation reward|direct electrical stimulation]] of dopamine pathways, using electrodes implanted in the brain, is experienced as pleasurable, and many types of animals are willing to work to obtain it.<ref name=Wise/> [[Antipsychotic drug]]s reduce dopamine levels and tend to cause [[anhedonia]], a diminished ability to experience pleasure.<ref name="Wise2">{{cite journal | vauthors = Wise RA | title = Dopamine and reward: the anhedonia hypothesis 30 years on | journal = Neurotoxicity Research | volume = 14 | issue = 2–3 | pages = 169–83 | date = October 2008 | pmid = 19073424 | pmc = 3155128 | doi = 10.1007/BF03033808 }}</ref> Many types of pleasurable experiences—such as sexual intercourse, eating, and playing video games—increase dopamine release.<ref name="fn5">{{cite journal |vauthors=Arias-Carrión O, Pöppel E |title=Dopamine, learning and reward-seeking behavior |journal=Acta Neurobiol Exp |volume=67 |issue=4 |pages=481–88 |year=2007|doi=10.55782/ane-2007-1664 |pmid=18320725 |doi-access=free }}</ref> All addictive drugs directly or indirectly affect dopamine neurotransmission in the nucleus accumbens;<ref name="NAcc function" /><ref name=Wise/> these drugs increase drug "wanting", leading to compulsive drug use, when repeatedly taken in high doses, presumably through the [[Addiction#Reward sensitization|sensitization of incentive-salience]].<ref name=Berridge2 /> Drugs that increase synaptic dopamine concentrations include [[psychostimulant]]s such as methamphetamine and cocaine. These produce increases in "wanting" behaviors, but do not greatly alter expressions of pleasure or change levels of satiation.<ref name=Berridge2/><ref name=Wise>{{cite journal | vauthors = Wise RA | title = Addictive drugs and brain stimulation reward | journal = Annual Review of Neuroscience | volume = 19 | pages = 319–40 | year = 1996 | pmid = 8833446 | doi = 10.1146/annurev.ne.19.030196.001535 }}</ref> However, [[opiate]] drugs such as heroin and morphine produce increases in expressions of "liking" and "wanting" behaviors.<ref name=Berridge2/> Moreover, animals in which the ventral tegmental dopamine system has been rendered inactive do not seek food, and will starve to death if left to themselves, but if food is placed in their mouths they will consume it and show expressions indicative of pleasure.<ref>{{cite journal | vauthors = Ikemoto S | title = Dopamine reward circuitry: two projection systems from the ventral midbrain to the nucleus accumbens-olfactory tubercle complex | journal = Brain Research Reviews | volume = 56 | issue = 1 | pages = 27–78 | date = November 2007 | pmid = 17574681 | pmc = 2134972 | doi = 10.1016/j.brainresrev.2007.05.004 }}</ref>
A clinical study from January 2019 that assessed the effect of a dopamine precursor ([[levodopa]]), dopamine antagonist ([[risperidone]]), and a placebo on reward responses to music – including the degree of pleasure experienced during [[musical chill]]s, as measured by changes in [[electrodermal activity]] as well as subjective ratings – found that the manipulation of dopamine neurotransmission bidirectionally regulates pleasure cognition (specifically, the [[Euphoria#Music-induced|hedonic impact of music]]) in human subjects.<ref name="Dopaminergic control of hedonic impact" /><ref name="Secondary source for 'Dopaminergic control of hedonic impact'" /> This research demonstrated that increased dopamine neurotransmission acts as a ''[[sine qua non]]'' condition for pleasurable hedonic reactions to music in humans.<ref name="Dopaminergic control of hedonic impact">{{cite journal | vauthors = Ferreri L, Mas-Herrero E, Zatorre RJ, Ripollés P, Gomez-Andres A, Alicart H, Olivé G, Marco-Pallarés J, Antonijoan RM, Valle M, Riba J, Rodriguez-Fornells A | title = Dopamine modulates the reward experiences elicited by music | journal = Proceedings of the National Academy of Sciences of the United States of America | year = 2019 | volume = 116| issue = 9| pages = 3793–98 | pmid = 30670642 | pmc = 6397525 | doi = 10.1073/pnas.1811878116 | bibcode = 2019PNAS..116.3793F | quote = Listening to pleasurable music is often accompanied by measurable bodily reactions such as goose bumps or shivers down the spine, commonly called "chills" or "frissons." ... Overall, our results straightforwardly revealed that pharmacological interventions bidirectionally modulated the reward responses elicited by music. In particular, we found that risperidone impaired participants' ability to experience musical pleasure, whereas levodopa enhanced it. ... Here, in contrast, studying responses to abstract rewards in human subjects, we show that manipulation of dopaminergic transmission affects both the pleasure (i.e., amount of time reporting chills and emotional arousal measured by EDA) and the motivational components of musical reward (money willing to spend). These findings suggest that dopaminergic signaling is a sine qua non condition not only for motivational responses, as has been shown with primary and secondary rewards, but also for hedonic reactions to music. This result supports recent findings showing that dopamine also mediates the perceived pleasantness attained by other types of abstract rewards (37) and challenges previous findings in animal models on primary rewards, such as food (42, 43).|doi-access = free }}</ref><ref name="Secondary source for 'Dopaminergic control of hedonic impact'">{{cite journal | vauthors = Goupil L, Aucouturier JJ | title = Musical pleasure and musical emotions | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 116 | issue = 9 | pages = 3364–66 | date = February 2019 | pmid = 30770455 | pmc = 6397567 | doi = 10.1073/pnas.1900369116 | bibcode = 2019PNAS..116.3364G | quote = In a pharmacological study published in PNAS, Ferreri et al. (1) present evidence that enhancing or inhibiting dopamine signaling using levodopa or risperidone modulates the pleasure experienced while listening to music. ... In a final salvo to establish not only the correlational but also the causal implication of dopamine in musical pleasure, the authors have turned to directly manipulating dopaminergic signaling in the striatum, first by applying excitatory and inhibitory transcranial magnetic stimulation over their participants' left dorsolateral prefrontal cortex, a region known to modulate striatal function (5), and finally, in the current study, by administrating pharmaceutical agents able to alter dopamine synaptic availability (1), both of which influenced perceived pleasure, physiological measures of arousal, and the monetary value assigned to music in the predicted direction. ... While the question of the musical expression of emotion has a long history of investigation, including in PNAS (6), and the 1990s psychophysiological strand of research had already established that musical pleasure could activate the autonomic nervous system (7), the authors' demonstration of the implication of the reward system in musical emotions was taken as inaugural proof that these were veridical emotions whose study has full legitimacy to inform the neurobiology of our everyday cognitive, social, and affective functions (8). Incidentally, this line of work, culminating in the article by Ferreri et al. (1), has plausibly done more to attract research funding for the field of music sciences than any other in this community.<br />The evidence of Ferreri et al. (1) provides the latest support for a compelling neurobiological model in which musical pleasure arises from the interaction of ancient reward/valuation systems (striatal–limbic–paralimbic) with more phylogenetically advanced perception/predictions systems (temporofrontal).| doi-access = free }}</ref>
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===Parkinson's disease===
Parkinson's disease is an age-related disorder characterized by [[movement disorder]]s such as stiffness of the body, slowing of movement, and trembling of limbs when they are not in use.<ref name=Jankovic>{{cite journal | vauthors = Jankovic J | title = Parkinson's disease: clinical features and diagnosis | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 79 | issue = 4 | pages = 368–76 | date = April 2008 | pmid = 18344392 | doi = 10.1136/jnnp.2007.131045 | url = http://jnnp.bmj.com/content/79/4/368.full | doi-access = free }}</ref> In advanced stages it progresses to [[dementia]] and eventually death.<ref name=Jankovic/> The main symptoms are caused by the loss of dopamine-secreting cells in the substantia nigra.<ref name=Dickson>{{cite book | vauthors = Dickson DV|chapter=Neuropathology of movement disorders | veditors = Tolosa E, Jankovic JJ| title=Parkinson's disease and movement disorders |publisher=Lippincott Williams & Wilkins |location=Hagerstown, MD |year=2007 |pages= 271–83 |isbn=978-0-7817-7881-7}}</ref> These dopamine cells are especially vulnerable to damage, and a variety of insults, including [[encephalitis]] (as depicted in the book and movie
The most widely used treatment for parkinsonism is administration of L-DOPA, the metabolic precursor for dopamine.<ref name="Nice-pharma"/> L-DOPA is converted to dopamine in the brain and various parts of the body by the enzyme DOPA decarboxylase.<ref name=Musacchio/> L-DOPA is used rather than dopamine itself because, unlike dopamine, it is capable of crossing the [[blood–brain barrier]].<ref name="Nice-pharma">{{cite book| chapter=Symptomatic pharmacological therapy in Parkinson's disease| editor=The National Collaborating Centre for Chronic Conditions| title=Parkinson's Disease| chapter-url=http://guidance.nice.org.uk/CG35/Guidance/pdf/English| access-date=24 September 2015| publisher=Royal College of Physicians| location=London| year=2006| isbn=978-1-86016-283-1| pages=59–100| archive-date=24 September 2010| archive-url=https://web.archive.org/web/20100924153546/http://guidance.nice.org.uk/CG35/Guidance/pdf/English| url-status=dead}}</ref> It is often co-administered with an [[enzyme inhibitor]] of peripheral [[decarboxylation]] such as [[carbidopa]] or [[benserazide]], to reduce the amount converted to dopamine in the periphery and thereby increase the amount of L-DOPA that enters the brain.<ref name="Nice-pharma"/> When L-DOPA is administered regularly over a long time period, a variety of unpleasant side effects such as [[dyskinesia]] often begin to appear; even so, it is considered the best available long-term treatment option for most cases of Parkinson's disease.<ref name="Nice-pharma"/>
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[[File:Bananas white background DS.jpg|thumb|right|Dopamine can be found in the [[Banana peel|peel]] and fruit pulp of [[bananas]].|alt=Photo of a bunch of bananas.]]
Many plants, including a variety of food plants, synthesize dopamine to varying degrees.<ref name=Kulma/> The highest concentrations have been observed in bananas—the fruit pulp of [[red banana|red]] and [[Cavendish banana|yellow bananas]] contains dopamine at levels of 40 to 50 parts per million by weight.<ref name=Kulma/> Potatoes, avocados, broccoli, and Brussels sprouts may also contain dopamine at levels of 1 part per million or more; oranges, tomatoes, spinach, beans, and other plants contain measurable concentrations less than 1 part per million.<ref name=Kulma>{{cite journal |vauthors=Kulma A, Szopa J |title=Catecholamines are active compounds in plants |journal=Plant Science |year=2007 |volume=172 |pages=433–40 |doi=10.1016/j.plantsci.2006.10.013 |issue=3|bibcode=2007PlnSc.172..433K }}</ref> The dopamine in plants is synthesized from the amino acid tyrosine, by biochemical mechanisms similar to those that animals use.<ref name=Kulma/> It can be metabolized in a variety of ways, producing [[melanin]] and a variety of [[alkaloid]]s as byproducts.<ref name=Kulma/> The functions of plant catecholamines have not been clearly established, but there is evidence that they play a role in the response to stressors such as bacterial infection, act as growth-promoting factors in some situations, and modify the way that sugars are metabolized. The receptors that mediate these actions have not yet been identified, nor have the intracellular mechanisms that they activate.<ref name=Kulma/>
Dopamine consumed in food cannot act on the brain, because it cannot cross the blood–brain barrier.<ref name="Nice-pharma"/> However, there are also a variety of plants that contain L-DOPA, the metabolic precursor of dopamine.<ref name=Ingle>{{cite journal | vauthors = Ingle PK |year=2003 |title=L-DOPA bearing plants |journal=Natural Product Radiance |volume=2 |pages=126–33 |url=http://nopr.niscair.res.in/bitstream/123456789/12261/1/NPR%202%283%29%20126-133.pdf |archive-url=https://web.archive.org/web/20140302114720/http://nopr.niscair.res.in/bitstream/123456789/12261/1/NPR%202%283%29%20126-133.pdf |archive-date=2014-03-02 |url-status=live |access-date=24 September 2015}}</ref> The highest concentrations are found in the leaves and bean pods of plants of the genus ''[[Mucuna]]'', especially in ''[[Mucuna pruriens]]'' (velvet beans), which have been used as a source for L-DOPA as a drug.<ref>{{cite journal |year=1993 |title=Occurrence of L-DOPA and dopamine in plants and cell cultures of ''Mucuna pruriens'' and effects of 2, 4-d and NaCl on these compounds |journal=Plant Cell, Tissue and Organ Culture |volume=33 |issue=3 |pages=259–64 |doi=10.1007/BF02319010 | vauthors = Wichers HJ, Visser JF, Huizing HJ, Pras N|s2cid=44814336 }}</ref> Another plant containing substantial amounts of L-DOPA is ''[[Vicia faba]]'', the plant that produces fava beans (also known as "broad beans"). The level of L-DOPA in the beans, however, is much lower than in the pod shells and other parts of the plant.<ref>{{cite journal | vauthors = Longo R, Castellani A, Sberze P, Tibolla M | title = Distribution of l-dopa and related amino acids in Vicia | journal = Phytochemistry | year = 1974 | volume = 13 | issue = 1 | pages = 167–71 | doi = 10.1016/S0031-9422(00)91287-1| bibcode = 1974PChem..13..167L }}</ref> The seeds of ''[[Cassia (genus)|Cassia]]'' and ''[[Bauhinia]]'' trees also contain substantial amounts of L-DOPA.<ref name=Ingle/>
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