Dopamine structure
Skeletal formula of dopamine
Ball-and-stick model of the dopamine molecule as found in solution. In the solid state, dopamine adopts a zwitterionic form.[1][2]
Clinical data
Other names
  • DA,
  • 2-(3,4-Dihydroxyphenyl)ethylamine,
  • 3,4-Dihydroxyphenethylamine,
  • 3-Hydroxytyramine,
  • Oxytyramine,
  • Prolactin inhibiting factor,
  • Prolactin inhibiting hormone,
  • Intropin,
  • Revivan
Physiological data
Source tissuesSubstantia nigra; ventral tegmental area; many others
Target tissuesSystem-wide
ReceptorsD1, D2, D3, D4, D5, TAAR1[3]
AgonistsDirect: apomorphine, bromocriptine
Indirect: cocaine, amphetamine
AntagonistsNeuroleptics, metoclopramide, domperidone
PrecursorPhenylalanine, tyrosine, and L-DOPA
BiosynthesisDOPA decarboxylase
MetabolismMAO, COMT[3]
  • 4-(2-Aminoethyl)benzene-1,2-diol
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.000.101 Edit this at Wikidata
Chemical and physical data
Molar mass153.181 g·mol−1
3D model (JSmol)
  • NCCc1cc(O)c(O)cc1
  • InChI=1S/C8H11NO2/c9-4-3-6-1-2-7(10)8(11)5-6/h1-2,5,10-11H,3-4,9H2

Dopamine (DA, a contraction of 3,4-dihydroxyphenethylamine) is a neuromodulatory molecule that plays several important roles in cells. It is an 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 chemical, L-DOPA, which is 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 neurons (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 dopamine pathways, one of which plays a major role in the motivational component of reward-motivated behavior. The anticipation of most types of rewards increases the level of dopamine in the brain,[4] and many addictive drugs increase dopamine release or block its reuptake into neurons following release.[5] Other brain dopamine pathways are involved in motor control and in controlling the release of various hormones. These pathways and cell groups form a dopamine system which is neuromodulatory.[5]

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;[6][7][8] 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.[8][9] It is the endocannabinoid, 2-Arachidonoylglycerol (2-AG: C23H38O4; 20:4, ω-6) that shape accumbal encoding of cue-motivated behavior via CB1 receptor activation in the ventral tegmentum, and thereby modulates cue-evoked dopamine transients during the pursuit of reward.[10]

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 (at normal concentrations); in the kidneys, it increases sodium excretion and urine output; in the pancreas, it reduces insulin production; in the digestive system, it reduces 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.

Several important diseases of the nervous system are associated with dysfunctions of the dopamine system, and some of the key medications used to treat them work by altering the effects of dopamine. Parkinson's disease, a degenerative condition causing tremor and motor impairment, is caused by a loss of dopamine-secreting neurons in an area of the midbrain called the substantia nigra. Its metabolic precursor L-DOPA can be manufactured; Levodopa, a pure form of L-DOPA, is the most widely used treatment for Parkinson's. There is evidence that schizophrenia involves altered levels of dopamine activity, and most antipsychotic drugs used to treat this are dopamine antagonists which reduce dopamine activity.[11] Similar dopamine antagonist drugs are also some of the most effective anti-nausea agents. Restless legs syndrome and attention deficit hyperactivity disorder (ADHD) are associated with decreased dopamine activity.[12] Dopaminergic stimulants can be addictive in high doses, but some are used at lower doses to treat ADHD. Dopamine itself is available as a manufactured medication for intravenous injection: although it cannot reach the brain from the bloodstream, its peripheral effects make it useful in the treatment of heart failure or shock, especially in newborn babies.

  1. ^ Cruickshank L, Kennedy AR, Shankland N (2013). "CSD Entry TIRZAX: 5-(2-Ammonioethyl)-2-hydroxyphenolate, Dopamine". Cambridge Structural Database: Access Structures. Cambridge Crystallographic Data Centre. doi:10.5517/cc10m9nl.
  2. ^ Cruickshank L, Kennedy AR, Shankland N (2013). "Tautomeric and ionisation forms of dopamine and tyramine in the solid state". J. Mol. Struct. 1051: 132–36. Bibcode:2013JMoSt1051..132C. doi:10.1016/j.molstruc.2013.08.002.
  3. ^ a b Cite error: The named reference DA IUPHAR was invoked but never defined (see the help page).
  4. ^ Berridge KC (April 2007). "The debate over dopamine's role in reward: the case for incentive salience". Psychopharmacology. 191 (3): 391–431. doi:10.1007/s00213-006-0578-x. PMID 17072591. S2CID 468204.
  5. ^ a b Wise RA, Robble MA (January 2020). "Dopamine and Addiction". Annual Review of Psychology. 71 (1): 79–106. doi:10.1146/annurev-psych-010418-103337. PMID 31905114. S2CID 210043316.
  6. ^ Cite error: The named reference NAcc function was invoked but never defined (see the help page).
  7. ^ Baliki MN, Mansour A, Baria AT, Huang L, Berger SE, Fields HL, Apkarian AV (October 2013). "Parceling human accumbens into putative core and shell dissociates encoding of values for reward and pain". The Journal of Neuroscience. 33 (41): 16383–93. doi:10.1523/JNEUROSCI.1731-13.2013. PMC 3792469. PMID 24107968.
  8. ^ a b Wenzel JM, Rauscher NA, Cheer JF, Oleson EB (January 2015). "A role for phasic dopamine release within the nucleus accumbens in encoding aversion: a review of the neurochemical literature". ACS Chemical Neuroscience. 6 (1): 16–26. doi:10.1021/cn500255p. PMC 5820768. PMID 25491156. 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 colleagues112 showing that, in anesthetized rats, the termination of tail pinch results in augmented dopamine release in the shell.
  9. ^ Puglisi-Allegra S, Ventura R (June 2012). "Prefrontal/accumbal catecholamine system processes high motivational salience". Front. Behav. Neurosci. 6: 31. doi:10.3389/fnbeh.2012.00031. PMC 3384081. PMID 22754514.
  10. ^ Oleson, Erik B. (26 January 2013). "Endocannabinoids shape accumbal encoding of cue-motivated behavior via CB1 receptor activation in the ventral tegmentum". Neuron. 73 (2): 360–373. doi:10.1016/j.neuron.2011.11.018. PMC 3269037. PMID 22284189.
  11. ^ Moncrieff J (2008). The myth of the chemical cure. A critique of psychiatric drug treatment. Basingstoke, UK: Palgrave MacMillan. ISBN 978-0-230-57432-8.
  12. ^ Volkow ND, Wang GJ, Kollins SH, Wigal TL, Newcorn JH, Telang F, Fowler JS, Zhu W, Logan J, Ma Y, Pradhan K, Wong C, Swanson JM (September 2009). "Evaluating dopamine reward pathway in ADHD: clinical implications". JAMA. 302 (10): 1084–91. doi:10.1001/jama.2009.1308. PMC 2958516. PMID 19738093.

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