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Dopamine

From Wikipedia
dopamine
type of chemical entity
Subclass ofcatecholamine, phenethylamine alkaloid Edit
Get useMedication Edit
Stylized nameDOPamine Edit
Chemical formulaC₈H₁₁NO₂ Edit
Canonical SMILESC1=CC(=C(C=C1CCN)O)O Edit
Medical condition treatedkidney disease, bradycardia, neurogenic shock Edit
Contributing factor ofdecision making Edit
Significant drug interactionphenelzine, linezolid, phenelzine, phenelzine, phenelzine Edit
ManufacturerPfizer Edit
Produced byDopaminergic cell groups Edit

Dopamine (DA, a contraction of 3,4-dihydroxyphenethylamine) be a neuromodulatory molecule wey dey play chaw important roles insyd cells. E be an organic chemical of de catecholamine den phenethylamine families. E be an amine synthesized by removing a carboxyl group from a molecule of ein precursor chemical, L-DOPA, wich be synthesized insyd de brain den kidneys. Dopamine sanso be synthesized insyd plants den chaw animals. Insyd de brain, dopamine dey function as a neurotransmitter—a chemical wey be released by neurons (nerve cells) to send signals to oda nerve cells. De brain dey include chaw distinct dopamine pathways, one of wich dey play a major role insyd de motivational component of reward-motivated behavior. De anticipation of chaw types of rewards dey increase de level of dopamine insyd de brain,[1] den chaw addictive drugs increase dopamine release anaa block ein reuptake into neurons dey follow release.[2] Oda brain dopamine pathways be involved insyd motor control den insyd controlling de release of various hormones. Dese pathways den cell groups dey form a dopamine system wich be neuromodulatory.[2]

Insyd popular culture den media, dopamine often be portrayed as de main chemical of pleasure, buh de current opinion insyd pharmacology be dat dopamine instead dey confer motivational salience;[3][4][5] insyd oda words, dopamine dey signal de perceived motivational prominence (i.e., de desirability anaa aversiveness) of an outcome, wich in turn dey propel de organism ein behavior toward anaa away from achieving dat outcome.[5][6]

Outsyd de central nervous system, dopamine dey function primarily as a local paracrine messenger. Insyd blood vessels, e dey inhibit norepinephrine release den dey act as a vasodilator; insyd de kidneys, e dey increase sodium excretion den urine output; insyd de pancreas, e dey reduce insulin production; insyd de digestive system, e dey reduce gastrointestinal motility den dey protect intestinal mucosa; den insyd de immune system, e dey reduce de activity of lymphocytes. Plus de exception of de blood vessels, dopamine insyd each of dese peripheral systems be synthesized locally den dey exert ein effects near de cells wey dey release am.

Chawl important diseases of de nervous system be associated plus dysfunctions of de dopamine system, den sam of de key medications dem use to treat dem dey work by altering de effects of dopamine. Parkinson's disease, a degenerative condition wey dey cause tremor den motor impairment, be caused by a loss of dopamine-secreting neurons insyd an area of de midbrain dem call de substantia nigra. Ein metabolic precursor L-DOPA fi be manufactured; Levodopa, a pure form of L-DOPA, be de most widely used treatment give Parkinson's. Der be evidence say schizophrenia dey involve altered levels of dopamine activity, den chaw antipsychotic drugs dem use to treat dis be dopamine antagonists wich dey reduce dopamine activity.[7] Similar dopamine antagonist drugs sanso be sam of de most effective anti-nausea agents. Restless legs syndrome den attention deficit hyperactivity disorder (ADHD) be associated plus decreased dopamine activity.[8] Dopaminergic stimulants fi be addictive insyd high doses, buh sam be used at lower doses to treat ADHD. Dopamine einself be available as a manufactured medication give intravenous injection. E be useful insyd de treatment of severe heart failure anaa cardiogenic shock.[9] Insyd newborn babies e fi be used for hypotension den septic shock.[10]

References

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  1. ↑ Berridge KC (April 2007). "The debate over dopamine's role in reward: the case for incentive salience". Psychopharmacology (in American English). 191 (3): 391–431. doi:10.1007/s00213-006-0578-x. PMID 17072591. S2CID 468204.
  2. 1 2 Wise RA, Robble MA (January 2020). "Dopamine and Addiction". Annual Review of Psychology (in American English). 71 (1): 79–106. doi:10.1146/annurev-psych-010418-103337. PMID 31905114. S2CID 210043316.
  3. ↑ Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (in American English) (2nd ed.). New York: McGraw-Hill Medical. pp. 147–48, 366–67, 375–76. ISBN 978-0-07-148127-4.
  4. ↑ 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 (in American English). 33 (41): 16383–93. doi:10.1523/JNEUROSCI.1731-13.2013. PMC 3792469. PMID 24107968.
  5. 1 2 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 (in American English). 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ "Dopamine infusion" (PDF). Retrieved 13 October 2023.
  10. ↑ "Shock and Hypotension in the Newborn Medication: Alpha/Beta Adrenergic Agonists, Vasodilators, Inotropic agents, Volume Expanders, Antibiotics, Other". emedicine.medscape.com (in American English). Retrieved 13 October 2023.

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