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For other uses, see Dopamine (disambiguation).

Dopamine Dopamine General Systematic name 	4-(2-aminoethyl)benzene-1,2-diol Other names 	2-(3,4-dihydroxyphenyl)ethylamine; 3,4-dihydroxyphenethylamine; 3-hydroxytyramine; DA; Intropin Revivan Molecular formula 	C8H11NO2 SMILES 	C1=CC(=C(C=C1CCN)O)O Molar mass 	153.18 g/mol Appearance 	white powder with distinctive smell CAS number 	[51-61-6] Properties Density and phase 	 ? g/cm3, ? Solubility in water 	 ? g/100 ml (? °C) Melting point 	128 °C (401 K) Boiling point 	 ? °C (? K) Acidity (pKa) 	 ? Basicity (pKb) 	 ? Chiral rotation [α]D 	 ?° Viscosity 	 ? cP at ? °C Structure Molecular shape 	 ? Coordination geometry 	 ? Crystal structure 	 ? Dipole moment 	 ? D Hazards MSDS 	External MSDS Main hazards 	 ? NFPA 704 	 ? Flash point 	 ? °C R/S statement 	R: 36/37/38 S: 26-36 RTECS number 	UX1088000 Supplementary data page Structure and properties 	n, εr, etc. Thermodynamic data 	Phase behaviour Solid, liquid, gas Spectral data 	UV, IR, NMR, MS Related compounds Other anions 	 ? Other cations 	 ? Related ? ? Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) Infobox disclaimer and references

Dopamine is a chemical naturally produced in the body. In the brain, dopamine functions as a neurotransmitter, activating dopamine receptors. Dopamine is also a neurohormone released by the hypothalamus. Its main function as a hormone is to inhibit the release of prolactin from the anterior lobe of the pituitary.

Dopamine can be supplied as a medication that acts on the sympathetic nervous system, producing effects such as increased heart rate and blood pressure. However, since dopamine cannot cross the blood-brain barrier, dopamine given as a drug does not directly affect the central nervous system. To increase the amount of dopamine in the brains of patients with diseases such as Parkinson's disease and Dopa-Responsive Dystonia, a synthetic precursor to dopamine such as L-DOPA can be given, since this will cross the blood-brain barrier. Contents [show]

* 1 Biochemistry * 2 Functions of dopamine in the brain o 2.1 Role in movement o 2.2 Role in cognition and frontal cortex function o 2.3 Role in regulating prolactin secretion o 2.4 Role in pleasure and motivation * 3 Dopamine and psychosis * 4 Therapeutic use * 5 Major dopamine pathways * 6 See also * 7 External links * 8 References

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Biochemistry

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

As a member of the catecholamine family, dopamine is a precursor to epinephrine (adrenaline) and norepinephrine (noradrenaline) in the biosynthetic pathways for these neurotransmitters. Arvid Carlsson won a share of the 2000 Nobel Prize in Physiology or Medicine for showing that dopamine is not just a precursor to these, but a neurotransmitter as well.

Dopamine is synthesized in the body (mainly by nervous tissue and adrenal glands) first by the dehydration of the amino acid tyrosine to DOPA by tyrosine hydroxylase and then by the decarboxylation of DOPA by aromatic-L-amino-acid decarboxylase. In neurons, dopamine is packaged after synthesis into vesicles, which are then released in response to the presynaptic action potential. The inactivation mechanism of neurotransmission are 1) uptake via a specific transporter; 2) enzymatic breakdown; and 3) diffusion. Uptake back to the presynaptic neuron via the dopamine transporter is the major role in the inactivation of dopamine neurotransmission. The recycled dopamine will face either breakdown by an enzyme or be re-packaged into vesicles and reused. [edit]

Functions of dopamine in the brain [edit]

Role in movement

Dopamine is critical to the way the brain controls our movements and is a crucial part of the basal ganglia motor loop. Shortage of dopamine, particularly the death of dopamine neurons in the nigrostriatal pathway, causes Parkinson's disease, in which a person loses the ability to execute smooth, controlled movements. [edit]

Role in cognition and frontal cortex function

In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention and problem-solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder and negative schizophrenia. [edit]

Role in regulating prolactin secretion

Dopamine is the primary neuroendocrine regulator of the secretion of prolactin from the anterior pituitary gland. Dopamine produced by neurons in the arcuate nucleus of the hypothalamus is secreted into the hypothalamo-hypophysial blood vessels of the median eminence, which supply the pituitary gland. The lactotrope cells that produce prolactin, in the absence of dopamine, secrete prolactin continuously; dopamine inhibits this secretion. [edit]

Role in pleasure and motivation

Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate us to do certain activities. Dopamine is released (particularly in areas such as the nucleus accumbens and striatum) by naturally-rewarding experiences such as food, sex, use of certain drugs and neutral stimuli that become associated with them. This theory is often discussed in terms of drugs (such as cocaine and amphetamines), which seem to be directly or indirectly related to the increase of dopamine in these areas, and in relation to neurobiological theories of chemical addiction, which argue that these dopamine pathways are pathologically altered in addicted persons. However, cocaine and amphetamine have different mechanisms of action. Cocaine is a dopamine transporter blocker: it competitively inhibits dopamine uptake to increase the lifetime of dopamine. On the other hand, amphetamines act as dopamine transporter substrates to competitively inhibit dopamine uptake and increase dopamine efflux via a dopamine transporter.

However, the idea that dopamine is the 'reward chemical' of the brain, a view held by many during early stages of its research, now seems too simple. Dopamine is released when unpleasant or aversive stimuli are encountered, so it is not associated only with 'rewards' or pleasure. Recent research has begun to examine whether or not the firing of dopamine neurons might function as a reward-prediction error signal, based on evidence that, when a reward is greater than expected, there is an increase in the firing of certain dopamine neurons (in contrast to when there is a lesser-than-expected reward, and there is a marked decrease in the firing of the same neurons). Some argue that dopamine may be involved in desire rather than pleasure.

Confusion of dopamine's role in pleasure comes from studies performed on animals. It has been shown experimentally that when the dopaminergic system of a rat is selectively abolished it will stop eating. However when the rat is force fed food it will still display the proper facial expressions which indicate whether they like or dislike it. Conversely mutant hyperdopaminergic mice show higher wanting of food but not liking.1 This research was taken to mean that dopamine mediated desire and incentive salience instead of pleasure. In humans, though, drugs that reduce dopamine activity (e.g., antipsychotics) have been shown to induce both amotivation (lack of desire) as well as anhedonia (inability to experience pleasure).2 The selective D2/D3 agonists pramipexole and ropinirole have anti-anhedonic and pro-motivational properties as measured by the Snaith-Hamilton Pleasure Scale.3 Opioid and cannabinoid transmission instead of dopamine is believed to be what modulates food reward and palatability (liking).4 This explains why animals would still have the same liking of food independent of brain dopamine concentrations. Other pleasures are likely dependent on dopamine. Libido can be increased by drugs that enhance dopaminergic functioning but not by ones that affect opioid peptides or other neurotransmitters. Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor binding is found in people with social anxiety. Traits common to negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a hypodopaminergic state in certain areas of the brain. In instances of bipolar mania subjects can become hypersocial as well as hypersexual. This is also believed to be due to an increase in dopamine, because it can be alleviated with dopamine blocking antipsychotics.

Other theories suggest that the crucial role of dopamine may be in predicting pleasurable activity. Related theories argue that dopamine function may be involved in the salience ('noticeableness') of perceived objects and events, with potentially important stimuli such as: 1) rewarding things or 2) dangerous or threatening things ~ seeming more noticeable or important. This hypothesis argues that dopamine assists decision-making by influencing the priority of such stimuli to the person concerned.

However, these theories are based on correlational, rather than causal, experimental evidence. The available evidence that examined causal relationships between dopamine and motivation does not seem to agree with any of the above-stated theories. For example, pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. The theories viewing dopamine as the mediator of 'desire/wanting,' 'predicting pleasurable activity,' 'noticeableness' or 'decision-making' cannot adequately explain this experimental evidence. Thus, the functional role of dopamine in motivation remains controversial.

Deficits in dopamine levels have also been implicated as one of several possible causes for Adult attention-deficit disorder (AADD), and some types of medications used to treat Attention-deficit hyperactivity disorder (ADHD/ADD) will help to stimulate dopaminergic systems, leading to potentially heightened, but preferably not distorted, sensation, for those who may be afflicted by it and be receiving treatment for it. [edit]

Dopamine and psychosis

Disruption to the dopamine system has also been strongly linked to psychosis and schizophrenia. Dopamine neurons in the mesolimbic pathway are particularly associated with these conditions. This is partly due to the discovery of a class of drugs called the phenothiazines (which block D2 dopamine receptors) that can reduce psychotic symptoms, and partly due to the finding that drugs such as amphetamine and cocaine (which are known to greatly increase dopamine levels) can cause psychosis. Because of this, most modern antipsychotic medication is designed to block dopamine function to varying degrees. Blocking the D2 dopamine receptor is known to cause relapse in patients that have achieved remission from depression, and such blocking also counteracts the effectiveness of SSRI medication.

See the article on the dopamine hypothesis of psychosis for a wider discussion of this topic. [edit]

Therapeutic use

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

Dopamine is also used as an inotropic drug in patients with shock to increase cardiac output and blood pressure. [edit]

Major dopamine pathways

* Mesocortical pathway * Mesolimbic pathway * Nigrostriatal pathway * Tuberoinfundibular pathway

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See also

* Addiction * Amphetamine * Antipsychotic * Catecholamine * Catechol-O-methyl transferase * Cocaine * Dopamine hypothesis of schizophrenia * Dopamine reuptake inhibitors * Methylphenidate * Neurotransmitter * Parkinson's disease * Prolactinoma * Schizophrenia * Selegiline

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External links

CID 681 from PubChem

* DrugBank APRD00085

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References

1. ↑ Pecina S, Cagniard B, Berridge KC, Aldridge JW, Zhuang X.(2003) Hyperdopaminergic mutant mice have higher "wanting" but not "liking" for sweet rewards.J Neurosci. 23(28):9395-402.  2. ↑ Lambert M, Schimmelmann BG, Karow A, Naber D.(2003) Subjective well-being and initial dysphoric reaction under antipsychotic drugs - concepts, measurement and clinical relevance.Pharmacopsychiatry., Nov;36 Suppl 3:S181-90. 3. ↑

* Matthias R. Lemke, M.D., H. Michael Brecht, M.D., Juergen Koester, Ph.D., Peter H. Kraus, M.D. and Heinz Reichmann, M.D.(2005) Anhedonia, Depression, and Motor Functioning in Parkinson’s Disease During Treatment With Pramipexole. J Neuropsychiatry Clin Neurosci. 17:214-220.

1. ↑ Susana Peciña and Kent C. Berridge .(2005) Hedonic Hot Spot in Nucleus Accumbens Shell: Where Do µ-Opioids Cause Increased Hedonic Impact of Sweetness?J Neurosci. 25(50):11777-11786.

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Phenethylamines edit

{2C-B} {2C-C} {2C-D} {2C-E} {2C-I} {2C-N} {2C-T-2} {2C-T-21} {2C-T-4} {2C-T-7} {2C-T-8} {3C-E} {4-FMP} {Amphetamine} {Bupropion} {Cathine} {Cathinone} {DESOXY} {Diethylcathinone} {Dimethylcathinone} {DOC} {DOB} {DOI} {DOM} {bk-MBDB} {Dopamine} {Br-DFLY} {Ephedrine} {Epinephrine} {Escaline} {Fenfluramine} {Levalbuterol} {Levmetamfetamine} {MBDB} {MDA} {MDMA} {MDMC/Methylone} {MDEA} {Mescaline} {Methamphetamine} {Methcathinone} {Methylphenidate} {Norepinephrine} {Phentermine} {Salbutamol} {Tyramine} {Venlafaxine} Retrieved from "http://en.wikipedia.org/wiki/Dopamine"

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