Quicknation    Dopamine

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Dopamine . 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 brain 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.

table 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 (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.

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.

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.

of the brain, providing feelings of enjoyment and reinforcement to motivate us to do, or continue doing, 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. The mechanisms of cocaine and amphetamine are different, however. Cocaine acts as a dopamine transporter blocker, competively inhibiting 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 the 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, seems too simple as more evidence has been gathered. Dopamine is known to be released when unpleasant or aversive stimuli are encountered, suggesting that it is not only associated 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 dopaminergic 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. Drugs that are known to reduce dopamine activity (e.g., antipsychotics) have been shown to reduce people's desire for pleasurable stimuli, despite the fact that they will rate them as just as pleasurable when they actually encounter or consume them. It seems that these drugs reduce the , providing more evidence for the desire theory.

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 (including rewarding things, but also things that may be dangerous or a threat) appearing more noticeable or more important. This theory argues that dopamine's role is to assist decision-making by influencing the priority of such stimuli to the person concerned.

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

Deficits in dopamine levels have also been implicated as one of a possible array of causes for Attention deficit disorder, and some types of medications used to treat ADD and ADHD will help to stimulate dopaminergic systems, leading to potentially ened, but preferably not distorted, sensation, for those who may be afflicted by it and be receiving treatment for it.

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 Dsub 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 Dsub 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.

Levodopa is a dopamine precursor used to treat Parkinson's disease. It is typically co-administered with an inhibitor of peripheral catechol-O-methyl transferase, such as carbidopa (co-careldopa) or benserazide (co-beneldopa).

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

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