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'''โดพามีน''' ([[ภาษาอังกฤษ|อังกฤษ]]:Dopamine) เป็นสารเคมีที่ผลิตขึ้นในร่างกาย ใน[[สมอง]]โดพามีนทำหน้าที่เป็น[[นิวโรทรานสมิตเตอร์]](neurotransmitter) คอยกระตุ้น[[โดพามีน รีเซพเตอร์]](dopamine receptor) โดพามีนทำหน้าที่เป็น[[นิวโรฮอร์โมน]] (neurohormone) ที่หลั่งมาจาก[[ไฮโปทาลามัส]] (hypothalamus) หน้าที่หลักของฮอร์โมนตัวนี้คือยับยั้งการหลั่ง[[โปรแลคติน]] (prolactin) จาก[[ต่อมใต้สมอง]]ส่วนหน้า (anterior pituitary)
โดพามีนสามารถใช้เป็นยา ซึ่งมีผลต่อระบบประสาทซิมพาเทติก (sympathetic nervous system) โดยมีผลลัพธ์คือ อัตราการเต้นของหัวใจเพิ่มขึ้น แรงดันโลหิตเพิ่มขึ้น อย่างไรก็ตาม เมื่อโพพามีนไม่สามารถผ่านโครงสร้างกั้นระหว่างเลือดและสมอง (blood-brain barrier) โดพามีนที่ใช้เป็นยา จะไม่มีผลโดยตรงต่อระบบประสาทส่วนกลาง การเพิ่มปริมาณของโดพามีนในสมองของผู้ป่วยที่เป็นโรคต่างๆ เช่น พาร์คินสัน สามารถให้สารตั้งต้นแบบสังเคราะห์แก่โดพามีน เช่น L-DOPA เพื่อให้สามารถผ่านโครงสร้างกั้นระหว่างเลือดและสมองได้
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Dopamine can be supplied as a [[drug]] which acts on the [[sympathetic
nervous system|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]], a synthetic precursor to
dopamine such as [[L-DOPA]] can be given, since this will cross the
blood-brain barrier.
== Biochemistry ==
Dopamine has the chemical formula (C<sub>6</sub>H<sub>3</sub> (OH) <sub>2</sub>-CH<sub>2</sub>-CH<sub>2</sub>-NH<sub>2</sub>). 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 is a neurotransmitter as well.
Dopamine is synthesized in the body (mainly by nervous tissue and adrenal glands) by the [[decarboxylation]] of [[DOPA]] by [[aromatic-L-amino-acid decarboxylase]]. In [[neuron]]s, 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-package into vesicles and reused.
== Functions of Dopamine in the Brain ==
=== 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.
=== Role in Cognition and Frontal Cortex Function ===
In the [[frontal lobe|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]]. This function is particularly related to the [[mesocortical pathway|mesocortical dopamine pathway]].
=== 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, or continue doing, certain activities. Certainly dopamine is released (particularly in areas such as the [[nucleus accumbens]] and [[striatum]]) by naturally rewarding experiences such as [[food]], [[Human sexual behaviour|sex]], use of certain drugs and neutral stimuli that become [[conditioning|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 [[neurobiology|neurobiological]] theories of 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. Also, the firing of dopamine [[neuron]]s occurs when a pleasurable activity is expected, regardless of whether it actually happens or not. This suggests that dopamine may be involved in [[desire]] rather than [[pleasure]]. Drugs that are known to reduce dopamine activity (e.g. [[antipsychotic]]s) 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 'wanting' but not the 'liking', 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 which 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. Importantly, the available experimental evidence which examined causal, rather than corrleational, relationships between dopamine and motivation, does not seem to agree with any of above 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 'desire/wanting,' 'predicting pleasurable activity,' 'noticeableness' or "decision making" can not adequately explain this experimental evidence. Thus, the functional role of dopamine in motivation remains to be the topic of controversy.
== 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 [[phenothiazine]]s (which block D<sub>2</sub> [[dopamine receptor]]s) that can reduce psychotic symptoms, and partly due to the finding that drugs such as [[amfetamine|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 D<sub>2</sub> [[dopamine receptor]] is known to cause relapse in patients that have achieved remission from depression, and such blocking also counteracts the effectiveness of [[Selective_serotonin_reuptake_inhibitor|SSRI]] medication.
See the article on the [[dopamine hypothesis of psychosis]] for a wider discussion of this topic.
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== Major Dopamine Pathways ==
* [[mesocortical pathway]]
* [[tuberoinfundibular pathway]]
== ดูเพิ่ม==
== See also ==
* [[addiction]]
* [[amfetamine|amphetamines]]
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