プロラクチン遊離阻害因子

関: prolactin release-inhibiting hormone

WordNet

part with a possession or right; "I am relinquishing my bedroom to the long-term house guest"; "resign a claim to the throne" (同)relinquish, resign, free, give_up
a process that liberates or discharges something; "there was a sudden release of oxygen"; "the release of iodine from the thyroid gland"
a device that when pressed will release part of a mechanism (同)button
activity that frees or expresses creative energy or emotion; "she had no other outlet for her feelings"; "he gave vent to his anger" (同)outlet, vent
(music) the act or manner of terminating a musical phrase or tone (同)tone ending
a formal written statement of relinquishment (同)waiver, discharge
merchandise issued for sale or public showing (especially a record or film); "a new release from the London Symphony Orchestra"
release (gas or energy) as a result of a chemical reaction or physical decomposition (同)free, liberate
be a contributing factor; "make things factor into a companys profitability"
any of the numbers (or symbols) that form a product when multiplied together
an independent variable in statistics
anything that contributes causally to a result; "a number of factors determined the outcome"
consider as relevant when making a decision; "You must factor in the recent developments" (同)factor in, factor out
resolve into factors; "a quantum computer can factor the number 15" (同)factor in, factor out
an event known to have happened or something known to have existed; "your fears have no basis in fact"; "how much of the story is fact and how much fiction is hard to tell"
a concept whose truth can be proved; "scientific hypotheses are not facts"
a piece of information about circumstances that exist or events that have occurred; "first you must collect all the facts of the case"
a statement or assertion of verified information about something that is the case or has happened; "he supported his argument with an impressive array of facts"
gonadotropic hormone secreted by the anterior pituitary; in females it stimulates growth of the mammary glands and lactation after parturition (同)lactogenic_hormone, luteotropin

PrepTutorEJDIC

(束縛・義務などから)〈人・動物など〉‘を'『自由にする』,解放する《+『名』+『from』+『名』》 / 〈矢など〉‘を'放つ,〈爆弾〉‘を'投下する;〈締めつけた物〉‘を'ゆるめて放す / 〈ニュースなど〉‘を'発表する;〈レコード・書籍など〉‘を'発売する,〈映画〉‘を'封切りする / (人に)〈権利など〉‘を'譲渡する《+『名』+『to』+『名』》 / (束縛・義務などからの)『解放』,放免,免除《+『from』+『名』》 / (ガスなどの)放出;(爆弾の)投下;(感情の)吐露《+『of』(『to』)+『名』》 / (ニュースなどの)発表;(映画などの)封切り,(レコードなどの)発表 / (機械の)作動装置,レリーズ
(…の)『要因』,(…を生み出す)要素《+『in』+『名』(do『ing』)》 / 囲数,約数 / 代理人,《おもに英》仲買人 / =factorize
〈C〉『事実』,実際にある(あった)事 / 〈U〉真相,真実(truth) / 《the~》(法律用語で)犯行

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/11/15 21:08:34」(JST)

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Dopamine is an organic chemical of the catecholamine and phenethylamine families that plays several important roles in the brain and body. Its name is derived from its chemical structure: it is an amine synthesized by removing a carboxyl group from a molecule of its precursor chemical L-DOPA, which occurs in human brain cells and adrenal cells.

In the brain, dopamine functions as a neurotransmitter—a chemical released by neurons (nerve cells) to send signals to other nerve cells. The brain includes several distinct dopamine pathways, one of which plays a major role in reward-motivated behavior. Most types of reward increase the level of dopamine in the brain, and most addictive drugs increase dopamine neuronal activity. Other brain dopamine pathways are involved in motor control and in controlling the release of various hormones.

Outside the nervous system, dopamine functions in several parts of the body as a local chemical 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, and in its pure form marketed as Levodopa is the most widely used treatment for the condition. There is evidence that schizophrenia involves altered levels of dopamine activity, and most antipsychotic drugs that are frequently used to treat it have a primary effect of reducing dopamine activity.^[1] 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.^[2] 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 Structure
2 Biochemistry
- 2.1 Synthesis
- 2.2 Degradation
3 Functions
- 3.1 Cellular effects
  - 3.1.1 Storage, release, and reuptake
- 3.2 Nervous system
  - 3.2.1 Basal ganglia
  - 3.2.2 Reward
- 3.3 Outside the nervous system
4 Medical uses
5 Disease, disorders, and pharmacology
- 5.1 Parkinson's disease
- 5.2 Psychostimulants and drug addiction
- 5.3 Psychosis and antipsychotic drugs
- 5.4 Attention deficit hyperactivity disorder
- 5.5 Pain
- 5.6 Nausea
6 Comparative biology and evolution
- 6.1 Microorganisms
- 6.2 Animals
- 6.3 Plants
- 6.4 As a precursor for melanin
7 History and development
- 7.1 Polydopamine
8 See also
9 References

Structure

A dopamine molecule consists of a catechol structure (a benzene ring with two hydroxyl side groups) with one amine group attached via an ethyl chain.^[3] As such, dopamine is the simplest possible catecholamine, a family that also includes the neurotransmitters norepinephrine and epinephrine.^[4] The presence of a benzene ring with this amine attachment makes it a substituted phenethylamine, a family that includes numerous psychoactive drugs.^[5]

Like most amines, dopamine is an organic base.^[6] In acidic environments, it is generally protonated.^[6] The protonated form is highly water-soluble and relatively stable, though it is capable of becoming oxidized if exposed to oxygen or other oxidants.^[6] In basic environments, dopamine is not protonated.^[6] In this free base form, it is less water-soluble and also more highly reactive.^[6] Because of the increased stability and water-solubility of the protonated form, dopamine is supplied for chemical or pharmaceutical use as dopamine hydrochloride—that is, the hydrochloride salt that is created when dopamine is combined with hydrochloric acid.^[6] In dry form, dopamine hydrochloride is a fine colorless powder.^[6]

Dopamine structure

Phenethylamine structure

Catechol structure

Biochemistry

Synthesis

The reaction from L-DOPA to dopamine

Dopamine is synthesized in a restricted set of cell types, mainly neurons and cells in the medulla of the adrenal glands.^[7] The metabolic pathway is:

L-Phenylalanine → L-Tyrosine → L-DOPA → Dopamine

The direct precursor of dopamine, L-DOPA, can be synthesized indirectly from the essential amino acid phenylalanine or directly from the non-essential amino acid tyrosine.^[8] These amino acids are found in nearly every protein and so are readily available in food, with tyrosine being the most common. Although dopamine is also found in many types of food, it is incapable of crossing the blood–brain barrier that surrounds and protects the brain.^[9] It must therefore be synthesized inside the brain to perform its neural actions.^[9]

L-Phenylalanine is converted into L-tyrosine by the enzyme phenylalanine hydroxylase (PAH), with molecular oxygen (O₂) and tetrahydrobiopterin (THB) as cofactors. L-Tyrosine is converted into L-DOPA by the enzyme tyrosine hydroxylase (TH), with tetrahydrobiopterin (THB), O₂, and probably iron (Fe²⁺) as cofactors.^[8] L-DOPA is converted into dopamine by the enzyme aromatic L-amino acid decarboxylase (AADC also known as DOPA decarboxylase (DDC)), with pyridoxal phosphate (PLP) as the cofactor.^[8]

Dopamine itself is used as precursor in the synthesis of the neurotransmitter norepinephrine and the hormone epinephrine.^[8] Dopamine is converted into norepinephrine by the enzyme dopamine β-hydroxylase (DBH), with O₂ and L-ascorbic acid as cofactors.^[8] Norepinephrine is converted into epinephrine by the enzyme phenylethanolamine N-methyltransferase (PNMT) with S-adenosyl-L-methionine (SAM) as the cofactor.^[8]

Some of the cofactors also require their own synthesis.^[8] Deficiency in any required amino acid or cofactor can impair the synthesis of dopamine, norepinephrine, and epinephrine.^[8]

Primary pathways for dopamine metabolism
MAO: Monoamine oxidase
COMT: catechol-O-methyltransferase

HVA: Homovanillic acid

Degradation

Dopamine is broken down into inactive metabolites by a set of enzymes, monoamine oxidase (MAO), catechol-O-methyl transferase (COMT), and aldehyde dehydrogenase (ALDH), acting in sequence.^[10] Both isoforms of monoamine oxidase, MAO-A and MAO-B, are effective.^[8] A variety of breakdown pathways are possible, but regardless of which pathway is followed, the primary final product is homovanillic acid, which has no known biological activity.^[10] From the bloodstream, homovanillic acid is filtered out by the kidneys and then excreted in the urine.^[10]

Research into the study of schizophrenia has tried to use the measure of homovanillic acid in plasma, to determine levels of dopamine activity in the brain. A difficulty in this approach however, is separating the high level of plasma homovanillic acid contributed by the metabolism of norepinephrine.^[11]^[12]

Although dopamine is normally broken down by oxidation catalyzed by enzymes, it is also susceptible to autoxidation—that is, direct reaction with oxygen, yielding quinones plus various free radicals as products.^[13] The rate of autoxidation can be increased by the presence of ferrous iron or other factors. Quinones and free radicals produced by autoxidation of dopamine can poison cells, and there is evidence that this mechanism may contribute to the cell loss that occurs in Parkinson's disease and other conditions.^[14]

Functions

Cellular effects

Dopamine receptors in the mammal brain
Family	Receptor	Gene	Type	Mechanism
D1-like	D₁	DRD1	G_s-coupled.	Increase intracellular levels of cAMP by activating adenylate cyclase.
D1-like	D₅	DRD5	G_s-coupled.
D2-like	D₂	DRD2	G_i/G_o-coupled.	Decrease intracellular levels of cAMP by inhibiting adenylate cyclase.
	D₃	DRD3
	D₄	DRD4

Dopamine exerts its effects by binding to and activating receptors located on the surface of cells.^[7] In mammals, five subtypes of dopamine receptors have been identified, labeled from D1 to D5.^[7] All of them function as G protein-coupled receptors, meaning that they exert their effects via a complex second messenger system.^[15] Dopamine receptors in mammals can be divided into two families, known as D1-like and D2-like.^[7] For receptors located on neurons in the nervous system, the ultimate effect of D1-like activation (D1 and D5) can be excitation (via opening of sodium channels) or inhibition (via opening of potassium channels); the ultimate effect of D2-like activation (D2, D3, and D4) is usually inhibition of the target neuron.^[15] Consequently, it is incorrect to describe dopamine itself as either excitatory or inhibitory: its effect on a target neuron depends on which types of receptors are present on the membrane of that neuron and on the internal responses of that neuron to cyclic AMP.^[15] D1 receptors are the most numerous dopamine receptors in the human nervous system; D2 receptors are next; D3, D4, and D5 receptors are present at significantly lower levels.^[15]

Storage, release, and reuptake

Dopamine processing in a synapse. After release dopamine can either be taken up again by the presynaptic terminal, or broken down by enzymes.
TH: tyrosine hydroxylase
DOPA: L-DOPA
DAT: dopamine transporter
DDC: DOPA decarboxylase
VMAT: vesicular monoamine transporter 2
MAO: Monoamine oxidase
COMT: Catechol-O-methyl transferase

HVA: Homovanillic acid

Inside the brain dopamine functions as a neurotransmitter, and is controlled by a set of mechanisms common to all monoamine neurotransmitters.^[7] After synthesis, dopamine is transported from the cytosol into synaptic vesicles by the vesicular monoamine transporter 2 (VMAT2).^[16] Dopamine is stored in these vesicles until it is ejected into the synaptic cleft through a process called exocytosis. In most cases exocytosis is caused by action potentials, but it can also be caused by mechanisms that do not require neural activity.^[17]

Once in the synapse, dopamine binds to and activates dopamine receptors, which can be located either on postsynaptic target cells or on the membrane of the presynaptic dopamine-releasing cell itself (i.e., D2 short autoreceptors).^[7] After an action potential, the dopamine molecules quickly become unbound from their receptors. They are then absorbed back into the presynaptic cell, via reuptake mediated either by the dopamine transporter or by the plasma membrane monoamine transporter.^[18] Once back in the cytosol, dopamine can either be broken down by monoamine oxidase or repackaged into vesicles by VMAT2, making it available for future release.^[16]

In the brain the level of extracellular dopamine is modulated by two mechanisms: phasic and tonic transmission.^[19] Phasic dopamine release, like most neurotransmitter release in the nervous system, is driven directly by action potentials in the dopamine-containing cells.^[19] Tonic dopamine transmission occurs when small amounts of dopamine are released without being preceded by presynaptic action potentials.^[19] Tonic transmission is regulated by a variety of factors, including the activity of other neurons and neurotransmitter reuptake.^[19]

Nervous system

Major dopamine pathways. As part of the reward pathway, dopamine is manufactured in nerve cell bodies located within the ventral tegmental area (VTA) and is released in the nucleus accumbens and the prefrontal cortex. The motor functions of dopamine are linked to a separate pathway, with cell bodies in the substantia nigra that manufacture and release dopamine into the striatum.

Inside the brain, dopamine plays important roles in executive functions, motor control, motivation, arousal, reinforcement, and reward, as well as lower-level functions including lactation, sexual gratification, and nausea.

Dopaminergic neurons (dopamine-producing nerve cells) are comparatively few in number—a total of around 400,000 in the human brain^[20]—and their cell bodies are confined in groups to a few relatively small brain areas.^[21] However their axons project to many other brain areas, and they exert powerful effects on their targets.^[21] These dopaminergic cell groups were first mapped in 1964 by Annica Dahlström and Kjell Fuxe, who assigned them labels starting with the letter "A" (for "aminergic").^[22] In their scheme, areas A1 through A7 contain the neurotransmitter norepinephrine, whereas A8 through A14 contain dopamine. The dopaminergic areas they identified are:

The substantia nigra, a small midbrain area that forms a component of the basal ganglia. This has two parts—an input area called the pars compacta and an output area the pars reticulata. The dopaminergic neurons are found mainly in the pars compacta (cell group A8) and nearby (group A9).^[21] In humans, the projection of dopaminergic neurons from the substantia nigra pars compacta to the dorsal striatum, termed the nigrostriatal pathway, plays a significant role in the control of motor function and in learning new motor programs.^[23] These neurons are especially vulnerable to damage, and when a large fraction of them die, the result is a parkinsonian syndrome.^[24]
The ventral tegmental area (VTA), another midbrain area. The most prominent group of VTA dopaminergic neurons (group A10) projects to the prefrontal cortex via the mesocortical pathway and another smaller group projects to the nucleus accumbens via the mesolimbic pathway. Together, these two pathways are collectively termed the mesocorticolimbic projection.^[21]^[23] The VTA also sends dopaminergic projections to the amygdala, cingulate gyrus, hippocampus, and olfactory bulb.^[21]^[23] Mesocorticolimbic neurons play a central role in reward and other aspects of motivation.^[23]
The posterior hypothalamus. These dopaminergic cells (group A11) project to the spinal cord, but their function is not well established.^[25] There is some evidence that pathology in this area plays a role in restless legs syndrome, a condition in which people have difficulty sleeping due to an overwhelming compulsion to constantly move parts of the body, especially the legs.^[25]
The arcuate nucleus (group A12) and periventricular nucleus (group A14) of the hypothalamus. An important projection from these dopaminergic neurons, termed the tuberoinfundibular pathway, goes to the pituitary gland, where it influences the secretion of the hormone prolactin.^[26] Dopamine is the primary neuroendocrine inhibitor of the secretion of prolactin from the anterior pituitary gland.^[26] Dopamine produced by neurons in the arcuate nucleus is secreted into the hypothalamo-hypophysial blood vessels of the median eminence, which supply the pituitary gland.^[26] The prolactin cells that produce prolactin, in the absence of dopamine, secrete prolactin continuously; dopamine inhibits this secretion.^[26] In the context of regulating prolactin secretion, dopamine is occasionally called prolactin-inhibiting factor, prolactin-inhibiting hormone, or prolactostatin.^[26]
The zona incerta. These cells (group A13) project to several areas of the hypothalamus, and participate in the control of gonadotropin-releasing hormone, which is necessary to activate the development of reproductive systems that occurs following puberty, both in males and females.^[26]

An additional group of dopamine-secreting neurons is found in the retina of the eye.^[27] These neurons are amacrine cells, meaning that they have no axons.^[27] They release dopamine into the extracellular medium, and are specifically active during daylight hours, becoming silent at night.^[27] This retinal dopamine acts to enhance the activity of cone cells in the retina while suppressing rod cells—the result is to increase sensitivity to color and contrast during bright light conditions, at the cost of reduced sensitivity when the light is dim.^[27]

Basal ganglia

Main circuits of the basal ganglia. The dopaminergic pathway from the substantia nigra pars compacta to the striatum is shown in light blue.

The largest and most important sources of dopamine in the vertebrate brain are the substantia nigra and ventral tegmental area.^[21] These structures are closely related to each other and functionally similar in many respects.^[21] Both are components of the basal ganglia, a complex network of structures located mainly at the base of the forebrain.^[21] The largest component of the basal ganglia is the striatum.^[28] The substantia nigra sends a dopaminergic projection to the dorsal striatum, while the ventral tegmental area sends a similar type of dopaminergic projection to the ventral striatum.^[21]

Progress in understanding the functions of the basal ganglia has been slow.^[28] The most popular hypotheses, broadly stated, propose that the basal ganglia play a central role in action selection.^[29] The action selection theory in its simplest form proposes that when a person or animal is in a situation where several behaviors are possible, activity in the basal ganglia determines which of them is executed, by releasing that response from inhibition while continuing to inhibit other motor systems that if activated would generate competing behaviors.^[30] Thus the basal ganglia, in this concept, are responsible for initiating behaviors, but not for determining the details of how they are carried out. In other words, they essentially form a decision-making system.^[30]

The basal ganglia can be divided into several sectors, and each is involved in controlling particular types of actions.^[31] The ventral sector of the basal ganglia (containing the ventral striatum and ventral tegmental area) operates at the highest level of the hierarchy, selecting actions at the whole-organism level.^[30] The dorsal sectors (containing the dorsal striatum and substantia nigra) operate at lower levels, selecting the specific muscles and movements that are used to implement a given behavior pattern.^[31]

Dopamine contributes to the action selection process in at least two important ways. First, it sets the "threshold" for initiating actions.^[29] The higher the level of dopamine activity, the lower the impetus required to evoke a given behavior.^[29] As a consequence, high levels of dopamine lead to high levels of motor activity and impulsive behavior; low levels of dopamine lead to torpor and slowed reactions.^[29] Parkinson's disease, in which dopamine levels in the substantia nigra circuit are greatly reduced, is characterized by stiffness and difficulty initiating movement—however, when people with the disease are confronted with strong stimuli such as a serious threat, their reactions can be as vigorous as those of a healthy person.^[32] In the opposite direction, drugs that increase the effects of dopamine, such as cocaine or amphetamine, produce heightened levels of activity, including at the highest levels psychomotor agitation and stereotyped movements.^[33]

The second important effect of dopamine is as a "teaching" signal.^[29] When an action is followed by an increase in dopamine activity, the basal ganglia circuit is altered in a way that makes the same response easier to evoke when similar situations arise in the future.^[29] This is a form of operant conditioning, in which dopamine plays the role of a reward signal.^[30]

Reward

The aspect of dopamine that has drawn the most interest is its connection with pleasure and reward. There is much evidence for a strong relationship, including:

Drugs that act rapidly and directly to increase dopamine levels, such as cocaine and methamphetamine, are among the most addictive substances known.^[34]
Many other addictive drugs that do not act directly on dopamine, such as heroin and nicotine, cause increases in dopamine levels by indirect mechanisms.^[34]
Conversely, drugs that reduce dopamine levels, such as the neuroleptic drugs often used to treat psychosis, tend to cause anhedonia, that is, diminished ability to experience pleasure.^[35]
Many types of pleasurable experiences—such as sex, eating good food, or playing video games—increase dopamine release.^[36]
Direct electrical stimulation of dopamine pathways, using electrodes implanted in the brain, is experienced as pleasurable, and many types of animals are willing to work to obtain it.^[34]
Microelectrode recordings from the brains of animals have shown that dopamine neurons in the ventral tegmental area and substantia nigra are strongly activated by a wide variety of rewarding events.^[37]

In spite of the overwhelming evidence showing a strong association between dopamine and reward, there has been a great deal of dispute about whether the function of dopamine should be described as reward per se, or as some more complex construct that relates strongly to reward. The difficulty arises from several observations, including: (1) in addition to being rewarding, dopamine is also arousing—it produces a general increase in movement of all sorts; (2) dopamine release can be caused by events that do not seem to have anything to do with reward, most notably pain; (3) some aspects of pleasure and reward do not rely on dopamine mechanisms.^[38] One of the most popular alternatives to the reward theory is the "incentive salience" theory, which argues that the function of dopamine is to increase the effects of motivators of all sorts, both positive and negative.^[38]

Until recently the "reward" and "incentive salience" theories competed, each favored by a group of investigators who argued that evidence for the other theory was misleading.^[39] Currently, however, the most popular view is that dopaminergic neurons have a range of functions, with some responding to salience (including aversive stimuli), while others behave as reward neurons.^[39] Reward-responsive neurons predominate in the ventral tegmental area, but can also be found in the substantia nigra.^[39]

Even if the basic validity of the reward concept is accepted, detailed studies have shown that dopamine cannot simply be equated with pleasure.^[40] Some aspects of pleasure and reward involve dopamine; others do not.^[40] In an effort to explain the distinction in easily understandable terms, Kent Berridge suggested that reward-related behaviors can be divided into two types, which he called "wanting" and "liking".^[40] "Wanting" occurs when an animal, given access to some stimulus such as food or a drug, executes some type of active behavior in order to acquire it.^[40] (Some writers such as Jaak Panksepp prefer to use the term "seeking" rather than "wanting", as it better conveys the idea that active behavior is involved.^[41]) "Liking" occurs when an animal, after having obtained access to something rewarding, continues to consume it until satiated, and shows expressions of pleasure.^[40] There is considerable evidence that the dopamine system is crucial for wanting but not for liking.^[42] Drugs that increase the effects of dopamine (most notably stimulants such as methamphetamine or cocaine) produce increases in "wanting" behaviors, but do not greatly alter expressions of pleasure or change levels of satiation.^[42] Conversely, opiate drugs such as heroin or morphine produce increases in expressions of pleasure but do not greatly alter "wanting" behaviors.^[42] Animals in which the ventral tegmental dopamine system has been rendered inactive do not seek food, and will starve to death if left to themselves, but if food is placed in their mouths they will consume it and show expressions indicative of pleasure.^[43]

Even the relationship of dopamine to the "wanting" aspect of reward shows complexity. A substantial body of evidence indicates that dopamine encodes not reward itself, but rather reward prediction error, that is, the degree to which reward is unexpected.^[37] According to this hypothesis, which derived initially from dopaminergic cell activity recordings made by Wolfram Schultz, rewards that are expected do not produce any activation of dopaminergic cells, but rewards that are unexpected, or greater than expected, produce a short-lasting increase in dopamine, whereas the omission of an expected reward actually causes dopamine release to drop below its background level.^[37] The "prediction error" hypothesis has drawn particular interest from computational neuroscientists, because an influential computational-learning method known as temporal difference learning makes heavy use of a signal that encodes prediction error.^[37] This confluence of theory and data has led to a fertile interaction between neuroscientists and computer scientists interested in machine learning.^[37]

Outside the nervous system

Dopamine does not cross the blood–brain barrier, so its synthesis and functions in peripheral areas are to a large degree independent of its synthesis and functions in the brain.^[9] A substantial amount of dopamine circulates in the bloodstream, but its functions there are not entirely clear.^[10] Dopamine is found in blood plasma at levels comparable to those of epinephrine, but in humans, over 95% of the dopamine in the plasma is in the form of dopamine sulphate, a conjugate produced by the enzyme Sulfotransferase 1A3/1A4 acting on free dopamine.^[10] The bulk of this dopamine sulphate is produced in the mesenteric organs that surround parts of the digestive system.^[10] The production of dopamine sulphate is thought to be a mechanism for detoxifying dopamine that is ingested as food or produced by the digestive process—levels in the plasma typically rise more than fifty-fold after a meal.^[10] Dopamine sulphate has no known biological functions and is excreted in urine.^[10]

The relatively small quantity of unconjugated dopamine in the bloodstream may be produced by the sympathetic nervous system, the digestive system, or possibly other organs.^[10] It may act on dopamine receptors in peripheral tissues, or be metabolized, or be converted to norepinephrine by the enzyme dopamine beta hydroxylase, which is released into the bloodstream by the adrenal medulla.^[10] Some dopamine receptors are located in the walls of arteries, where they act as a vasodilator and an inhibitor of norepinephrine release.^[44] These responses might be activated by dopamine released from the carotid body under conditions of low oxygen, but whether arterial dopamine receptors perform other biologically useful functions is not known.^[44]

Beyond its role in modulating blood flow, there are several peripheral systems in which dopamine circulates within a limited area and performs an exocrine or paracrine function.^[10] The peripheral systems in which dopamine plays an important role include:

The immune system. Dopamine acts upon receptors present on immune cells, especially lymphocytes.^[45] Dopamine can also affect immune cells in the spleen, bone marrow, and circulatory system.^[46] In addition, dopamine can be synthesized and released by immune cells themselves.^[45] The main effect of dopamine on lymphocytes is to reduce their activation level. The functional significance of this system is unclear, but it affords a possible route for interactions between the nervous system and immune system, and may be relevant to some autoimmune disorders.^[46]
The kidneys. Multiple types of dopamine receptors are present in cells of the kidneys. Dopamine is also synthesized there, by tubule cells, and discharged into the tubular fluid. Its actions include increasing the blood supply to the kidneys, increasing filtration by the glomeruli, and increasing excretion of sodium in the urine. Defects in renal dopamine function can be produced by high blood pressure or by genetic problems, and can lead to reduced sodium excretion as well as hypertension.^[47]
The pancreas. The role of dopamine here is somewhat complex. The pancreas consists of two parts, known as exocrine and endocrine. The exocrine part synthesizes enzymes and other substances, and secretes them into the small intestine, where food is digested.^[48] One of the substances synthesized and secreted by the exocrine pancreas is dopamine.^[48] The function of this secreted dopamine after it enters the small intestine is not clearly established—the possibilities include protecting the intestinal mucosa from damage and reducing gastrointestinal motility (the rate at which food moves through the intestines).^[48]

The endocrine part of the pancreas, also known as the islets of Langerhans, synthesizes hormones including insulin, and secretes them into the bloodstream.^[48] There is evidence that the beta cells that synthesize insulin contain dopamine receptors, and that dopamine acts to reduce the amount of insulin they release.^[48] The source of their dopamine input is not clearly established—it may come from dopamine that circulates in the bloodstream and derives from the sympathetic nervous system, or it may be synthesized locally by other types of pancreatic cells.^[48]

Medical uses

Dopamine HCl preparation, single dose vial for intravenous administration

Dopamine as a manufactured medication is sold under the trade names Intropin, Dopastat, and Revimine, among others, and is widely used: it is on the World Health Organization's List of Essential Medicines.^[49] It is most commonly used as a stimulant drug in the treatment of severe low blood pressure, slow heart rate, and cardiac arrest. It is especially important in treating these in newborn infants.^[50] It is given intravenously. Since the half-life of dopamine in plasma is very short—approximately one minute in adults, two minutes in newborn infants and up to five minutes in preterm infants—it is usually given in a continuous intravenous drip rather than a single injection.^[51]

Its effects, depending on dosage, include an increase in sodium excretion by the kidneys, an increase in urine output, an increase in heart rate, and an increase in blood pressure.^[51] At low doses it acts through the sympathetic nervous system to increase heart muscle contraction force and heart rate, thereby increasing cardiac output and blood pressure.^[52] Higher doses also cause vasoconstriction that further increases blood pressure.^[52]^[53] Older literature also describes very low doses thought to improve kidney function without other consequences, but recent reviews have concluded that doses at such low levels are not effective and may sometimes be harmful.^[54]

Side effects of dopamine include negative effects on kidney function and cardiac arrhythmias.^[52] The LD₅₀, or toxic dose which is expected to be lethal in 50% of the population, has been found to be: 59 mg/kg (mouse; administered intravenously); 950 mg/kg (mouse; administered intraperitoneally); 163 mg/kg (rat; administered intraperitoneally); 79 mg/kg (dog; administered intravenously).^[55]

Disease, disorders, and pharmacology

The dopamine system plays a central role in important medical conditions including Parkinson's disease, attention deficit hyperactivity disorder, schizophrenia, and drug addiction. Aside from dopamine itself, there are many other important drugs that exert their effects by acting on dopamine systems in various parts of the brain or body. Some are used for medical or recreational purposes, but neurochemists have also developed a variety of research drugs, some of which bind with high affinity to specific types of dopamine receptors and agonize or antagonize their effects, and many that affect other aspects of dopamine physiology.^[56]

Parkinson's disease

Parkinson's disease is an age-related disorder characterized by stiffness of the body, slowing of movement, and trembling of limbs when they are not in use.^[32] In advanced stages it progresses to dementia and eventually death.^[32] The main symptoms are caused by a massive loss of dopamine-secreting cells in the substantia nigra.^[57] These dopamine cells are especially vulnerable to damage, and a variety of insults, including encephalitis (as depicted in the book and movie "Awakenings"), repeated sports-related concussions, and some forms of chemical poisoning such as MPTP, can lead to substantial cell loss, producing a parkinsonian syndrome that is similar in its main features to Parkinson's disease.^[58] Most cases of Parkinson's disease, however, are idiopathic, meaning that the cause of cell death cannot be identified.^[58]

The most widely used treatment for parkinsonism is administration of L-DOPA, the metabolic precursor for dopamine.^[9] L-DOPA is converted to dopamine in the brain and various parts of the body by the enzyme DOPA decarboxylase.^[8] L-DOPA is used rather than dopamine itself because, unlike dopamine, it is capable of crossing the blood-brain barrier.^[9] It is often co-administered with an inhibitor of peripheral decarboxylation such as carbidopa or benserazide, to reduce the amount converted to dopamine in the periphery and thereby increase the amount of L-DOPA that enters the brain.^[9] When L-DOPA is administered regularly over a long time period, a variety of unpleasant side effects such as dyskinesia often begin to appear; even so, it is considered the best available long-term treatment option for most cases of Parkinson's disease.^[9]

L-DOPA treatment cannot restore the dopamine cells that have been lost, but it causes the remaining cells to produce more dopamine, thereby compensating for the loss to at least some degree.^[9] In advanced stages the treatment begins to fail because the cell loss is so severe that the remaining ones cannot produce enough dopamine regardless of L-DOPA levels.^[9] As this stage is approached, the metabolic regulatory mechanisms in the dopamine cells, operating far above their normal level, become erratic, producing dopamine dysregulation syndrome, in which patients fluctuate unpredictably between states of hyperactivity and paralysis.^[59] Other drugs that enhance dopamine function, such as bromocryptine and pergolide, are also sometimes used to treat Parkinsonism, but in most cases L-DOPA appears to give the best tradeoff between positive effects and negative side-effects.^[9]

Psychostimulants and drug addiction

Cocaine increases dopamine levels by blocking dopamine transporters (DAT), which transport dopamine back into a synaptic terminal after it has been emitted.

Cocaine, substituted amphetamines (including methamphetamine), Adderall, methylphenidate (marketed as Ritalin or Concerta), MDMA (ecstasy) and other psychostimulants exert their effects primarily or partly by increasing dopamine levels in the brain by a variety of mechanisms.^[60] Cocaine and methylphenidate are dopamine transporter blockers: they non-competitively inhibit dopamine reuptake, resulting in increased dopamine concentrations in the synaptic cleft.^[61]^[62]^:54–58 Like cocaine, substituted amphetamines increase the concentration of dopamine in the synaptic cleft, but by a different mechanism, involving complex intracellular effects.^[17] MDMA also increases dopamine levels by a complex combination of mechanisms.^[62]^:147–150

The effects of psychostimulants include increases in heart rate, body temperature, and sweating; improvements in alertness, attention, and endurance; increases in pleasure produced by rewarding events; but at higher doses agitation, anxiety, or even loss of contact with reality.^[60] Drugs in this group can have a high addiction potential, due to their activating effects on the dopamine-mediated reward system in the brain.^[60] However some can also be useful, at lower doses, for treating attention deficit hyperactivity disorder (ADHD).^[63] An important differentiating factor is the onset and duration of action.^[60] Cocaine can take effect in seconds if it is injected or inhaled in free-base form; the effects last from 5 to 90 minutes.^[64] This rapid and brief action gives it high addiction potential.^[60] Methylphenidate taken in pill form, in contrast, can take two hours to reach peak levels in the bloodstream, and depending on formulation the effects can last for up to 12 hours.^[63] These slow and sustained actions reduce the addiction potential and make it more useful for treating ADHD.^[63]

Metamphetamine hydrochloride also known as crystal meth

A variety of addictive drugs produce an increase in reward-related dopamine activity.^[60] For some addictive drugs such as heroin, altered dopamine levels in the reward system may play only a minor role in addiction, but for other drugs, including nicotine and psychomotor stimulants such as cocaine and methamphetamine, increased postsynaptic dopamine receptor activation or increased levels of synaptic dopamine appear to be the primary factor.^[65] When people addicted to stimulants go through withdrawal, they do not experience the physical suffering associated with withdrawal from alcohol or opiates; instead they experience "craving", an intense desire for the drug characterized by irritability, restlessness, and other arousal symptoms.^[66]

The dopamine system plays a crucial role in several aspects of addiction. At the earliest stage, genetic differences that alter the expression of dopamine receptors in the brain can predict whether a person will find stimulants appealing or aversive.^[67] Consumption of stimulants produces increases in brain dopamine levels that last from minutes to hours.^[60] Finally, the chronic elevation in dopamine that comes with repetitive stimulant consumption triggers a wide-ranging set of structural changes in the brain, one of which is a reduction in responses to dopamine in the basal ganglia, with the consequence that every type of experience is perceived as less rewarding than before drug consumption began.^[68] Treatment of stimulant addiction is very difficult, because even if consumption ceases, the "craving" that comes with psychological withdrawal does not.^[66] Even when the craving seems to be extinct, it may re-emerge when a person experiences environmental stimuli (friends, locations, situations, etc.) that are associated with the drug.^[66]

Psychosis and antipsychotic drugs

Psychiatrists in the early 1950s discovered that a class of drugs known as major tranquilizers were often effective at reducing the psychotic symptoms of schizophrenia.^[69] By the 1970s researchers came to an understanding that the primary neural effect of these antipsychotic drugs is to reduce the activity of dopamine systems.^[69] The realization that all then-known antipsychotic drugs reduce dopamine activity led researchers in the 1970s to propose the so-called dopamine hypothesis of schizophrenia, which postulates that schizophrenia is caused, at least in the majority of cases, by hyperactivity of brain dopamine systems.^[70] The dopamine hypothesis drew additional support from the observation that psychotic symptoms were often intensified by dopamine-enhancing stimulants such as methamphetamine, and that these drugs could produce psychosis even in healthy people if taken in large doses.^[70]

Other observations, however, have caused the dopamine hypothesis to lose popularity, at least in its simple original form.^[70] For one thing, patients with schizophrenia do not typically show measurably increased levels of brain dopamine activity.^[70] Also, a variety of drugs acting by mechanisms that don't appear to involve dopamine can produce psychotic symptoms, most notably ketamine and phencyclidine (PCP), whose direct effects are on glutamate NMDA receptors.^[70] Perhaps most importantly, drugs that reduce dopamine activity are a very imperfect treatment for schizophrenia: they only reduce a subset of symptoms, while producing severe short-term and long-term side effects.^[71] Even so, many psychiatrists and neuroscientists continue to believe that schizophrenia involves some sort of dopamine system dysfunction.^[69] As the "dopamine hypothesis" has evolved over time, however, the sorts of dysfunctions it postulates have tended to become increasingly subtle and complex.^[69]

A range of drugs that reduce dopamine activity have been found useful in the treatment of schizophrenia and other disorders that produce psychosis,^[69] mainly by antagonizing D2 receptors.^[72] Antipsychotic drugs have a broadly suppressive effect on most types of active behavior, and particularly reduce the delusional and agitated behavior characteristic of overt psychosis.^[72] The introduction of the first widely used antipsychotic drug, chlorpromazine (Thorazine), in the 1950s, led to the release of many patients with schizophrenia from institutions in the years that followed.^[69]

Even so, the widespread use of antipsychotic drugs has long been controversial.^[73] There are several reasons for this. First, antipsychotic drugs are perceived as very aversive by people who have to take them, because they produce a general dullness of thought and suppress the ability to experience pleasure.^[74] Second, it is difficult to show that they act specifically against psychotic behaviors rather than merely suppressing all types of active behavior.^[73] Third, they can produce a range of serious side effects, including weight gain, diabetes, fatigue, sexual dysfunction, hormonal changes, and a type of movement disorder known as tardive dyskinesia.^[71] Some of these side effects may continue long after the cessation of drug use, or even permanently.^[71]

The first drugs introduced specifically for the treatment of psychosis all had strong direct effects on dopamine receptors of the D2 class.^[72] Drugs of this type are known as typical antipsychotics.^[69] In the following decades other types of antipsychotic drugs with fewer serious side-effects were developed, known as atypical antipsychotics.^[69] Many of these newer drugs do not act directly on dopamine receptors, but detailed investigation has shown that almost all of them produce alterations in dopamine activity indirectly.^[75] There remains substantial dispute, however, about how much of an improvement in the patient experience these drugs produce.^[73]

Attention deficit hyperactivity disorder

Altered dopamine neurotransmission is implicated in attention deficit hyperactivity disorder (ADHD), a condition associated with impaired cognitive control, in turn leading to problems with regulating attention (attentional control), inhibiting behaviors (inhibitory control), and forgetting things or missing details (working memory), among other problems.^[76] There are genetic links between dopamine receptors, the dopamine transporter, and ADHD, in addition to links to other neurotransmitter receptors and transporters.^[77] The most important relationship between dopamine and ADHD involves the drugs that are used to treat ADHD.^[42] Some of the most effective therapeutic agents for ADHD are psychostimulants such as methylphenidate (Ritalin, Concerta) and amphetamine (Adderall, Dexedrine), drugs that increase both dopamine and norepinephrine levels in the brain.^[78] In 2015, a systematic review and a meta-analysis of high quality clinical trials found that, when used at low (therapeutic) doses, stimulants produce unambiguous improvements in working memory, episodic memory, and inhibitory control in adults.^[79]^[80] These clinical effects of psychostimulants are mediated through the indirect activation of dopamine and norepinephrine receptors, specifically dopamine receptor D₁ and adrenoceptor A₂, in the prefrontal cortex.^[76]

Pain

Dopamine plays a role in pain processing in multiple levels of the central nervous system including the spinal cord, periaqueductal gray, thalamus, basal ganglia, and cingulate cortex.^[81] Decreased levels of dopamine have been associated with painful symptoms that frequently occur in Parkinson's disease.^[81] Abnormalities in dopaminergic neurotransmission also occur in several painful clinical conditions, including burning mouth syndrome, fibromyalgia, and restless legs syndrome.^[81]

Nausea

Nausea and vomiting are largely determined by activity in an area of the medulla of the brainstem known as the chemoreceptor trigger zone.^[82] This area contains a large population of type D2 dopamine receptors.^[82] Consequently, drugs that activate D2 receptors have a high potential to cause nausea.^[82] This group includes some medications that are administered for Parkinson's disease, as well as other dopamine agonists such as apomorphine.^[83] In some cases, D2-receptor antagonists such as metoclopramide are useful as anti-nausea drugs.^[82]

Comparative biology and evolution

Microorganisms

There are no reports of dopamine in archaea, but it has been detected in some types of bacteria and in the protozoan called Tetrahymena.^[84] Perhaps more importantly, there are types of bacteria that contain homologs of all the enzymes that animals use to synthesize dopamine.^[85] It has been proposed that animals derived their dopamine-synthesizing machinery from bacteria, via horizontal gene transfer that may have occurred relatively late in evolutionary time, perhaps as a result of the symbiotic incorporation of bacteria into eukaryotic cells that gave rise to mitochondria.^[85]

Animals

Dopamine is used as an intercellular messenger in virtually all multicellular animals.^[86] In sponges only a single report exists of the presence of dopamine, with no indication of its function;^[87] however, dopamine has been reported in the nervous systems of numerous radially symmetric species, including the jellyfish, hydra and some coral species of the cnidaria phylum.^[88] This dates the emergence of dopamine as a neurotransmitter back to the earliest appearance of the nervous system, over 500 million years ago in the Cambrian era. Dopamine functions as a neurotransmitter in vertebrates, echinoderms, arthropods, molluscs, and several types of worm.^[89]^[90]

In every type of animal that has been examined, dopamine has been seen to modify motor behavior.^[86] In the model organism, nematode Caenorhabditis elegans, it reduces locomotion and increases food-exploratory movements; in planarian flatworms it produces "screw-like" movements; in leeches it inhibits swimming and promotes crawling. Across a wide range of vertebrates, dopamine has an "activating" effect on behavior-switching and response selection, comparable to its effect in mammals.^[86]

Dopamine also consistently plays a role in reward learning, in all animal groups that have been examined except arthropods, although recent evidence suggests that dopamine at least mediates reward learning in fruit flies.^[91] In nematodes, planarians, molluscs, D. melanogaster and vertebrates, animals can be trained to repeat an action if it is consistently followed by an increase in dopamine levels.^[86] Arthropods have long been believed to be an exception. In these species—insects, crustaceans, etc.—dopamine was thought to have an aversive effect, with reward instead mediated by octopamine, a neurotransmitter that is not found in vertebrates but is closely related to norepinephrine.^[91] More recent studies, however, have found that the rewarding effect of octopamine comes from its activation of a set of dopaminergic neurons that had not been accessed in previous efforts.^[91]

Plants

Dopamine can be found in the peel and fruit pulp of bananas.

Many plants, including a variety of food plants, synthesize dopamine to varying degrees.^[92] The highest concentrations have been observed in bananas—the fruit pulp of red and yellow bananas contains dopamine at levels of 40 to 50 parts per million by weight.^[92] Potatoes, avocados, broccoli, and Brussels sprouts may also contain dopamine at levels of 1 part per million or more; oranges, tomatoes, spinach, beans, and other plants contain measurable concentrations less than 1 part per million.^[92] The dopamine in plants is synthesized from the amino acid tyrosine, by biochemical mechanisms similar to those that animals use.^[92] It can be metabolized in a variety of ways, producing melanin and a variety of alkaloids as byproducts.^[92] The functions of plant catecholamines have not been clearly established, but there is evidence that they play a role in the response to stressors such as bacterial infection, act as growth-promoting factors in some situations, and modify the way that sugars are metabolized. The receptors that mediate these actions have not yet been identified, nor have the intracellular mechanisms that they activate.^[92]

Dopamine consumed in food cannot act on the brain, because it cannot cross the blood–brain barrier.^[9] However, there are also a variety of plants that contain L-DOPA, the metabolic precursor of dopamine.^[93] The highest concentrations are found in the leaves and bean pods of plants of the genus Mucuna, especially in Mucuna pruriens (velvet beans), which have been used as a source for L-DOPA as a drug.^[94] Another plant containing substantial amounts of L-DOPA is Vicia faba, the plant that produces fava beans (also known as "broad beans"). The level of L-DOPA in the beans, however, is much lower than in the pod shells and other parts of the plant.^[95] The seeds of Cassia and Bauhinia trees also contain substantial amounts of L-DOPA.^[93]

In a species of marine green algae Ulvaria obscura, a major component of some algal blooms, dopamine is present in very high concentrations, estimated at 4.4% of dry weight. There is evidence that this dopamine functions as an anti-herbivore defense, reducing consumption by snails and isopods.^[96]

As a precursor for melanin

Melanins are a family of dark-pigmented substances found in a wide range of organisms.^[97] Chemically they are closely related to dopamine, and there is a type of melanin, known as dopamine-melanin, that can be synthesized by oxidation of dopamine via the enzyme tyrosinase.^[97] The melanin that darkens human skin is not of this type: it is synthesized by a pathway that uses L-DOPA as a precursor but not dopamine.^[97] However, there is substantial evidence that the neuromelanin that gives a dark color to the brain's substantia nigra is at least in part dopamine-melanin.^[98]

Dopamine-derived melanin probably appears in at least some other biological systems as well. Some of the dopamine in plants is likely to be used as a precursor for dopamine-melanin.^[99] The complex patterns that appear on butterfly wings, as well as black-and-white stripes on the bodies of insect larvae, are also thought to be caused by spatially structured accumulations of dopamine-melanin.^[100]

History and development

Dopamine was first synthesized in 1910 by George Barger and James Ewens at Wellcome Laboratories in London, England^[101] and first identified in the human brain by Kathleen Montagu in 1957. It was named dopamine because it is a monoamine whose precursor in the Barger-Ewens synthesis is 3,4-dihydroxyphenylalanine (levodopamine or L-DOPA). Dopamine's function as a neurotransmitter was first recognized in 1958 by Arvid Carlsson and Nils-Åke Hillarp at the Laboratory for Chemical Pharmacology of the National Heart Institute of Sweden.^[102] Carlsson was awarded the 2000 Nobel Prize in Physiology or Medicine for showing that dopamine is not only a precursor of norepinephrine (noradrenaline) and epinephrine (adrenaline), but is also itself a neurotransmitter.^[103]

Polydopamine

Research motivated by adhesive polyphenolic proteins in mussels led to the discovery in 2007 that a wide variety of materials, if placed in a solution of dopamine at slightly basic pH, will become coated with a layer of polymerized dopamine, often referred to as polydopamine.^[104]^[105] This polymerized dopamine forms by a spontaneous oxidation reaction, and is formally a type of melanin.^[106] Synthesis usually involves reaction of dopamine hydrochloride with Tris as a base in water. The structure of polydopamine is unknown.^[105]

Polydopamine coatings can form on objects ranging in size from nanoparticles to large surfaces.^[106] Polydopamine layers have chemical properties that have the potential to be extremely useful, and numerous studies have examined their possible applications.^[106] At the simplest level, they can be used for protection against damage by light, or to form capsules for drug delivery.^[106] At a more sophisticated level, their adhesive properties may make them useful as substrates for biosensors or other biologically active macromolecules.^[106]

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UpToDate Contents

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1. 原発性無月経の病因、診断、および治療 etiology diagnosis and treatment of primary amenorrhea
2. 女性の不妊評価 evaluation of female infertility
3. 思春期における多嚢胞性卵巣症候群の定義、臨床的特徴、および鑑別診断 definition clinical features and differential diagnosis of polycystic ovary syndrome in adolescents
4. 思春期における多嚢胞性卵巣症候群の診断的評価 diagnostic evaluation of polycystic ovary syndrome in adolescents
5. 関節リウマチおよび妊娠 rheumatoid arthritis and pregnancy

English Journal

Ontogenic characterization of gene expression in the developing neuroendocrine system of the chick.

Ellestad LE, Saliba J, Porter TE.SourceMolecular and Cell Biology Program, University of Maryland, College Park, MD 20742, USA. ellestad@umd.edu
General and comparative endocrinology.Gen Comp Endocrinol.2011 Mar 1;171(1):82-93. doi: 10.1016/j.ygcen.2010.12.006. Epub 2010 Dec 17.
The neuroendocrine system consists of five major hypothalamic-pituitary hormone axes that regulate several important metabolic processes, and it develops in all vertebrates during embryogenesis. In order to define initiation and establishment of these five axes, mRNA expression profiles of hypothala
PMID 21168412

The influence of regulatory T cells and diurnal hormone rhythms on T helper cell activity.

Bollinger T, Bollinger A, Naujoks J, Lange T, Solbach W.SourceInstitute of Medical Microbiology and Hygiene, University of Luebeck, Luebeck, Germany. Thomas.Bollinger@uk-sh.de
Immunology.Immunology.2010 Dec;131(4):488-500. doi: 10.1111/j.1365-2567.2010.03320.x.
Symptoms of diseases such as rheumatoid arthritis, which is T helper 1 (Th1) dependent, and asthma, which is T helper 2 (Th2) dependent, are influenced by diurnal rhythms and natural regulatory T cells (nTreg). However, the mechanisms responsible for the diurnal rhythm of disease activity have not b
PMID 20646075

The effect of sex hormones on bone metabolism of the otic capsule--an overview.

Horner KC.SourceDept Physiologie Neurovégétative, CRN2M-UMR 6231, Université Paul Cézanne, Boulevard Normandie Niémen, 13397 Marseille Cedex 20, France. kathleen.horner@univ-cezanne.fr
Hearing research.Hear Res.2009 Jun;252(1-2):56-60. doi: 10.1016/j.heares.2008.12.004. Epub 2008 Dec 24.
Bone resorption, which can occur after the menopause, has long been considered to due to the decrease of estrogen and so estrogen and estrogen/progestin treatment in women has been employed with the aim of slowing down the process. Other important factors have recently been considered, including fol
PMID 19121641

Japanese Journal

Isolation of the gene and hypothalamic cDNA for the common precursor of gonadotropin-releasing hormone and prolactin release-inhibiting factor in human and rat

ADELMAN JP.
Proc Natl Acad Sci USA 83, 179-183, 1986
NAID 80002802731

Extraction and Partial Purification of Prolactin-Release Stimulating Factor in Bovine Hypothalami

KOKUBU TOMOKUNI,SAWANO SHINJI,SHIRAKI MASARU,YAMASAKI MAKOTO,ISHIZUKA YUSAKU
Endocrinologia Japonica 22(3), 213-217, 1975
… Partial purification of prolactin-release stimulating factor (PRF) was performed by Sephadex G-25 gel filtration of bovine hypothalamic extracts. … PRF activity was evaluated on the basis of the measurement of immunoreactive prolactin released from the isolated rat hemipituitary <I>in vitro</I>. …
NAID 130000956342

Related Pictures

★リンクテーブル★

リンク元	「プロラクチン遊離阻害因子」「prolactin release-inhibiting hormone」
関連記事	「fact」「factor」「release」「inhibiting」「prolactin」

「プロラクチン遊離阻害因子」

Dopamine
IUPAC name	4-(2-Aminoethyl)benzene-1,2-diol
Synonyms	2-(3,4-Dihydroxyphenyl)ethylamine; 3,4-Dihydroxyphenethylamine; 3-hydroxytyramine; Intropin; Revivan; Oxytyramine; Prolactin inhibiting factor; Prolactin inhibiting hormone
Abbreviation	DA
Sources	substantia nigra; ventral tegmental area; many others
Targets	system-wide
Receptors	D1; D2; D3; D4; D5
Agonists	cocaine; amphetamines; apomorphine; bromocryptine
Antagonists	neuroleptics, metoclopramide
Precursor	L-DOPA
Synthesizing enzyme	DOPA decarboxylase
Metabolizing enzyme	MAO; COMT
Database links
CAS Registry Number	51-61-6 62-31-7 (hydrochloride)
PubChem	CID: 681
DrugBank	DB00988
ChemSpider	661
KEGG	D07870

　　[★]

英: prolactin release-inhibiting factor
関: プロラクチン放出抑制ホルモン

「prolactin release-inhibiting hormone」

　　[★]

プロラクチン放出抑制ホルモン

関: prolactin release-inhibiting factor

「fact」

　　[★]

n.

事実、現状、実際、実態

関: actual、actually、in fact、in practice、indeed、practically

「factor」

　　[★]

n.

因子、要因、要素、ファクター

関: element、elementary、factorial、parameter

「release」

　　[★]

n.

遊離、放出、リリース、

v.

遊離する、放出する

「inhibiting」

　　[★]

抑制性の、阻害性の

関: inhibitory、suppressive

「prolactin」

　　[★] プロラクチン

同: PRL

同: PRL

同: PRL

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