Mental disorder

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Mental disorder
Classification and external resources
Eight women representing prominent mental diagnoses in the 19th century. (Armand Gautier)
ICD-10	F.
MeSH	D001523

A mental disorder or mental illness is a psychological or behavioral pattern generally associated with subjective distress or disability that occurs in an individual, and which are not a part of normal development or culture. The recognition and understanding of mental health conditions has changed over time and across cultures, and there are still variations in the definition, assessment, and classification of mental disorders, although standard guideline criteria are widely accepted. A few mental disorders are diagnosed based on the harm to others, regardless of the subject's perception of distress. Over a third of people in most countries report meeting criteria for the major categories at some point in their life.
The causes are often explained in terms of a diathesis-stress model or biopsychosocial model. In biological psychiatry, mental disorders are conceptualized as disorders of brain circuits likely caused by developmental processes shaped by a complex interplay of genetics and experience.^[1]
Services are based in psychiatric hospitals or in the community. Diagnoses are made by psychiatrists or clinical psychologists using various methods, often relying on observation and questioning in interviews. Treatments are provided by various mental health professionals. Psychotherapy and psychiatric medication are two major treatment options as are social interventions, peer support and self-help. In some cases there may be involuntary detention and involuntary treatment where legislation allows.
Stigma and discrimination add to the suffering associated with the disorders, and have led to various social movements campaign for change.^{[clarification needed]}

Contents [show] 1 Classifications 1.1 Disorders 2 Causes 2.1 Gender-specific influences 3 Diagnosis 4 Management 4.1 Psychotherapy 4.2 Medication 4.3 Other 5 Prognosis 6 Epidemiology 7 History 7.1 Ancient civilizations 7.2 Europe 7.2.1 Middle Ages 7.2.2 Eighteenth century 7.2.3 Nineteenth century 7.2.4 Twentieth century 7.3 Europe and the U.S. 8 Society and culture 8.1 Professions and fields 8.2 Movements 8.3 Intangible experiences 8.4 Western bias 8.5 Relationships and morality 8.6 Laws and policies 8.7 Perception and discrimination 9 In animals 10 See also 11 Notes 11.1 Further reading 12 External links

[edit] Classifications

Main article: Classification of mental disorders

The definition and classification of mental disorders is a key issue for mental health and for users and providers of mental health services. Most international clinical documents use the term "mental disorder". There are currently two widely established systems that classify mental disorders—ICD-10 Chapter V: Mental and behavioural disorders, part of the International Classification of Diseases produced by the World Health Organization (WHO), and the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) produced by the American Psychiatric Association (APA). Both list categories of disorder and provide standardized criteria for diagnosis. They have deliberately converged their codes in recent revisions so that the manuals are often broadly comparable, although significant differences remain. Other classification schemes may be used in non-western cultures (see, for example, the Chinese Classification of Mental Disorders), and other manuals may be used by those of alternative theoretical persuasions, for example the Psychodynamic Diagnostic Manual. In general, mental disorders are classified separately to neurological disorders, learning disabilities or mental retardation.
Unlike most of the above systems, some approaches to classification do not employ distinct categories of disorder or dichotomous cut-offs intended to separate the abnormal from the normal. There is significant scientific debate about the different kinds of categorization and the relative merits of categorical versus non-categorical (or hybrid) schemes, with the latter including spectrum, continuum or dimensional systems.

[edit] Disorders

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There are many different categories of mental disorder, and many different facets of human behavior and personality that can become disordered.^{[2][3][4][5][6]}
Anxiety or fear that interferes with normal functioning may be classified as an anxiety disorder.^[7] Commonly recognized categories include specific phobias, generalized anxiety disorder, social anxiety disorder, panic disorder, agoraphobia, obsessive-compulsive disorder and post-traumatic stress disorder.
Other affective (emotion/mood) processes can also become disordered. Mood disorder involving unusually intense and sustained sadness, melancholia or despair is known as Major depression or Clinical depression (milder but still prolonged depression can be diagnosed as dysthymia). Bipolar disorder (also known as manic depression) involves abnormally "high" or pressured mood states, known as mania or hypomania, alternating with normal or depressed mood. Whether unipolar and bipolar mood phenomena represent distinct categories of disorder, or whether they usually mix and merge together along a dimension or spectrum of mood, is under debate in the scientific literature.^[8]
Patterns of belief, language use and perception can become disordered (e.g. delusions, thought disorder, hallucinations). Psychotic disorders in this domain include schizophrenia, and delusional disorder. Schizoaffective disorder is a category used for individuals showing aspects of both schizophrenia and affective disorders. Schizotypy is a category used for individuals showing some of the characteristics associated with schizophrenia but without meeting cut-off criteria.
Personality—the fundamental characteristics of a person that influence his or her thoughts and behaviors across situations and time—may be considered disordered if judged to be abnormally rigid and maladaptive. Categorical schemes list a number of different such personality disorders, including those sometimes classed as eccentric (e.g. paranoid, schizoid and schizotypal personality disorders), to those sometimes classed as dramatic or emotional (antisocial, borderline, histrionic or narcissistic personality disorders) or those seen as fear-related (avoidant, dependent, or obsessive-compulsive personality disorders). If an inability to sufficiently adjust to life circumstances begins within three months of a particular event or situation, and ends within six months after the stressor stops or is eliminated, it may instead be classed as an adjustment disorder. There is an emerging consensus that so-called "personality disorders", like personality traits in general, actually incorporate a mixture of acute dysfunctional behaviors that resolve in short periods, and maladaptive temperamental traits that are more stable.^[9] Furthermore, there are also non-categorical schemes that rate all individuals via a profile of different dimensions of personality rather than using a cut-off from normal personality variation, for example through schemes based on the Big Five personality traits.^[10]
Eating disorders involve disproportionate concern in matters of food and weight.^[7] Categories of disorder in this area include anorexia nervosa, bulimia nervosa, exercise bulimia or binge eating disorder.
Sleep disorders such as insomnia involve disruption to normal sleep patterns, or a feeling of tiredness despite sleep appearing normal.
Sexual and gender identity disorders may be diagnosed, including dyspareunia, gender identity disorder and ego-dystonic homosexuality. Various kinds of paraphilia are considered mental disorders (sexual arousal to objects, situations, or individuals that are considered abnormal or harmful to the person or others).
People who are abnormally unable to resist certain urges or impulses that could be harmful to themselves or others, may be classed as having an impulse control disorder, including various kinds of tic disorders such as Tourette's syndrome, and disorders such as kleptomania (stealing) or pyromania (fire-setting). Various behavioral addictions, such as gambling addiction, may be classed as a disorder. Obsessive-compulsive disorder can sometimes involve an inability to resist certain acts but is classed separately as being primarily an anxiety disorder.
The use of drugs (legal or illegal), when it persists despite significant problems related to the use, may be defined as a mental disorder termed substance dependence or substance abuse (a broader category than drug abuse). The DSM does not currently use the common term drug addiction and the ICD simply talks about "harmful use". Disordered substance use may be due to a pattern of compulsive and repetitive use of the drug that results in tolerance to its effects and withdrawal symptoms when use is reduced or stopped.
People who suffer severe disturbances of their self-identity, memory and general awareness of themselves and their surroundings may be classed as having a dissociative identity disorder, such as depersonalization disorder or Dissociative Identity Disorder itself (which has also been called multiple personality disorder, or "split personality"). Other memory or cognitive disorders include amnesia or various kinds of old age dementia.
A range of developmental disorders that initially occur in childhood may be diagnosed, for example autism spectrum disorders, oppositional defiant disorder and conduct disorder, and attention deficit hyperactivity disorder (ADHD), which may continue into adulthood.
Conduct disorder, if continuing into adulthood, may be diagnosed as antisocial personality disorder (dissocial personality disorder in the ICD). Popularist labels such as psychopath (or sociopath) do not appear in the DSM or ICD but are linked by some to these diagnoses.
Disorders appearing to originate in the body, but thought to be mental, are known as somatoform disorders, including somatization disorder and conversion disorder. There are also disorders of the perception of the body, including body dysmorphic disorder. Neurasthenia is an old diagnosis involving somatic complaints as well as fatigue and low spirits/depression, which is officially recognized by the ICD-10 but no longer by the DSM-IV.^[11]
Factitious disorders, such as Munchausen syndrome, are diagnosed where symptoms are thought to be experienced (deliberately produced) and/or reported (feigned) for personal gain.
There are attempts to introduce a category of relational disorder, where the diagnosis is of a relationship rather than on any one individual in that relationship. The relationship may be between children and their parents, between couples, or others. There already exists, under the category of psychosis, a diagnosis of shared psychotic disorder where two or more individuals share a particular delusion because of their close relationship with each other.
Various new types of mental disorder diagnosis are occasionally proposed. Among those controversially considered by the official committees of the diagnostic manuals include self-defeating personality disorder, sadistic personality disorder, passive-aggressive personality disorder and premenstrual dysphoric disorder.
Two recent unique isolated proposals are solastalgia by Glenn Albrecht and hubris syndrome by David Owen. The application of the concept of mental illness to the phenomena described by these authors has in turn been critiqued by Seamus Mac Suibhne.^[12]

Hyperplasia (false dignoses of "cancer")

FALSE DIAGNOSES OF "CANCER"
Damaging if intentionally caused and left untreated and also in combination with other conditions such metal toxicities.

Hyperplasia

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-plasia
Anaplasia – dedifferentiation
Hyperplasia – physiological proliferation
Neoplasia – abnormal proliferation
Dysplasia – maturation abnormality
Metaplasia – cell type conversion
Desmoplasia – connective tissue growth

Hyperplasia
Classification and external resources
MeSH	D006965

Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue beyond that which is ordinarily seen. Hyperplasia may result in the gross enlargement of an organ and the term is sometimes mixed with benign neoplasia/ benign tumor.

Hyperplasia is a common preneoplastic response to stimulus. Microscopically cells resemble normal cells but are increased in numbers. Sometimes cells may be also increased in size (hypertrofia)^[1]. Hyperplasia is different from hypertrophy in that the adaptive cell change in hypertrophy is an increase in cell size, whereas hyperplasia involves an increase in the number of cells.

Simple illustration to show the difference between hyperplasia and hypertrophy.

Contents [show] 1 Difference from neoplasia 2 Causes 3 Examples in human biology and disease 4 References 5 External links

[edit] Difference from neoplasia

Hyperplasia is considered to be a physiological (normal) response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasiacancer and benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.^[2] (the process underlying

As seen in examples below, such physiological proliferation of cells may in fact be secondarily due to a pathological cause. Still, the proliferation itself is a normal response to another abnormal condition, in contrast to neoplasia, where the proliferation in itself is abnormal.

[edit] Causes

Hyperplasia may be due to any number of causes, including increased demand (for example, proliferation of basal layer of epidermis to compensate skin loss), chronic inflammatory response, hormonal dysfunctions, or compensation for damage or disease elsewhere. Hyperplasia may be harmless and occur on a particular tissue. An example of a normal hyperplastic response would be the growth and multiplication of milk-secreting glandular cells in the breast as a response to pregnancy, thus preparing for future breast feeding.

Hyperplasia may also be induced artificially by injecting hormones such as IGF-1 and human growth hormone. Perhaps the most interesting and potent effect IGF has on the human body is its ability to cause hyperplasia, which is an actual splitting of cells.^{[original research?]} By contrast, hypertrophy is what occurs, for example, to skeletal muscle cells during weight training and steroid use and is simply an increase in the size of the cells. With IGF use, one is able to cause hyperplasia which actually increases the number of muscle cells present in the tissue. Weight training with or without anabolic steroid use enables these new cells to mature in size and strength. In addition, animal tests have shown that stretching a muscle can trigger hyperplasia, though this phenomenon has yet to be confirmed in humans. Hyperplasia may also be induced through specific power output training for athletic performance, thus increasing the number of muscle fibers instead of increasing the size of a single fiber. ^[3]

Hyperplasia may also occur abnormally, and is associated with a variety of clinical diseases.

[edit] Examples in human biology and disease

Some of the more commonly-known clinical forms of hyperplasia, or conditions leading to hyperplasia, are:

• Cushing's disease – Physiopathology of hyperplasia of adrenal cortex due to increased circulating level of ACTH (adrenocorticotropic hormone).
• Congenital adrenal hyperplasia
• Endometrial hyperplasia – Hyperproliferation of the endometrium, usually in response to unopposed estrogen stimulation in the setting of polycystic ovary syndrome or exogenous administration of hormones. Atypical endometrial hyperplasia may represent an early neoplastic process which can lead to endometrial adenocarcinoma.
• Benign prostatic hyperplasia, also known as prostate enlargement.
• Hyperplasia of the breast – "Hyperplastic" lesions of the breast include usual ductal hyperplasia, a focal expansion of the number of cells in a terminal breast duct, and atypical ductal hyperplasia, in which a more abnormal pattern of growth is seen, and which is associated with an increased risk of developing breast cancer. The biology of these lesions is the subject of dispute, with some authorities arguing that both of these lesions are the result of neoplasia, and that the application of the term "hyperplasia" in this instance is "inaccurate."^[4]
• Intimal hyperplasia – The thickening of the Tunica intima of a blood vessel as a complication of a reconstruction procedure or endarterectomy. Intimal hyperplasia is the universal response of a vessel to injury and is an important reason of late bypass graft failure, particularly in vein and synthetic vascular grafts.
• Focal epithelial hyperplasia (also known as Heck's disease) – This is a wart-like growth in the mucous tissues of the mouth or, rarely, throat that is caused by certain sub-types of the human papillomavirus (HPV). Heck's disease has not been known to cause cancer.
• Sebaceous hyperplasia – In this condition, small yellowish growths develop on the skin, usually on the face. This condition is neither contagious nor dangerous.
• Compensatory liver hyperplasia – The liver undergoes cellular division after acute injury, resulting in new cells that restore liver function back to baseline. Approximately 75% of the liver can be acutely damaged or resected with seemingly full regeneration through hepatocyte division, i.e., hyperplasia. This is the basis for living-donor liver transplants.

[edit] References

1. ^ M. Donald McGavin, James F. Zachary (2007). Pathologic Basis of Veterinary Disease, Fourth Edition. Mosby Elsevier. 
2. ^ Ramzi Cotran, Vinay Kumar, Tucker Collins (1999). Robbins Pathologic Basis of Disease, Sixth Edition. W.B. Saunders. ISBN 0-7216-7335-X. OCLC 222671811. 
3. ^ Antonio J, Gonyea WJ (Aug 1994). "Muscle fiber splitting in stretch-enlarged avian muscle". Med Sci Sports Exerc. 26 (8): 973–977. PMID 7968431. 
4. ^ Tavassoli FA (2005). "Breast pathology: rationale for adopting the ductal intraepithelial neoplasia (DIN) classification". Nature Clinical Practice. Oncology 2 (3): 116–117. doi:10.1038/ncponc0109. PMID 16264885.

Dopaminergic (modern diseases)

Dopaminergic

Main article: Dopamine

The chemical structure of the neurotransmitter dopamine

Look up dopaminergic in Wiktionary, the free dictionary.

Dopaminergic means related to the neurotransmitter dopamine.^[1] For example, certain proteins such as the dopamine transporter (DAT), vesicular monoamine transporter 2 (VMAT₂), and dopamine receptors can be classified as dopaminergic, and neurons which synthesize or contain dopamine and synapses with dopamine receptors in them may also be labeled as dopaminergic. Enzymes which regulate the biosynthesis or metabolism of dopamine such as aromatic L-amino acid decarboxylase (AAAD) or DOPA decarboxylasemonoamine oxidase (MAO), and catechol O-methyl transferase (COMT) may be referred to as dopaminergic as well. Lastly, any endogenous or exogenous chemical substance which acts to affect dopamine receptors or dopamine release through indirect actions (for example, on neurons that synapse onto neurons that release dopamine or express dopamine receptors) can also be said to have dopaminergic effects, two prominent examples being opioids which enhance dopamine release indirectly in the reward pathways, and amphetamines, which enhance dopamine release directly by binding to, and inhibiting VMAT₂. (DDC),

[edit] Supplements and drugs

A complete list of dopaminergic substances used as supplements and drugs includes:

• Dopamine (DA; Intropan, Inovan, Revivan, Rivimine, Dopastat, Dynatra, etc) itself, which is used in the treatment of severe hypotension, circulatory shock, and cardiac arrest as a vasopressor or antihypotensive agent.

• Precursors including L-phenylalanine (PHE), L-tyrosine (TYR), and L-DOPA (Levodopa; Sinemet, Parcopa, Atamet, Stalevo, Madopar, Prolopa, etc; also found in Mucuna pruriens (Velvet Bean)), which are all used as dietary supplements, and the latter of which is also used in the treatment of Parkinson's disease (PD).

• Cofactors including ferrous iron (Fe²⁺), tetrahydrobiopterin (THB, BH₄), vitamin B₃ (niacin, niacinamide) → NADPH, vitamin B₆ (pyridoxine, pyridoxamine, pyridoxal → pyridoxal phosphatevitamin B₉ (folic acid) → tetrahydrofolic acid (THFA, H₄FA), vitamin C (ascorbic acid), and zinc (Zn²⁺), which are used as dietary supplements. (PLP),

• Dopamine receptor agonists such as apomorphine (Apokyn, Uprima), bromocriptine (Parolodel), cabergoline (Dostinex), dihydrexidine (LS-186,899), dopamine (Intropin, Revivan), fenoldopampiribedil (Trivastal), lisuride (Dopergin), pergolide (Permax), pramipexole (Mirapex), ropinirole (Requip), and rotigotine (Neupro), which are used in the treatment of Parkinson's diseaserestless legs syndrome (RLS), hyperprolactinemia (HPA), and sexual dysfunction (SD), as well as are being investigated in the treatment of depression and anxiety as antidepressants and anxiolytics, respectively. (Corlopam), (PD),

• Dopamine receptor antagonists including typical antipsychotics such as chlorpromazine (Thorazine), fluphenazine (Prolixin), haloperidol (Haldol), loxapine (Loxitane), molindone (Moban), perphenazinepimozide (Orap), thioridazine (Mellaril), thiothixene (Navane), and trifluoperazineatypical antipsychotics such as amisulpride (Solian), clozapine (Clozaril), olanzapinequetiapine (Seroquel), risperidone (Risperdal), sulpiride (Dogmatil), and ziprasidoneantiemetics like domperidone, metoclopramide (Reglan), and prochlorperazineschizophrenia (SCZ) and bipolar disorder (BD) as antipsychotics, and nausea and vomiting. (Trilafon), (Stelazine), the (Zyprexa), (Geodon), and (Compazine), among others, which are used in the treatment of schizophrenia (SCZ) and bipolar disorder (BD) as antipsychotics, and nausea and vomiting.

• Dopamine reuptake inhibitors (DRIs) or dopamine transporter (DAT) inhibitors such as methylphenidate (Ritalin, Focalin, Concerta), bupropion (Wellbutrin, Zyban), amineptine (Survector, Maneon, Directin), and nomifensine (Merital, Alival), as well as cocaine ("Coke", "Crack", etc), methylenedioxypyrovalerone (MDPV; "Sonic"), ketamine (K; Ketalar, Ketanest, Ketaset; "Special-K", "Kit Kat", etc), and phencyclidine (PCP; Sernyl; "Angel Dust", "Rocket Fuel", etc), among others, which are used in the treatment of attention-deficit hyperactivity disorder (ADHD) and narcolepsy as psychostimulants, obesity as anorectics, depression and anxiety as antidepressants and anxiolytics, respectively, drug addiction as anticraving agents, and sexual dysfunction, as well as illicitstreet drugs.

• Dopamine releasing agents (DRAs) such as amphetamine (Adderall, Dexedrine; "Speed"), lisdexamfetamine (Vyvanse), methamphetamine (Desoxyn; "Meth", "Crank", "Crystal", etc), methylenedioxymethamphetamine (MDMA; "Ecstasy", "E", "X", "XTC", etc), phenmetrazine (Preludin; "Prellies"), pemoline (Cylert), 4-methylaminorex (4-MAR; "Ice", "Euphoria", etc), and benzylpiperazineattention-deficit hyperactivity disorder (ADHD) and narcolepsy as psychostimulants, obesity as anorectics, depression and anxiety as antidepressants and anxiolytics, respectively, drug addiction as anticraving agents, and sexual dysfunction, as well as illicit street drugs. (BZP; "Bennies", "A2", "Sunrise", "Frenzy", etc), among many others, which, like DRIs, are used in the treatment of

• Dopamine activity enhancers such as BPAP and PPAP, which are currently only research chemicals, but are being investigated for clinical development in the treatment of a number of medical disorders.

• Vesicular monoamine transporter 2 (VMAT₂) inhibitors such as reserpine (Serpasil), tetrabenazinedeserpidine (Harmonyl), which are used as sympatholytics or antihypertensives, and in the past as antipsychotics. (Nitoman, Xenazine), and

• Monoamine oxidase (MAO) inhibitors (MAOIs) including nonselective agents such as phenelzinetranylcypromine (Parnate), and isocarboxazid (Marplan), MAO_A selective agents like moclobemide (Aurorix, Manerix), and MAO_B selective agents such as selegiline (Eldepryl, Zelapar, Emsam), rasagiline (Azilect), and pargyline (Eutonyl), as well as the harmala alkaloids like harmine, harmaline, tetrahydroharmine, harmalol, harman, and norharman, which are found to varying degrees in Nicotiana tabacum (Tobacco; also cigarettes, cigars, chew, hookah, etc), Banisteriopsis caapiPeganum harmala (Harmal, Syrian Rue), Passiflora incarnata (Passion Flower), and Tribulus terrestris (Puncture Vine), among others, which are used in the treatment of depression and anxiety as antidepressants and anxiolytics, respectively, in the treatment of Parkinson's disease (PD) and dementia, and for the recreational purpose of boosting the effects of certain drugsphenethylamine (PEA) and psychedelics like dimethyltryptamine (DMT) via inhibiting their metabolism. (Nardil), (Ayahausca, Caapi, Yage), like

• Catechol O-methyl transferase (COMT) inhibitors such as entacapone (Comtan, Stalevo) and tolcapone (Tasmar), which are used in the treatment of Parkinson's disease (PD).

• Dopamine β-hydroxylase (DBH) inhibitors like disulfiram (Antabuse), which is used in the treatment of drug addiction as an anticraving agent.

• Phenylalanine hydroxylase (PAH) inhibitors like 3,4-dihydroxystyrene (DHS) which is currently only a research chemical with no suitable therapeutic indications, likely on account of the fact that such drugs would induce the potentially highly dangerous hyperphenylalaninemia (HPA) and/or phenylketonuria (PKU).

• Tyrosine hydroxylase (TH) inhibitors like metirosine (Demser), which is used in the treatment of pheochromocytoma (PCC) as a sympatholytic or antihypertensive agent.

• Aromatic L-amino acid decarboxylase (AAAD) or DOPA decarboxylase (DDC) inhibitors including benserazide (Prolopa, Madopar, etc), carbidopa (Lodosyn, Atamet, Parcopa, Sinemet, Stalevo, etc), and methyldopa (Aldomet, Aldoril, Dopamet, Dopegyt, etc), which are used in the treatment of Parkinson's disease (PD) in augmentation of L-DOPA ((Levodopa; Sinemet, Parcopa, Atamet, Stalevo, Madopar, Prolopa, etc)) to block the peripheral conversion of dopamine thereby inhibiting undesirable side effects, and as sympatholytic or antihypertensive agents.

Others such as hyperforin and adhyperforin (both found in Hypericum perforatum (St. John's Wort (SJW))), L-theanine (found in Camellia sinensis (Tea Plant, also known as Black, White, Oolong, Pu-erh, or Green Tea)), and S-adenosyl-L-methionine (SAMe), which are all dietary supplements used mainly  for the remedification of depression and anxietyantidepressants and anxiolytics, respectively.

Dopamine Dopaminergic system (misinformation included)

 Dopamine

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Jump to: navigation, search

For other uses, see Dopamine (disambiguation).

Dopamine
IUPAC name[hide] 4-(2-aminoethyl)benzene-1,2-diol
Other names[hide] 2-(3,4-dihydroxyphenyl)ethylamine; 3,4-dihydroxyphenethylamine; 3-hydroxytyramine; DA; Intropin; Revivan; Oxytyramine
Identifiers
CAS number	51-61-6 Y, 62-31-7 (hydrochloride)
PubChem	681
ChemSpider	661
UNII	VTD58H1Z2X Y
SMILES	[show] c1cc(c(cc1CCN)O)O
InChI	[show] 1/C8H11NO2/c9-4-3-6-1-2-7(10)8(11)5-6/h1-2,5,10-11H,3-4,9H2
InChI key	[show] VYFYYTLLBUKUHU-UHFFFAOYAA
Properties
Molecular formula	C8H11NO2
Molar mass	153.18 g/mol
Density	1.26 g/cm3
Melting point	128 °C, 401 K, 262 °F
Boiling point	decomposes
Solubility in water	60.0 g/100 ml
Hazards
R-phrases	R36/37/38
S-phrases	S26 S36
(what is this?)  (verify) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)Y
Infobox references

Dopamine is a catecholamine neurotransmitter present in a wide variety of animals, including both vertebrates and invertebrates. In the brain, this phenethylamine functions as a neurotransmitter, activating the five types of dopamine receptors—D₁, D₂, D₃, D₄, and D₅—and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.^[1] Dopamine is also a neurohormonehypothalamus. Its main function as a hormone is to inhibit the release of prolactin from the anterior lobe of the pituitary. released by the

Dopamine is available as an intravenous medication acting on the sympathetic nervous system, producing effects such as increased heart rate and blood pressure. However, because 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, L-DOPA, which is the precursor of dopamine, can be given because it can cross the blood-brain barrier.

Contents [show] 1 History 2 Biochemistry 2.1 Name and family 2.2 Biosynthesis 2.3 Inactivation and degradation 3 Functions in the brain 3.1 Anatomy 3.2 Tonic and phasic activity 3.3 Movement 3.4 Cognition and frontal cortex 3.5 Regulating prolactin secretion 3.6 Motivation and pleasure 3.6.1 Reinforcement 3.6.2 Reuptake inhibition, expulsion 3.6.3 Incentive salience 3.6.4 Dopamine, learning, and reward-seeking behavior 3.6.5 Animal studies 3.6.6 The effects of drugs that reduce dopamine activity 3.6.7 Opioid and cannabinoid transmission 3.6.8 Sociability 3.6.9 Processing of pain 3.6.10 Salience 3.6.11 Behavior disorders 3.7 Latent inhibition and creative drive 3.8 Chemoreceptor trigger zone 3.9 Dopaminergic mind hypothesis 4 Links to psychosis 5 Therapeutic use 6 Nonneural functions 6.1 Immunoregulatory 6.2 Peripheral effects 6.3 Renal effects 7 Dopamine and fruit browning 8 See also 9 References 10 External links

[edit] History

Dopamine was first synthesized in 1910 by George Barger and James Ewens at Wellcome Laboratories in London, England.^[2] It was named dopamine because it was a monoamine, and its synthetic precursor was 3,4-dihydroxyphenylalanine (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.^[3] Carlsson was awarded the 2000 Nobel Prize in Physiology or Medicine for showing that dopamine is not just a precursor of norepinephrine (noradrenaline) and epinephrine (adrenaline), but a neurotransmitter as well.

[edit] Biochemistry

Biosynthesis of dopamine

[edit] Name and family

Dopamine has the chemical formula C₆H₃(OH)₂-CH₂-CH₂-NH₂. Its chemical name is "4-(2-aminoethyl)benzene-1,2-diol" and its abbreviation is "DA."
As a member of the catecholamine family, dopamine is a precursor to norepinephrine (noradrenaline) and then epinephrine (adrenaline) in the biosynthetic pathways for these neurotransmitters.

The effects of drugs that reduce dopamine activity

In humans, drugs that reduce dopamine activity (neuroleptics, e.g. antipsychotics) have been shown to reduce motivation, cause anhedonia (inability to experience pleasure), and long-term use has been associated with the irreversible movement disorder, tardive dyskinesia.^[26] Furthermore, antipsychotic drugs are associated with weight gain, diabetes, lactation, gynecomastia, drooling, dysphoria, fatigue, sexual dysfunction, and heart rhythm problems. Selective D2/D3 agonists pramipexole and ropinirole, used to treat restless legs syndrome^[27] (RLS), have limited anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale (SHAPS).

[edit] Opioid and cannabinoid transmission

Opioid and cannabinoid transmission instead of dopamine may modulate consummatory pleasure and food palatability (liking).^[28] This could explain why animals' "liking" of food is independent of brain dopamine concentration. Other consummatory pleasures, however, may be more associated with dopamine. One study found that both anticipatory and consummatory measures of sexual behavior (male rats) were disrupted by DA receptor antagonists.^[29] Libido can be increased by drugs that affect dopamine, but not by drugs that affect opioid peptides or other neurotransmitters.

[edit] Sociability

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 disorder, manic subjects can become hypersocial, as well as hypersexual.^{[citation needed]} This is credited to an increase in dopamine, because mania can be reduced by dopamine-blocking anti-psychotics.^[30]

[edit] Processing of pain

Dopamine has been demonstrated to play a role in pain processing in multiple levels of the central nervous system including the spinal cord,^[31] periaqueductal gray (PAG),^[32] thalamus,^[33] basal ganglia,^[34][35] insular cortex,^[36][37] and cingulate cortex.^[38] Accordingly, decreased levels of dopamine have been associated with painful symptoms that frequently occur in Parkinson's disease.^[39] Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including burning mouth syndrome,^[40] fibromyalgia,^[41][42] and restless legs syndrome.^[43] In general, the analgesic capacity of dopamine occurs as a result of dopamine D2 receptor activation; however, exceptions to this exist in the PAG, in which dopamine D1 receptor activation attenuates pain presumably via activation of neurons involved in descending inhibition.^[44] In addition, D1 receptor activation in the insular cortex appears to attenuate subsequent pain-related behavior.

[edit] Salience

Dopamine may also have a role in the salience of potentially important stimuli, such as sources of reward or of danger.^[45] This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.

[edit] Behavior disorders

Deficient dopamine neurotransmission is implicated in attention-deficit hyperactivity disorder, and stimulant medications used to successfully treat the disorder increase dopamine neurotransmission, leading to decreased symptoms.^[46] Consistent with this hypothesis, dopaminergic pathways have a role in inhibitory action control and the inhibition of the tendency to make unwanted actions.^[47]

The long term use of levodopa in Parkinson's disease has been linked to dopamine dysregulation syndrome.^[48]

[edit] Latent inhibition and creative drive

Dopamine in the mesolimbic pathway increases general arousal and goal directed behaviors and decreases latent inhibition; all three effects increase the creative drive of idea generation. This has led to a three-factor model of creativity involving the frontal lobes, the temporal lobes, and mesolimbic dopamine.^[49]

[edit] Chemoreceptor trigger zone

Dopamine is one of the neurotransmitters implicated in the control of nausea and vomiting via interactions in the chemoreceptor trigger zone. Metoclopramide is a D2-receptor antagonist that functions as a prokinetic/antiemetic.

[edit] Dopaminergic mind hypothesis

The dopaminergic mind hypothesis seeks to explain the differences between modern humans and their hominid relatives by focusing on changes in dopamine.^[50] It theorizes that increased levels of dopamine were part of a general physiological adaptation due to an increased consumption of meat around two million years ago in Homo habilis, and later enhanced by changes in diet and other environmental and social factors beginning approximately 80,000 years ago. Under this theory, the "high-dopamine" personality is characterized by high intelligence, a sense of personal destiny, a religious/cosmic preoccupation, an obsession with achieving goals and conquests, an emotional detachment that in many cases leads to ruthlessness, and a risk-taking mentality. High levels of dopamine are proposed to underlie increased psychological disorders in industrialized societies. According to this hypothesis, a "dopaminergic society" is an extremely goal-oriented, fast-paced, and even manic society, "given that dopamine is known to increase activity levels, speed up our internal clocks and create a preference for novel over unchanging environments."^[50] In the same way that high-dopamine individuals lack empathy and exhibit a more masculine behavioral style, dopaminergic societies are "typified by more conquest, competition, and aggression than nurturance and communality."^[50] Although behavioral evidence and some indirect anatomical evidence (e.g., enlargement of the dopamine-rich striatum in humans)^[51] support a dopaminergic expansion in humans, there is still no direct evidence that dopamine levels are markedly higher in humans relative to other apes.^[52] However, recent discoveries about the sea-side settlements of early man may provide evidence of dietary changes consistent with this hypothesis.^[53]

[edit] Links to psychosis

Main article: Dopamine hypothesis of schizophrenia

Abnormally high dopaminergic transmission has been linked to psychosis and schizophrenia.^[54] Increased dopaminergic functional activity, specifically in the mesolimbic pathway, is found in schizophrenic individuals. Anti-psychotic medications act largely as dopamine antagonists, inhibiting dopamine at the receptor level, and thereby blocking the effects of the neurochemical in a dose-dependant manner. The older, so-called typical antipsychotics most commonly act on D2 receptors,^[55] while the atypical drugs also act on D1, D3 and D4 receptors.^[56][57] The finding that drugs such as amphetamines, methamphetamine and cocaine, which can increase dopamine levels by more than tenfold,^[58] can temporarily cause psychosis, provides further evidence for this link.^[5

Therapeutic use

Main article: L-DOPA

Levodopa is a dopamine precursor used in various forms to treat Parkinson's disease and dopa-responsive dystonia. 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.