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Addiction and dependence glossary[1][2][3][4] | |
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Amphetamine[note 1] (contracted from alpha-methylphenethylamine) is a potent central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity.[8][9] Amphetamine was discovered in 1887 and exists as two enantiomers:[note 2] levoamphetamine and dextroamphetamine.[8][11][12] Amphetamine properly refers to a specific chemical,[13] the racemic free base,[14][15] which is equal parts of the two enantiomers, levoamphetamine and dextroamphetamine, in their pure amine forms. The term is frequently used informally to refer to any combination of the enantiomers, or to either of them alone.[6][13][15] Historically, it has been used to treat nasal congestion and depression.[16] Amphetamine is also used as an athletic performance enhancer and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant.[sources 1] It is a prescription drug in many countries, and unauthorized possession and distribution of amphetamine are often tightly controlled due to the significant health risks associated with recreational use.[21][22]
The first amphetamine pharmaceutical was Benzedrine, a brand which was used to treat a variety of conditions.[8][16] Currently, pharmaceutical amphetamine is prescribed as racemic amphetamine, Adderall,[note 3] dextroamphetamine, or the inactive prodrug lisdexamfetamine.[8][9][23][24] Amphetamine increases monoamine and excitatory neurotransmission in the brain, with its most pronounced effects targeting the norepinephrine and dopamine neurotransmitter systems.[sources 2]
At therapeutic doses, amphetamine causes emotional and cognitive effects such as euphoria, change in desire for sex, increased wakefulness, and improved cognitive control.[sources 3] It induces physical effects such as improved reaction time, fatigue resistance, and increased muscle strength.[18][32] Larger doses of amphetamine may impair cognitive function and induce rapid muscle breakdown.[17][21] Drug addiction is a serious risk with large recreational doses but is unlikely to arise from typical long-term medical use at therapeutic doses.[33][34][35] Very high doses can result in psychosis (e.g., delusions and paranoia) which rarely occurs at therapeutic doses even during long-term use.[24][36] Recreational doses are generally much larger than prescribed therapeutic doses and carry a far greater risk of serious side effects.[31][37]
Amphetamine belongs to the phenethylamine class.[38][39][40] It is also the parent compound of its own structural class, the substituted amphetamines,[note 4] which includes prominent substances such as bupropion, cathinone, MDMA, and methamphetamine.[38][39][40] Amphetamine is also chemically related to the naturally occurring trace amine neuromodulators, specifically phenethylamine and N-methylphenethylamine, both of which are produced within the human body.[38] Phenethylamine is the parent compound of amphetamine, while N-methylphenethylamine is a positional isomer of amphetamine that differs only in the placement of the methyl group.[42]
Amphetamine[note 5] (contracted from alpha-methylphenethylamine) is a potent central nervous system (CNS) stimulant that is used in the treatment of attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity.[8][9] Amphetamine was discovered in 1887 and exists as two enantiomers:[note 6] levoamphetamine and dextroamphetamine.[8][11] Amphetamine properly refers to a specific chemical,[13] the racemic free base,[14][15] which is equal parts of the two enantiomers, levoamphetamine and dextroamphetamine, in their pure amine forms. The term is frequently used informally to refer to any combination of the enantiomers, or to either of them alone.[6][13][15] Historically, it has been used to treat nasal congestion and depression.[16] Amphetamine is also used as an athletic performance enhancer and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant.[sources 4] It is a prescription drug in many countries, and unauthorized possession and distribution of amphetamine are often tightly controlled due to the significant health risks associated with recreational use.[21][22]
The first amphetamine pharmaceutical was Benzedrine, a brand which was used to treat a variety of conditions.[8][16] Currently, pharmaceutical amphetamine is prescribed as racemic amphetamine, Adderall,[note 3] dextroamphetamine, or the inactive prodrug lisdexamfetamine.[8][9][23][24] Amphetamine increases monoamine and excitatory neurotransmission in the brain, with its most pronounced effects targeting the norepinephrine and dopamine neurotransmitter systems.[sources 5]
At therapeutic doses, amphetamine causes emotional and cognitive effects such as euphoria, change in desire for sex, increased wakefulness, and improved cognitive control.[sources 6] It induces physical effects such as improved reaction time, fatigue resistance, and increased muscle strength.[18] Larger doses of amphetamine may impair cognitive function and induce rapid muscle breakdown.[17][21] Drug addiction is a serious risk with large recreational doses but is unlikely to arise from typical long-term medical use at therapeutic doses.[33][34][35] Very high doses can result in psychosis (e.g., delusions and paranoia) which rarely occurs at therapeutic doses even during long-term use.[24][36] Recreational doses are generally much larger than prescribed therapeutic doses and carry a far greater risk of serious side effects.[31][37]
Amphetamine belongs to the phenethylamine class.[38][39][40] It is also the parent compound of its own structural class, the substituted amphetamines,[note 7] which includes prominent substances such as bupropion, cathinone, MDMA, and methamphetamine.[38][39][40] Amphetamine is also chemically related to the naturally occurring trace amine neuromodulators, specifically phenethylamine and N-methylphenethylamine, both of which are produced within the human body.[38] Phenethylamine is the parent compound of amphetamine, while N-methylphenethylamine is a positional isomer of amphetamine that differs only in the placement of the methyl group.[42]
PMID 29259540 - review covering+citing the primary source on EAAT3 endocytosis
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
PubChem Header
was invoked but never defined (see the help page).DrugBank1
was invoked but never defined (see the help page).Acute amph toxicity
was invoked but never defined (see the help page).Amph Uses
was invoked but never defined (see the help page).One of a pair of molecular entities which are mirror images of each other and non-superposable.
Amphetamine was first synthesised in 1887 by Lazar Edeleanu at the University of Berlin
In principle, INNs are selected only for the active part of the molecule which is usually the base, acid or alcohol. In some cases, however, the active molecules need to be expanded for various reasons, such as formulation purposes, bioavailability or absorption rate. In 1975 the experts designated for the selection of INN decided to adopt a new policy for naming such molecules. In future, names for different salts or esters of the same active substance should differ only with regard to the inactive moiety of the molecule. ... The latter are called modified INNs (INNMs).
Amphetamine, in the singular form, properly applies to the racemate of 2-amino-1-phenylpropane. ... In its broadest context, however, the term [amphetamines] can even embrace a large number of structurally and pharmacologically related substances.
Benzedrine
was invoked but never defined (see the help page).Malenka_2009
was invoked but never defined (see the help page).Amphetamines and caffeine are stimulants that increase alertness, improve focus, decrease reaction time, and delay fatigue, allowing for an increased intensity and duration of training ...
Physiologic and performance effects
• Amphetamines increase dopamine/norepinephrine release and inhibit their reuptake, leading to central nervous system (CNS) stimulation
• Amphetamines seem to enhance athletic performance in anaerobic conditions 39 40
• Improved reaction time
• Increased muscle strength and delayed muscle fatigue
• Increased acceleration
• Increased alertness and attention to task
Nonmedical
was invoked but never defined (see the help page).Libido
was invoked but never defined (see the help page).FDA Abuse & OD
was invoked but never defined (see the help page).UN Convention
was invoked but never defined (see the help page).Adderall IR
was invoked but never defined (see the help page).Miller
was invoked but never defined (see the help page).Miller+Grandy 2016
was invoked but never defined (see the help page).E Weihe
was invoked but never defined (see the help page).EAAT3
was invoked but never defined (see the help page).SLC1A1
was invoked but never defined (see the help page).FDA Effects
was invoked but never defined (see the help page).Westfall
was invoked but never defined (see the help page).In 1980, Chandler and Blair47 showed significant increases in knee extension strength, acceleration, anaerobic capacity, time to exhaustion during exercise, pre-exercise and maximum heart rates, and time to exhaustion during maximal oxygen consumption (VO2 max) testing after administration of 15 mg of dextroamphetamine versus placebo. Most of the information to answer this question has been obtained in the past decade through studies of fatigue rather than an attempt to systematically investigate the effect of ADHD drugs on exercise.
NHM-Addiction doses
was invoked but never defined (see the help page).Addiction risk
was invoked but never defined (see the help page).EncycOfPsychopharm
was invoked but never defined (see the help page).Cochrane
was invoked but never defined (see the help page).Stimulant Misuse
was invoked but never defined (see the help page).Trace Amines
was invoked but never defined (see the help page).Amphetamine - a substituted amphetamine
was invoked but never defined (see the help page).Substituted amphetamines, FMO, and DBH
was invoked but never defined (see the help page).