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Addiction and dependence glossary[1][2][3][4]
  • addiction – a brain disorder characterized by compulsive engagement in rewarding stimuli despite adverse consequences
  • addictive behavior – a behavior that is both rewarding and reinforcing
  • addictive drug – a drug that is both rewarding and reinforcing
  • dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
  • drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
  • drug withdrawal – symptoms that occur upon cessation of repeated drug use
  • physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens)
  • psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
  • reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
  • rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
  • sensitization – an amplified response to a stimulus resulting from repeated exposure to it
  • substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
  • tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose

Article section for stimulant

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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]

For Amphetamine's lead

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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]

Review on Amphetamine-induced EAAT3 endocytosis

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PMID 29259540 - review covering+citing the primary source on EAAT3 endocytosis

Notes

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  1. ^ Synonyms and alternate spellings include: 1-phenylpropan-2-amine (IUPAC name), α-methylphenethylamine, amfetamine (International Nonproprietary Name [INN]), β-phenylisopropylamine, and speed.[5][6][7]
  2. ^ Enantiomers are molecules that are mirror images of one another; they are structurally identical, but of the opposite orientation.[10]
    Levoamphetamine and dextroamphetamine are also known as L-amph or levamfetamine (INN) and D-amph or dexamfetamine (INN) respectively.[5]
  3. ^ a b "Adderall" is a brand name as opposed to a nonproprietary name; because the latter ("dextroamphetamine sulfate, dextroamphetamine saccharate, amphetamine sulfate, and amphetamine aspartate"[23]) is excessively long, this article exclusively refers to this amphetamine mixture by the brand name. Cite error: The named reference "Adderall" was defined multiple times with different content (see the help page).
  4. ^ The term "amphetamines" also refers to a chemical class, but, unlike the class of substituted amphetamines,[41] the "amphetamines" class does not have a standardized definition in academic literature.[15] One of the more restrictive definitions of this class includes only the racemate and enantiomers of amphetamine and methamphetamine.[15] The most general definition of the class encompasses a broad range of pharmacologically and structurally related compounds.[15]
    Due to confusion that may arise from use of the plural form, this article will only use the terms "amphetamine" and "amphetamines" to refer to racemic amphetamine, levoamphetamine, and dextroamphetamine and reserve the term "substituted amphetamines" for its structural class.
  5. ^ Synonyms and alternate spellings include: 1-phenylpropan-2-amine (IUPAC name), α-methylphenethylamine, amfetamine (International Nonproprietary Name [INN]), β-phenylisopropylamine, and speed.[5][6][7]
  6. ^ Enantiomers are molecules that are mirror images of one another; they are structurally identical, but of the opposite orientation.[10]
    Levoamphetamine and dextroamphetamine are also known as L-amph or levamfetamine (INN) and D-amph or dexamfetamine (INN) respectively.[5]
  7. ^ The term "amphetamines" also refers to a chemical class, but, unlike the class of substituted amphetamines,[41] the "amphetamines" class does not have a standardized definition in academic literature.[15] One of the more restrictive definitions of this class includes only the racemate and enantiomers of amphetamine and methamphetamine.[15] The most general definition of the class encompasses a broad range of pharmacologically and structurally related compounds.[15]
    Due to confusion that may arise from use of the plural form, this article will only use the terms "amphetamine" and "amphetamines" to refer to racemic amphetamine, levoamphetamine, and dextroamphetamine and reserve the term "substituted amphetamines" for its structural class.

Reference notes

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  1. ^ [17][18][19][20]
  2. ^ [17][25][26][27][28][29]
  3. ^ [17][20][30][31]
  4. ^ [17][18][19][20]
  5. ^ [17][25][26][27][28][29]
  6. ^ [17][20][30][31]

References

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  1. ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274.
  2. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410. 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.
  3. ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015.
  4. ^ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMID 26816013. 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.
  5. ^ a b c d Cite error: The named reference PubChem Header was invoked but never defined (see the help page).
  6. ^ a b c d Cite error: The named reference DrugBank1 was invoked but never defined (see the help page).
  7. ^ a b Cite error: The named reference Acute amph toxicity was invoked but never defined (see the help page).
  8. ^ a b c d e f g h Cite error: The named reference Amph Uses was invoked but never defined (see the help page).
  9. ^ a b c d "Evekeo Prescribing Information" (PDF). Arbor Pharmaceuticals LLC. April 2014. pp. 1–2. Retrieved 11 August 2015.
  10. ^ a b "Enantiomer". IUPAC Goldbook. International Union of Pure and Applied Chemistry. doi:10.1351/goldbook.E02069. Archived from the original on 17 March 2013. Retrieved 14 March 2014. One of a pair of molecular entities which are mirror images of each other and non-superposable.
  11. ^ a b "Historical overview of methamphetamine". Vermont Department of Health. Government of Vermont. Retrieved 29 January 2012.
  12. ^ Rassool GH (2009). Alcohol and Drug Misuse: A Handbook for Students and Health Professionals. London, England: Routledge. p. 113. ISBN 9780203871171. Amphetamine was first synthesised in 1887 by Lazar Edeleanu at the University of Berlin
  13. ^ a b c d "Amphetamine". Medical Subject Headings. United States National Library of Medicine. Retrieved 16 December 2013.
  14. ^ a b "Guidelines on the Use of International Nonproprietary Names (INNS) for Pharmaceutical Substances". World Health Organization. 1997. Retrieved 1 December 2014. 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).
  15. ^ a b c d e f g h i j Yoshida T (1997). "Chapter 1: Use and Misuse of Amphetamines: An International Overview". In Klee H (ed.). Amphetamine Misuse: International Perspectives on Current Trends. Amsterdam, Netherlands: Harwood Academic Publishers. p. 2. ISBN 9789057020810. Retrieved 1 December 2014. 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.
  16. ^ a b c d Cite error: The named reference Benzedrine was invoked but never defined (see the help page).
  17. ^ a b c d e f g h Cite error: The named reference Malenka_2009 was invoked but never defined (see the help page).
  18. ^ a b c d Liddle DG, Connor DJ (June 2013). "Nutritional supplements and ergogenic AIDS". Prim. Care. 40 (2): 487–505. doi:10.1016/j.pop.2013.02.009. PMID 23668655. 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
  19. ^ a b Cite error: The named reference Nonmedical was invoked but never defined (see the help page).
  20. ^ a b c d Cite error: The named reference Libido was invoked but never defined (see the help page).
  21. ^ a b c d Cite error: The named reference FDA Abuse & OD was invoked but never defined (see the help page).
  22. ^ a b Cite error: The named reference UN Convention was invoked but never defined (see the help page).
  23. ^ a b c d "National Drug Code Amphetamine Search Results". National Drug Code Directory. United States Food and Drug Administration. Archived from the original on 16 December 2013. Retrieved 16 December 2013.
  24. ^ a b c d Cite error: The named reference Adderall IR was invoked but never defined (see the help page).
  25. ^ a b Cite error: The named reference Miller was invoked but never defined (see the help page).
  26. ^ a b Cite error: The named reference Miller+Grandy 2016 was invoked but never defined (see the help page).
  27. ^ a b Cite error: The named reference E Weihe was invoked but never defined (see the help page).
  28. ^ a b Cite error: The named reference EAAT3 was invoked but never defined (see the help page).
  29. ^ a b Cite error: The named reference SLC1A1 was invoked but never defined (see the help page).
  30. ^ a b Cite error: The named reference FDA Effects was invoked but never defined (see the help page).
  31. ^ a b c d Cite error: The named reference Westfall was invoked but never defined (see the help page).
  32. ^ Parr JW (July 2011). "Attention-deficit hyperactivity disorder and the athlete: new advances and understanding". Clin. Sports Med. 30 (3): 591–610. doi:10.1016/j.csm.2011.03.007. PMID 21658550. 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.
  33. ^ a b Cite error: The named reference NHM-Addiction doses was invoked but never defined (see the help page).
  34. ^ a b Cite error: The named reference Addiction risk was invoked but never defined (see the help page).
  35. ^ a b Cite error: The named reference EncycOfPsychopharm was invoked but never defined (see the help page).
  36. ^ a b Cite error: The named reference Cochrane was invoked but never defined (see the help page).
  37. ^ a b Cite error: The named reference Stimulant Misuse was invoked but never defined (see the help page).
  38. ^ a b c d e f Cite error: The named reference Trace Amines was invoked but never defined (see the help page).
  39. ^ a b c d "Amphetamine". European Monitoring Centre for Drugs and Drug Addiction. Retrieved 19 October 2013.
  40. ^ a b c d Cite error: The named reference Amphetamine - a substituted amphetamine was invoked but never defined (see the help page).
  41. ^ a b Cite error: The named reference Substituted amphetamines, FMO, and DBH was invoked but never defined (see the help page).
  42. ^ a b Mosnaim AD, Callaghan OH, Hudzik T, Wolf ME (April 2013). "Rat brain-uptake index for phenylethylamine and various monomethylated derivatives". Neurochem. Res. 38 (4): 842–846. doi:10.1007/s11064-013-0988-1. PMID 23389662.
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