苯丙胺 (Chinese Wikipedia)

Analysis of information sources in references of the Wikipedia article "苯丙胺" in Chinese language version.

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Greydanus D. Stimulant Misuse: Strategies to Manage a Growing Problem (PDF). American College Health Association (Review Article). ACHA Professional Development Program: 20. [2013-11-02]. （原始内容 (PDF)存档于2013-11-03）.

archive.org

Horwitz D, Alexander RW, Lovenberg W, Keiser HR. Human serum dopamine-β-hydroxylase. Relationship to hypertension and sympathetic activity. Circ. Res. May 1973, 32 (5): 594–599. PMID 4713201. doi:10.1161/01.RES.32.5.594. Subjects with exceptionally low levels of serum dopamine-β-hydroxylase activity showed normal cardiovascular function and normal β-hydroxylation of an administered synthetic substrate, hydroxyamphetamine.
Yoshida T. Chapter 1: Use and Misuse of Amphetamines: An International Overview. Klee H (编). Amphetamine Misuse: International Perspectives on Current Trends. Amsterdam, Netherlands: Harwood Academic Publishers. 1997: 2 [1 December 2014]. ISBN 9789057020810. 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.
Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K. Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects. JAMA Psychiatry. February 2013, 70 (2): 185–198. PMID 23247506. doi:10.1001/jamapsychiatry.2013.277.
Spencer TJ, Brown A, Seidman LJ, Valera EM, Makris N, Lomedico A, Faraone SV, Biederman J. Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies. J. Clin. Psychiatry. September 2013, 74 (9): 902–917. PMC 3801446 . PMID 24107764. doi:10.4088/JCP.12r08287.
Pringsheim T, Steeves T. Pringsheim T , 编. Pharmacological treatment for Attention Deficit Hyperactivity Disorder (ADHD) in children with comorbid tic disorders. Cochrane Database Syst. Rev. April 2011, (4): CD007990. PMID 21491404. doi:10.1002/14651858.CD007990.pub2.
Parr JW. Attention-deficit hyperactivity disorder and the athlete: new advances and understanding. Clin. Sports Med. July 2011, 30 (3): 591–610. PMID 21658550. doi:10.1016/j.csm.2011.03.007. 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.
Kessler S. Drug therapy in attention-deficit hyperactivity disorder. South. Med. J. January 1996, 89 (1): 33–38. PMID 8545689. doi:10.1097/00007611-199601000-00005. statements on package inserts are not intended to limit medical practice. Rather they are intended to limit claims by pharmaceutical companies. ... the FDA asserts explicitly, and the courts have upheld that clinical decisions are to be made by physicians and patients in individual situations.
Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J. Clin. Psychiatry. November 2004, 65 (11): 1520–1524. PMID 15554766. doi:10.4088/jcp.v65n1113.
Rytting E, Audus KL. Novel organic cation transporter 2-mediated carnitine uptake in placental choriocarcinoma (BeWo) cells. J. Pharmacol. Exp. Ther. January 2005, 312 (1): 192–198. PMID 15316089. doi:10.1124/jpet.104.072363.
Vicentic A, Jones DC. The CART (cocaine- and amphetamine-regulated transcript) system in appetite and drug addiction. J. Pharmacol. Exp. Ther. February 2007, 320 (2): 499–506. PMID 16840648. doi:10.1124/jpet.105.091512. The physiological importance of CART was further substantiated in numerous human studies demonstrating a role of CART in both feeding and psychostimulant addiction. ... Colocalization studies also support a role for CART in the actions of psychostimulants. ... CART and DA receptor transcripts colocalize (Beaudry et al., 2004). Second, dopaminergic nerve terminals in the NAc synapse on CART-containing neurons (Koylu et al., 1999), hence providing the proximity required for neurotransmitter signaling. These studies suggest that DA plays a role in regulating CART gene expression possibly via the activation of CREB.

books.google.com

Glennon RA. Phenylisopropylamine stimulants: amphetamine-related agents. Lemke TL, Williams DA, Roche VF, Zito W (编). Foye's principles of medicinal chemistry 7th. Philadelphia, USA: Wolters Kluwer Health/Lippincott Williams & Wilkins. 2013: 646–648 [2015-09-11]. ISBN 9781609133450. （原始内容存档于2019-06-09）. The phase 1 metabolism of amphetamine analogs is catalyzed by two systems: cytochrome P450 and flavin monooxygenase. ... Amphetamine can also undergo aromatic hydroxylation to p-hydroxyamphetamine. ... Subsequent oxidation at the benzylic position by DA β-hydroxylase affords p-hydroxynorephedrine. Alternatively, direct oxidation of amphetamine by DA β-hydroxylase can afford norephedrine.
Yoshida T. Chapter 1: Use and Misuse of Amphetamines: An International Overview. Klee H (编). Amphetamine Misuse: International Perspectives on Current Trends. Amsterdam, Netherlands: Harwood Academic Publishers. 1997: 2 [1 December 2014]. ISBN 9789057020810. 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.

brenda-enzymes.info

Monoamine oxidase (Homo sapiens). BRENDA. Technische Universität Braunschweig. 1 January 2014 [4 May 2014]. （原始内容存档于2020-07-27）.

doi.org

Heal DJ, Smith SL, Gosden J, Nutt DJ. Amphetamine, past and present – a pharmacological and clinical perspective. J. Psychopharmacol. June 2013, 27 (6): 479–496. PMC 3666194 . PMID 23539642. doi:10.1177/0269881113482532. The intravenous use of d-amphetamine and other stimulants still pose major safety risks to the individuals indulging in this practice. Some of this intravenous abuse is derived from the diversion of ampoules of d-amphetamine, which are still occasionally prescribed in the UK for the control of severe narcolepsy and other disorders of excessive sedation. ... For these reasons, observations of dependence and abuse of prescription d-amphetamine are rare in clinical practice, and this stimulant can even be prescribed to people with a history of drug abuse provided certain controls, such as daily pick-ups of prescriptions, are put in place (Jasinski and Krishnan, 2009b).
Santagati NA, Ferrara G, Marrazzo A, Ronsisvalle G. Simultaneous determination of amphetamine and one of its metabolites by HPLC with electrochemical detection. J. Pharm. Biomed. Anal. September 2002, 30 (2): 247–255. PMID 12191709. doi:10.1016/S0731-7085(02)00330-8.
Brams M, Mao AR, Doyle RL. Onset of efficacy of long-acting psychostimulants in pediatric attention-deficit/hyperactivity disorder. Postgrad. Med. September 2008, 120 (3): 69–88. PMID 18824827. doi:10.3810/pgm.2008.09.1909.
Brams M, Mao AR, Doyle RL. Onset of efficacy of long-acting psychostimulants in pediatric attention-deficit/hyperactivity disorder. Postgrad. Med. September 2008, 120 (3): 69–88. PMID 18824827. doi:10.3810/pgm.2008.09.1909.
Mignot EJ. A practical guide to the therapy of narcolepsy and hypersomnia syndromes. Neurotherapeutics. October 2012, 9 (4): 739–752. PMC 3480574 . PMID 23065655. doi:10.1007/s13311-012-0150-9.
Horwitz D, Alexander RW, Lovenberg W, Keiser HR. Human serum dopamine-β-hydroxylase. Relationship to hypertension and sympathetic activity. Circ. Res. May 1973, 32 (5): 594–599. PMID 4713201. doi:10.1161/01.RES.32.5.594. Subjects with exceptionally low levels of serum dopamine-β-hydroxylase activity showed normal cardiovascular function and normal β-hydroxylation of an administered synthetic substrate, hydroxyamphetamine.
Krueger SK, Williams DE. Mammalian flavin-containing monooxygenases: structure/function, genetic polymorphisms and role in drug metabolism. Pharmacol. Ther. 2005-06, 106 (3): 357–387. PMC 1828602 . PMID 15922018. doi:10.1016/j.pharmthera.2005.01.001.
"Table 5: N-containing drugs and xenobiotics oxygenated by FMO （页面存档备份，存于互联网档案馆）"
Enantiomer. IUPAC Goldbook. International Union of Pure and Applied Chemistry. [2014-03-14]. doi:10.1351/goldbook.E02069. （原始内容存档于2013-03-17）. One of a pair of molecular entities which are mirror images of each other and non-superposable.
Miller GM. The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity. J. Neurochem. January 2011, 116 (2): 164–176. PMC 3005101 . PMID 21073468. doi:10.1111/j.1471-4159.2010.07109.x.
Liddle DG, Connor DJ. Nutritional supplements and ergogenic AIDS. Prim. Care. June 2013, 40 (2): 487–505. PMID 23668655. doi:10.1016/j.pop.2013.02.009. 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
Broadley KJ. The vascular effects of trace amines and amphetamines. Pharmacol. Ther. March 2010, 125 (3): 363–375. PMID 19948186. doi:10.1016/j.pharmthera.2009.11.005.
Hagel JM, Krizevski R, Marsolais F, Lewinsohn E, Facchini PJ. Biosynthesis of amphetamine analogs in plants. Trends Plant Sci. 2012, 17 (7): 404–412. PMID 22502775. doi:10.1016/j.tplants.2012.03.004. Substituted amphetamines, which are also called phenylpropylamino alkaloids, are a diverse group of nitrogen-containing compounds that feature a phenethylamine backbone with a methyl group at the α-position relative to the nitrogen (Figure 1). ... Beyond (1R,2S)-ephedrine and (1S,2S)-pseudoephedrine, myriad other substituted amphetamines have important pharmaceutical applications. ... For example, (S)-amphetamine (Figure 4b), a key ingredient in Adderall^® and Dexedrine^®, is used to treat attention deficit hyperactivity disorder (ADHD) [79]. ...
[Figure 4](b) Examples of synthetic, pharmaceutically important substituted amphetamines.
Carvalho M, Carmo H, Costa VM, Capela JP, Pontes H, Remião F, Carvalho F, Bastos Mde L. Toxicity of amphetamines: an update. Arch. Toxicol. August 2012, 86 (8): 1167–1231. PMID 22392347. doi:10.1007/s00204-012-0815-5.
Berman S, O'Neill J, Fears S, Bartzokis G, London ED. Abuse of amphetamines and structural abnormalities in the brain. Ann. N. Y. Acad. Sci. October 2008, 1141: 195–220. PMC 2769923 . PMID 18991959. doi:10.1196/annals.1441.031.
Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K. Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects. JAMA Psychiatry. February 2013, 70 (2): 185–198. PMID 23247506. doi:10.1001/jamapsychiatry.2013.277.
Spencer TJ, Brown A, Seidman LJ, Valera EM, Makris N, Lomedico A, Faraone SV, Biederman J. Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies. J. Clin. Psychiatry. September 2013, 74 (9): 902–917. PMC 3801446 . PMID 24107764. doi:10.4088/JCP.12r08287.
Frodl T, Skokauskas N. Meta-analysis of structural MRI studies in children and adults with attention deficit hyperactivity disorder indicates treatment effects.. Acta psychiatrica Scand. February 2012, 125 (2): 114–126. PMID 22118249. doi:10.1111/j.1600-0447.2011.01786.x. Basal ganglia regions like the right globus pallidus, the right putamen, and the nucleus caudatus are structurally affected in children with ADHD. These changes and alterations in limbic regions like ACC and amygdala are more pronounced in non-treated populations and seem to diminish over time from child to adulthood. Treatment seems to have positive effects on brain structure.
Arnold LE, Hodgkins P, Caci H, Kahle J, Young S. Effect of treatment modality on long-term outcomes in attention-deficit/hyperactivity disorder: a systematic review. PLoS ONE. February 2015, 10 (2): e0116407. PMC 4340791 . PMID 25714373. doi:10.1371/journal.pone.0116407. The highest proportion of improved outcomes was reported with combination treatment (83% of outcomes). Among significantly improved outcomes, the largest effect sizes were found for combination treatment. The greatest improvements were associated with academic, self-esteem, or social function outcomes. Figure 3: Treatment benefit by treatment type and outcome group （页面存档备份，存于互联网档案馆）
Arnold, L. Eugene; Hodgkins, Paul; Caci, Hervé; Kahle, Jennifer; Young, Susan. Effect of Treatment Modality on Long-Term Outcomes in Attention-Deficit/Hyperactivity Disorder: A Systematic Review. PLoS ONE. [2017-05-15]. PMID 25714373. doi:10.1371/journal.pone.0116407. （原始内容存档于2020-11-09）.
Huang YS, Tsai MH. Long-term outcomes with medications for attention-deficit hyperactivity disorder: current status of knowledge. CNS Drugs. July 2011, 25 (7): 539–554. PMID 21699268. doi:10.2165/11589380-000000000-00000. Recent studies have demonstrated that stimulants, along with the non-stimulants atomoxetine and extended-release guanfacine, are continuously effective for more than 2-year treatment periods with few and tolerable adverse effects. The effectiveness of long-term therapy includes not only the core symptoms of ADHD, but also improved quality of life and academic achievements. The most concerning short-term adverse effects of stimulants, such as elevated blood pressure and heart rate, waned in long-term follow-up studies. ... In the longest follow-up study (of more than 10 years), lifetime stimulant treatment for ADHD was effective and protective against the development of adverse psychiatric disorders.
Bidwell LC, McClernon FJ, Kollins SH. Cognitive enhancers for the treatment of ADHD. Pharmacol. Biochem. Behav. August 2011, 99 (2): 262–274. PMC 3353150 . PMID 21596055. doi:10.1016/j.pbb.2011.05.002.
Parker J, Wales G, Chalhoub N, Harpin V. The long-term outcomes of interventions for the management of attention-deficit hyperactivity disorder in children and adolescents: a systematic review of randomized controlled trials. Psychol. Res. Behav. Manag. (systematic review (secondary source)). September 2013, 6: 87–99. PMC 3785407 . PMID 24082796. doi:10.2147/PRBM.S49114. Only one paper⁵³ examining outcomes beyond 36 months met the review criteria. ... There is high level evidence suggesting that pharmacological treatment can have a major beneficial effect on the core symptoms of ADHD (hyperactivity, inattention, and impulsivity) in approximately 80% of cases compared with placebo controls, in the short term.
Scholten RJ, Clarke M, Hetherington J. The Cochrane Collaboration. Eur. J. Clin. Nutr. August 2005,. 59 Suppl 1: S147–S149; discussion S195–S196. PMID 16052183. doi:10.1038/sj.ejcn.1602188.
Castells X, Ramos-Quiroga JA, Bosch R, Nogueira M, Casas M. Castells X , 编. Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults. Cochrane Database Syst. Rev. June 2011, (6): CD007813. PMID 21678370. doi:10.1002/14651858.CD007813.pub2.
Punja S, Shamseer L, Hartling L, Urichuk L, Vandermeer B, Nikles J, Vohra S. Amphetamines for attention deficit hyperactivity disorder (ADHD) in children and adolescents. Cochrane Database Syst. Rev. February 2016, 2: CD009996. PMID 26844979. doi:10.1002/14651858.CD009996.pub2.
Pringsheim T, Steeves T. Pringsheim T , 编. Pharmacological treatment for Attention Deficit Hyperactivity Disorder (ADHD) in children with comorbid tic disorders. Cochrane Database Syst. Rev. April 2011, (4): CD007990. PMID 21491404. doi:10.1002/14651858.CD007990.pub2.
Spencer RC, Devilbiss DM, Berridge CW. The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex. Biol. Psychiatry. June 2015, 77 (11): 940–950. PMID 25499957. doi:10.1016/j.biopsych.2014.09.013. The procognitive actions of psychostimulants are only associated with low doses. Surprisingly, despite nearly 80 years of clinical use, the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors. ... This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors. Collectively, this evidence indicates that at low, clinically relevant doses, psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFC-dependent function). ... In particular, in both animals and humans, lower doses maximally improve performance in tests of working memory and response inhibition, whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses.
Ilieva IP, Hook CJ, Farah MJ. Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis. J. Cogn. Neurosci. January 2015: 1–21. PMID 25591060. doi:10.1162/jocn_a_00776. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. ... The results of this meta-analysis ... do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.
Bagot KS, Kaminer Y. Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review. Addiction. April 2014, 109 (4): 547–557. PMC 4471173 . PMID 24749160. doi:10.1111/add.12460. Amphetamine has been shown to improve consolidation of information (0.02 ≥ P ≤ 0.05), leading to improved recall.
Wood S, Sage JR, Shuman T, Anagnostaras SG. Psychostimulants and cognition: a continuum of behavioral and cognitive activation. Pharmacol. Rev. January 2014, 66 (1): 193–221. PMID 24344115. doi:10.1124/pr.112.007054.
Parr JW. Attention-deficit hyperactivity disorder and the athlete: new advances and understanding. Clin. Sports Med. July 2011, 30 (3): 591–610. PMID 21658550. doi:10.1016/j.csm.2011.03.007. 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.
Roelands B, de Koning J, Foster C, Hettinga F, Meeusen R. Neurophysiological determinants of theoretical concepts and mechanisms involved in pacing. Sports Med. May 2013, 43 (5): 301–311. PMID 23456493. doi:10.1007/s40279-013-0030-4. In high-ambient temperatures, dopaminergic manipulations clearly improve performance. The distribution of the power output reveals that after dopamine reuptake inhibition, subjects are able to maintain a higher power output compared with placebo. ... Dopaminergic drugs appear to override a safety switch and allow athletes to use a reserve capacity that is ‘off-limits’ in a normal (placebo) situation.
Docherty JR. Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA). Br. J. Pharmacol. June 2008, 154 (3): 606–622. PMC 2439527 . PMID 18500382. doi:10.1038/bjp.2008.124.
Parker KL, Lamichhane D, Caetano MS, Narayanan NS. Executive dysfunction in Parkinson's disease and timing deficits. Front. Integr. Neurosci. October 2013, 7: 75. PMC 3813949 . PMID 24198770. doi:10.3389/fnint.2013.00075. Manipulations of dopaminergic signaling profoundly influence interval timing, leading to the hypothesis that dopamine influences internal pacemaker, or “clock,” activity. For instance, amphetamine, which increases concentrations of dopamine at the synaptic cleft advances the start of responding during interval timing, whereas antagonists of D2 type dopamine receptors typically slow timing;... Depletion of dopamine in healthy volunteers impairs timing, while amphetamine releases synaptic dopamine and speeds up timing.
Rattray B, Argus C, Martin K, Northey J, Driller M. Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance?. Front. Physiol. March 2015, 6: 79. PMC 4362407 . PMID 25852568. doi:10.3389/fphys.2015.00079. Aside from accounting for the reduced performance of mentally fatigued participants, this model rationalizes the reduced RPE and hence improved cycling time trial performance of athletes using a glucose mouthwash (Chambers et al., 2009) and the greater power output during a RPE matched cycling time trial following amphetamine ingestion (Swart, 2009). ... Dopamine stimulating drugs are known to enhance aspects of exercise performance (Roelands et al., 2008)
Roelands B, De Pauw K, Meeusen R. Neurophysiological effects of exercise in the heat. Scand. J. Med. Sci. Sports. June 2015,. 25 Suppl 1: 65–78. PMID 25943657. doi:10.1111/sms.12350. This indicates that subjects did not feel they were producing more power and consequently more heat. The authors concluded that the “safety switch” or the mechanisms existing in the body to prevent harmful effects are overridden by the drug administration (Roelands et al., 2008b). Taken together, these data indicate strong ergogenic effects of an increased DA concentration in the brain, without any change in the perception of effort.
Kessler S. Drug therapy in attention-deficit hyperactivity disorder. South. Med. J. January 1996, 89 (1): 33–38. PMID 8545689. doi:10.1097/00007611-199601000-00005. statements on package inserts are not intended to limit medical practice. Rather they are intended to limit claims by pharmaceutical companies. ... the FDA asserts explicitly, and the courts have upheld that clinical decisions are to be made by physicians and patients in individual situations.
Feinberg SS. Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication. J. Clin. Psychiatry. November 2004, 65 (11): 1520–1524. PMID 15554766. doi:10.4088/jcp.v65n1113.
Stewart JW, Deliyannides DA, McGrath PJ. How treatable is refractory depression?. J. Affect. Disord. June 2014, 167: 148–152. PMID 24972362. doi:10.1016/j.jad.2014.05.047.
Vitiello B. Understanding the risk of using medications for attention deficit hyperactivity disorder with respect to physical growth and cardiovascular function. Child Adolesc. Psychiatr. Clin. N. Am. April 2008, 17 (2): 459–474. PMC 2408826 . PMID 18295156. doi:10.1016/j.chc.2007.11.010.
Cooper WO, Habel LA, Sox CM, Chan KA, Arbogast PG, Cheetham TC, Murray KT, Quinn VP, Stein CM, Callahan ST, Fireman BH, Fish FA, Kirshner HS, O'Duffy A, Connell FA, Ray WA. ADHD drugs and serious cardiovascular events in children and young adults. N. Engl. J. Med. 2011-11, 365 (20): 1896–1904. PMC 4943074 . PMID 22043968. doi:10.1056/NEJMoa1110212.
Habel LA, Cooper WO, Sox CM, Chan KA, Fireman BH, Arbogast PG, Cheetham TC, Quinn VP, Dublin S, Boudreau DM, Andrade SE, Pawloski PA, Raebel MA, Smith DH, Achacoso N, Uratsu C, Go AS, Sidney S, Nguyen-Huynh MN, Ray WA, Selby JV. ADHD medications and risk of serious cardiovascular events in young and middle-aged adults. JAMA. 2011-12, 306 (24): 2673–2683. PMC 3350308 . PMID 22161946. doi:10.1001/jama.2011.1830.
Shoptaw SJ, Kao U, Ling W. Shoptaw SJ, Ali R , 编. Treatment for amphetamine psychosis. Cochrane Database Syst. Rev. January 2009, (1): CD003026. PMID 19160215. doi:10.1002/14651858.CD003026.pub3. A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals. In such cases, symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation. More common (about 18%) is for frequent amphetamine users to report psychotic symptoms that are sub-clinical and that do not require high-intensity intervention ...
About 5–15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983) ...
Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis.
Childs E, de Wit H. Amphetamine-induced place preference in humans. Biol. Psychiatry. May 2009, 65 (10): 900–904. PMC 2693956 . PMID 19111278. doi:10.1016/j.biopsych.2008.11.016. This study demonstrates that humans, like nonhumans, prefer a place associated with amphetamine administration. These findings support the idea that subjective responses to a drug contribute to its ability to establish place conditioning.
Spiller HA, Hays HL, Aleguas A. Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation, mechanisms of toxicity, and management. CNS Drugs. June 2013, 27 (7): 531–543. PMID 23757186. doi:10.1007/s40263-013-0084-8. Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter. The mechanism of toxicity is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin.
Collaborators. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013 (PDF). Lancet. 2015, 385 (9963): 117–171 [2015-03-03]. PMC 4340604 . PMID 25530442. doi:10.1016/S0140-6736(14)61682-2. Amphetamine use disorders ... 3,788 (3,425–4,145)
Ruffle JK. Molecular neurobiology of addiction: what's all the (Δ)FosB about?. Am. J. Drug Alcohol Abuse. November 2014, 40 (6): 428–437. PMID 25083822. doi:10.3109/00952990.2014.933840. ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure.
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Olsen CM. Natural rewards, neuroplasticity, and non-drug addictions. Neuropharmacology. December 2011, 61 (7): 1109–1122. PMC 3139704 . PMID 21459101. doi:10.1016/j.neuropharm.2011.03.010. Similar to environmental enrichment, studies have found that exercise reduces self-administration and relapse to drugs of abuse (Cosgrove et al., 2002; Zlebnik et al., 2010). There is also some evidence that these preclinical findings translate to human populations, as exercise reduces withdrawal symptoms and relapse in abstinent smokers (Daniel et al., 2006; Prochaska et al., 2008), and one drug recovery program has seen success in participants that train for and compete in a marathon as part of the program (Butler, 2005). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al., 2006; Aiken, 2007; Lader, 2008).
Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA. Exercise as a novel treatment for drug addiction: a neurobiological and stage-dependent hypothesis. Neurosci. Biobehav. Rev. September 2013, 37 (8): 1622–1644. PMC 3788047 . PMID 23806439. doi:10.1016/j.neubiorev.2013.06.011. These findings suggest that exercise may “magnitude”-dependently prevent the development of an addicted phenotype possibly by blocking/reversing behavioral and neuroadaptive changes that develop during and following extended access to the drug. ... Exercise has been proposed as a treatment for drug addiction that may reduce drug craving and risk of relapse. Although few clinical studies have investigated the efficacy of exercise for preventing relapse, the few studies that have been conducted generally report a reduction in drug craving and better treatment outcomes ... Taken together, these data suggest that the potential benefits of exercise during relapse, particularly for relapse to psychostimulants, may be mediated via chromatin remodeling and possibly lead to greater treatment outcomes.
Zhou Y, Zhao M, Zhou C, Li R. Sex differences in drug addiction and response to exercise intervention: From human to animal studies. Front. Neuroendocrinol. July 2015, 40: 24–41. PMID 26182835. doi:10.1016/j.yfrne.2015.07.001. Collectively, these findings demonstrate that exercise may serve as a substitute or competition for drug abuse by changing ΔFosB or cFos immunoreactivity in the reward system to protect against later or previous drug use. ... The postulate that exercise serves as an ideal intervention for drug addiction has been widely recognized and used in human and animal rehabilitation.
Linke SE, Ussher M. Exercise-based treatments for substance use disorders: evidence, theory, and practicality. Am. J. Drug Alcohol Abuse. January 2015, 41 (1): 7–15. PMC 4831948 . PMID 25397661. doi:10.3109/00952990.2014.976708. The limited research conducted suggests that exercise may be an effective adjunctive treatment for SUDs. In contrast to the scarce intervention trials to date, a relative abundance of literature on the theoretical and practical reasons supporting the investigation of this topic has been published. ... numerous theoretical and practical reasons support exercise-based treatments for SUDs, including psychological, behavioral, neurobiological, nearly universal safety profile, and overall positive health effects.
Greene SL, Kerr F, Braitberg G. Review article: amphetamines and related drugs of abuse. Emerg. Med. Australas. 2008-10, 20 (5): 391–402. PMID 18973636. doi:10.1111/j.1742-6723.2008.01114.x.
Volkow, Nora D.; Koob, George F.; McLellan, A. Thomas. Longo, Dan L. , 编. Neurobiologic Advances from the Brain Disease Model of Addiction. New England Journal of Medicine. 2016-01-28, 374 (4): 363–371. ISSN 0028-4793. PMC 6135257 . PMID 26816013. doi:10.1056/NEJMra1511480 （英语）.
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Robison AJ, Nestler EJ. Transcriptional and epigenetic mechanisms of addiction. Nat. Rev. Neurosci. November 2011, 12 (11): 623–637. PMC 3272277 . PMID 21989194. doi:10.1038/nrn3111.
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Perez-Mana C, Castells X, Torrens M, Capella D, Farre M. Efficacy of psychostimulant drugs for amphetamine abuse or dependence. Cochrane Database Syst. Rev. September 2013, 9: CD009695. PMID 23996457. doi:10.1002/14651858.CD009695.pub2. To date, no pharmacological treatment has been approved for [addiction], and psychotherapy remains the mainstay of treatment. ... Results of this review do not support the use of psychostimulant medications at the tested doses as a replacement therapy
Forray A, Sofuoglu M. Future pharmacological treatments for substance use disorders. Br. J. Clin. Pharmacol. February 2014, 77 (2): 382–400. PMC 4014020 . PMID 23039267. doi:10.1111/j.1365-2125.2012.04474.x.
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Carroll ME, Smethells JR. Sex Differences in Behavioral Dyscontrol: Role in Drug Addiction and Novel Treatments. Front. Psychiatry. February 2016, 6: 175. PMC 4745113 . PMID 26903885. doi:10.3389/fpsyt.2015.00175. Physical Exercise
There is accelerating evidence that physical exercise is a useful treatment for preventing and reducing drug addiction ... In some individuals, exercise has its own rewarding effects, and a behavioral economic interaction may occur, such that physical and social rewards of exercise can substitute for the rewarding effects of drug abuse. ... The value of this form of treatment for drug addiction in laboratory animals and humans is that exercise, if it can substitute for the rewarding effects of drugs, could be self-maintained over an extended period of time. Work to date in [laboratory animals and humans] regarding exercise as a treatment for drug addiction supports this hypothesis. ... Animal and human research on physical exercise as a treatment for stimulant addiction indicates that this is one of the most promising treatments on the horizon.
Shoptaw SJ, Kao U, Heinzerling K, Ling W. Shoptaw SJ , 编. Treatment for amphetamine withdrawal. Cochrane Database Syst. Rev. April 2009, (2): CD003021. PMID 19370579. doi:10.1002/14651858.CD003021.pub2. The prevalence of this withdrawal syndrome is extremely common (Cantwell 1998; Gossop 1982) with 87.6% of 647 individuals with amphetamine dependence reporting six or more signs of amphetamine withdrawal listed in the DSM when the drug is not available (Schuckit 1999) ... The severity of withdrawal symptoms is greater in amphetamine dependent individuals who are older and who have more extensive amphetamine use disorders (McGregor 2005). Withdrawal symptoms typically present within 24 hours of the last use of amphetamine, with a withdrawal syndrome involving two general phases that can last 3 weeks or more. The first phase of this syndrome is the initial "crash" that resolves within about a week (Gossop 1982;McGregor 2005) ...
Cantwell, Bernadette; McBride, Andrew J. Self detoxication by amphetamine dependent patients: a pilot study. Drug and Alcohol Dependence (Elsevier BV). 1998, 49 (2): 157–163 [2017-05-09]. doi:10.1016/s0376-8716(97)00160-9.
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Bowyer JF, Hanig JP. Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity. Temperature (Austin). November 2014, 1 (3): 172–182. PMC 5008711 . PMID 27626044. doi:10.4161/23328940.2014.982049. Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia (≥40°C) are minimally neurotoxic. Hyperthermia likely enhances AMPH and METH neurotoxicity directly through disruption of protein function, ion channels and enhanced ROS production. ... The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier (BBB) resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals. ... In animal models that evaluate the neurotoxicity of AMPH and METH, it is quite clear that hyperthermia is one of the essential components necessary for the production of histological signs of dopamine terminal damage and neurodegeneration in cortex, striatum, thalamus and hippocampus.
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Sulzer D. How addictive drugs disrupt presynaptic dopamine neurotransmission. Neuron. February 2011, 69 (4): 628–649. PMC 3065181 . PMID 21338876. doi:10.1016/j.neuron.2011.02.010. They did not confirm the predicted straightforward relationship between uptake and release, but rather that some compounds including AMPH were better releasers than substrates for uptake. Zinc, moreover, stimulates efflux of intracellular [3H]DA despite its concomitant inhibition of uptake (Scholze et al., 2002).
Scholze P, Nørregaard L, Singer EA, Freissmuth M, Gether U, Sitte HH. The role of zinc ions in reverse transport mediated by monoamine transporters. J. Biol. Chem. June 2002, 277 (24): 21505–21513. PMID 11940571. doi:10.1074/jbc.M112265200. The human dopamine transporter (hDAT) contains an endogenous high affinity Zn²⁺ binding site with three coordinating residues on its extracellular face (His193, His375, and Glu396). ... Although Zn²⁺ inhibited uptake, Zn²⁺ facilitated [3H]MPP+ release induced by amphetamine, MPP+, or K+-induced depolarization specifically at hDAT but not at the human serotonin and the norepinephrine transporter (hNET).
Scassellati C, Bonvicini C, Faraone SV, Gennarelli M. Biomarkers and attention-deficit/hyperactivity disorder: a systematic review and meta-analyses. J. Am. Acad. Child Adolesc. Psychiatry. October 2012, 51 (10): 1003–1019.e20. PMID 23021477. doi:10.1016/j.jaac.2012.08.015. With regard to zinc supplementation, a placebo controlled trial reported that doses up to 30 mg/day of zinc were safe for at least 8 weeks, but the clinical effect was equivocal except for the finding of a 37% reduction in amphetamine optimal dose with 30 mg per day of zinc.¹¹⁰
Eiden LE, Weihe E. VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse. Ann. N. Y. Acad. Sci. January 2011, 1216: 86–98. PMC 4183197 . PMID 21272013. doi:10.1111/j.1749-6632.2010.05906.x. VMAT2 is the CNS vesicular transporter for not only the biogenic amines DA, NE, EPI, 5-HT, and HIS, but likely also for the trace amines TYR, PEA, and thyronamine (THYR) ... [Trace aminergic] neurons in mammalian CNS would be identifiable as neurons expressing VMAT2 for storage, and the biosynthetic enzyme aromatic amino acid decarboxylase (AADC). ... AMPH release of DA from synapses requires both an action at VMAT2 to release DA to the cytoplasm and a concerted release of DA from the cytoplasm via "reverse transport" through DAT.
Borowsky B, Adham N, Jones KA, Raddatz R, Artymyshyn R, Ogozalek KL, Durkin MM, Lakhlani PP, Bonini JA, Pathirana S, Boyle N, Pu X, Kouranova E, Lichtblau H, Ochoa FY, Branchek TA, Gerald C. Trace amines: identification of a family of mammalian G protein-coupled receptors. Proc. Natl. Acad. Sci. U.S.A. July 2001, 98 (16): 8966–8971. PMC 55357 . PMID 11459929. doi:10.1073/pnas.151105198.
Underhill SM, Wheeler DS, Li M, Watts SD, Ingram SL, Amara SG. Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons. Neuron. 2014-07, 83 (2): 404–416. PMC 4159050 . PMID 25033183. doi:10.1016/j.neuron.2014.05.043. AMPH also increases intracellular calcium (Gnegy et al., 2004) that is associated with calmodulin/CamKII activation (Wei et al., 2007) and modulation and trafficking of the DAT (Fog et al., 2006; Sakrikar et al., 2012). ... For example, AMPH increases extracellular glutamate in various brain regions including the striatum, VTA and NAc (Del Arco et al., 1999; Kim et al., 1981; Mora and Porras, 1993; Xue et al., 1996), but it has not been established whether this change can be explained by increased synaptic release or by reduced clearance of glutamate. ... DHK-sensitive, EAAT2 uptake was not altered by AMPH (Figure 1A). The remaining glutamate transport in these midbrain cultures is likely mediated by EAAT3 and this component was significantly decreased by AMPH
Zhu HJ, Appel DI, Gründemann D, Markowitz JS. Interaction of organic cation transporter 3 (SLC22A3) and amphetamine. J. Neurochem. 2010-07, 114 (1): 142–149. PMC 3775896 . PMID 20402963. doi:10.1111/j.1471-4159.2010.06738.x.
Rytting E, Audus KL. Novel organic cation transporter 2-mediated carnitine uptake in placental choriocarcinoma (BeWo) cells. J. Pharmacol. Exp. Ther. January 2005, 312 (1): 192–198. PMID 15316089. doi:10.1124/jpet.104.072363.
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Zhang M, Han L, Xu Y. Roles of cocaine- and amphetamine-regulated transcript in the central nervous system. Clin. Exp. Pharmacol. Physiol. June 2012, 39 (6): 586–592. PMID 22077697. doi:10.1111/j.1440-1681.2011.05642.x. Recently, it was demonstrated that CART, as a neurotrophic peptide, had a cerebroprotective against focal ischaemic stroke and inhibited the neurotoxicity of β-amyloid protein, which focused attention on the role of CART in the central nervous system (CNS) and neurological diseases. ... The literature indicates that there are many factors, such as regulation of the immunological system and protection against energy failure, that may be involved in the cerebroprotection afforded by CART
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Colasanti A, Searle GE, Long CJ, Hill SP, Reiley RR, Quelch D, Erritzoe D, Tziortzi AC, Reed LJ, Lingford-Hughes AR, Waldman AD, Schruers KR, Matthews PM, Gunn RN, Nutt DJ, Rabiner EA. Endogenous opioid release in the human brain reward system induced by acute amphetamine administration. Biol. Psychiatry. September 2012, 72 (5): 371–377. PMID 22386378. doi:10.1016/j.biopsych.2012.01.027.
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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
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[Figure 4](b) Examples of synthetic, pharmaceutically important substituted amphetamines.
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Bidwell LC, McClernon FJ, Kollins SH. Cognitive enhancers for the treatment of ADHD. Pharmacol. Biochem. Behav. August 2011, 99 (2): 262–274. PMC 3353150 . PMID 21596055. doi:10.1016/j.pbb.2011.05.002.
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Ilieva IP, Hook CJ, Farah MJ. Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis. J. Cogn. Neurosci. January 2015: 1–21. PMID 25591060. doi:10.1162/jocn_a_00776. Specifically, in a set of experiments limited to high-quality designs, we found significant enhancement of several cognitive abilities. ... The results of this meta-analysis ... do confirm the reality of cognitive enhancing effects for normal healthy adults in general, while also indicating that these effects are modest in size.
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Parker KL, Lamichhane D, Caetano MS, Narayanan NS. Executive dysfunction in Parkinson's disease and timing deficits. Front. Integr. Neurosci. October 2013, 7: 75. PMC 3813949 . PMID 24198770. doi:10.3389/fnint.2013.00075. Manipulations of dopaminergic signaling profoundly influence interval timing, leading to the hypothesis that dopamine influences internal pacemaker, or “clock,” activity. For instance, amphetamine, which increases concentrations of dopamine at the synaptic cleft advances the start of responding during interval timing, whereas antagonists of D2 type dopamine receptors typically slow timing;... Depletion of dopamine in healthy volunteers impairs timing, while amphetamine releases synaptic dopamine and speeds up timing.
Rattray B, Argus C, Martin K, Northey J, Driller M. Is it time to turn our attention toward central mechanisms for post-exertional recovery strategies and performance?. Front. Physiol. March 2015, 6: 79. PMC 4362407 . PMID 25852568. doi:10.3389/fphys.2015.00079. Aside from accounting for the reduced performance of mentally fatigued participants, this model rationalizes the reduced RPE and hence improved cycling time trial performance of athletes using a glucose mouthwash (Chambers et al., 2009) and the greater power output during a RPE matched cycling time trial following amphetamine ingestion (Swart, 2009). ... Dopamine stimulating drugs are known to enhance aspects of exercise performance (Roelands et al., 2008)
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· Amphetamine
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About 5–15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983) ...
Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis.
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Olsen CM. Natural rewards, neuroplasticity, and non-drug addictions. Neuropharmacology. December 2011, 61 (7): 1109–1122. PMC 3139704 . PMID 21459101. doi:10.1016/j.neuropharm.2011.03.010. Similar to environmental enrichment, studies have found that exercise reduces self-administration and relapse to drugs of abuse (Cosgrove et al., 2002; Zlebnik et al., 2010). There is also some evidence that these preclinical findings translate to human populations, as exercise reduces withdrawal symptoms and relapse in abstinent smokers (Daniel et al., 2006; Prochaska et al., 2008), and one drug recovery program has seen success in participants that train for and compete in a marathon as part of the program (Butler, 2005). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al., 2006; Aiken, 2007; Lader, 2008).
Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA. Exercise as a novel treatment for drug addiction: a neurobiological and stage-dependent hypothesis. Neurosci. Biobehav. Rev. September 2013, 37 (8): 1622–1644. PMC 3788047 . PMID 23806439. doi:10.1016/j.neubiorev.2013.06.011. These findings suggest that exercise may “magnitude”-dependently prevent the development of an addicted phenotype possibly by blocking/reversing behavioral and neuroadaptive changes that develop during and following extended access to the drug. ... Exercise has been proposed as a treatment for drug addiction that may reduce drug craving and risk of relapse. Although few clinical studies have investigated the efficacy of exercise for preventing relapse, the few studies that have been conducted generally report a reduction in drug craving and better treatment outcomes ... Taken together, these data suggest that the potential benefits of exercise during relapse, particularly for relapse to psychostimulants, may be mediated via chromatin remodeling and possibly lead to greater treatment outcomes.
Zhou Y, Zhao M, Zhou C, Li R. Sex differences in drug addiction and response to exercise intervention: From human to animal studies. Front. Neuroendocrinol. July 2015, 40: 24–41. PMID 26182835. doi:10.1016/j.yfrne.2015.07.001. Collectively, these findings demonstrate that exercise may serve as a substitute or competition for drug abuse by changing ΔFosB or cFos immunoreactivity in the reward system to protect against later or previous drug use. ... The postulate that exercise serves as an ideal intervention for drug addiction has been widely recognized and used in human and animal rehabilitation.
Linke SE, Ussher M. Exercise-based treatments for substance use disorders: evidence, theory, and practicality. Am. J. Drug Alcohol Abuse. January 2015, 41 (1): 7–15. PMC 4831948 . PMID 25397661. doi:10.3109/00952990.2014.976708. The limited research conducted suggests that exercise may be an effective adjunctive treatment for SUDs. In contrast to the scarce intervention trials to date, a relative abundance of literature on the theoretical and practical reasons supporting the investigation of this topic has been published. ... numerous theoretical and practical reasons support exercise-based treatments for SUDs, including psychological, behavioral, neurobiological, nearly universal safety profile, and overall positive health effects.
Greene SL, Kerr F, Braitberg G. Review article: amphetamines and related drugs of abuse. Emerg. Med. Australas. 2008-10, 20 (5): 391–402. PMID 18973636. doi:10.1111/j.1742-6723.2008.01114.x.
Volkow, Nora D.; Koob, George F.; McLellan, A. Thomas. Longo, Dan L. , 编. Neurobiologic Advances from the Brain Disease Model of Addiction. New England Journal of Medicine. 2016-01-28, 374 (4): 363–371. ISSN 0028-4793. PMC 6135257 . PMID 26816013. doi:10.1056/NEJMra1511480 （英语）.
Kollins SH. A qualitative review of issues arising in the use of psycho-stimulant medications in patients with ADHD and co-morbid substance use disorders. Curr. Med. Res. Opin. May 2008, 24 (5): 1345–1357. PMID 18384709. doi:10.1185/030079908X280707. When oral formulations of psychostimulants are used at recommended doses and frequencies, they are unlikely to yield effects consistent with abuse potential in patients with ADHD.
Perez-Mana C, Castells X, Torrens M, Capella D, Farre M. Pérez-Mañá C , 编. Efficacy of psychostimulant drugs for amphetamine abuse or dependence. Cochrane Database Syst. Rev. September 2013, 9: CD009695. PMID 23996457. doi:10.1002/14651858.CD009695.pub2.
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Robison AJ, Nestler EJ. Transcriptional and epigenetic mechanisms of addiction. Nat. Rev. Neurosci. November 2011, 12 (11): 623–637. PMC 3272277 . PMID 21989194. doi:10.1038/nrn3111.
Steiner H, Van Waes V. Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants. Prog. Neurobiol. January 2013, 100: 60–80. PMC 3525776 . PMID 23085425. doi:10.1016/j.pneurobio.2012.10.001.
Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P. Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens. Proc. Natl. Acad. Sci. U.S.A. 2009-02, 106 (8): 2915–2920. PMC 2650365 . PMID 19202072. doi:10.1073/pnas.0813179106.
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Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M. Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms. J. Psychoactive Drugs. March 2012, 44 (1): 38–55. PMC 4040958 . PMID 22641964. doi:10.1080/02791072.2012.662112.
Pitchers KK, Vialou V, Nestler EJ, Laviolette SR, Lehman MN, Coolen LM. Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator. J. Neurosci. February 2013, 33 (8): 3434–3442. PMC 3865508 . PMID 23426671. doi:10.1523/JNEUROSCI.4881-12.2013.
Beloate LN, Weems PW, Casey GR, Webb IC, Coolen LM. Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats. Neuropharmacology. February 2016, 101: 154–164. PMID 26391065. doi:10.1016/j.neuropharm.2015.09.023.
Stoops WW, Rush CR. Combination pharmacotherapies for stimulant use disorder: a review of clinical findings and recommendations for future research. Expert Rev Clin Pharmacol. May 2014, 7 (3): 363–374. PMC 4017926 . PMID 24716825. doi:10.1586/17512433.2014.909283. Despite concerted efforts to identify a pharmacotherapy for managing stimulant use disorders, no widely effective medications have been approved.
Perez-Mana C, Castells X, Torrens M, Capella D, Farre M. Efficacy of psychostimulant drugs for amphetamine abuse or dependence. Cochrane Database Syst. Rev. September 2013, 9: CD009695. PMID 23996457. doi:10.1002/14651858.CD009695.pub2. To date, no pharmacological treatment has been approved for [addiction], and psychotherapy remains the mainstay of treatment. ... Results of this review do not support the use of psychostimulant medications at the tested doses as a replacement therapy
Forray A, Sofuoglu M. Future pharmacological treatments for substance use disorders. Br. J. Clin. Pharmacol. February 2014, 77 (2): 382–400. PMC 4014020 . PMID 23039267. doi:10.1111/j.1365-2125.2012.04474.x.
Grandy DK, Miller GM, Li JX. "TAARgeting Addiction"-The Alamo Bears Witness to Another Revolution: An Overview of the Plenary Symposium of the 2015 Behavior, Biology and Chemistry Conference. Drug Alcohol Depend. February 2016, 159: 9–16. PMID 26644139. doi:10.1016/j.drugalcdep.2015.11.014. When considered together with the rapidly growing literature in the field a compelling case emerges in support of developing TAAR1-selective agonists as medications for preventing relapse to psychostimulant abuse.
Jing L, Li JX. Trace amine-associated receptor 1: A promising target for the treatment of psychostimulant addiction. Eur. J. Pharmacol. August 2015, 761: 345–352. PMC 4532615 . PMID 26092759. doi:10.1016/j.ejphar.2015.06.019. Existing data provided robust preclinical evidence supporting the development of TAAR1 agonists as potential treatment for psychostimulant abuse and addiction.
Carroll ME, Smethells JR. Sex Differences in Behavioral Dyscontrol: Role in Drug Addiction and Novel Treatments. Front. Psychiatry. February 2016, 6: 175. PMC 4745113 . PMID 26903885. doi:10.3389/fpsyt.2015.00175. Physical Exercise
There is accelerating evidence that physical exercise is a useful treatment for preventing and reducing drug addiction ... In some individuals, exercise has its own rewarding effects, and a behavioral economic interaction may occur, such that physical and social rewards of exercise can substitute for the rewarding effects of drug abuse. ... The value of this form of treatment for drug addiction in laboratory animals and humans is that exercise, if it can substitute for the rewarding effects of drugs, could be self-maintained over an extended period of time. Work to date in [laboratory animals and humans] regarding exercise as a treatment for drug addiction supports this hypothesis. ... Animal and human research on physical exercise as a treatment for stimulant addiction indicates that this is one of the most promising treatments on the horizon.
Shoptaw SJ, Kao U, Heinzerling K, Ling W. Shoptaw SJ , 编. Treatment for amphetamine withdrawal. Cochrane Database Syst. Rev. April 2009, (2): CD003021. PMID 19370579. doi:10.1002/14651858.CD003021.pub2. The prevalence of this withdrawal syndrome is extremely common (Cantwell 1998; Gossop 1982) with 87.6% of 647 individuals with amphetamine dependence reporting six or more signs of amphetamine withdrawal listed in the DSM when the drug is not available (Schuckit 1999) ... The severity of withdrawal symptoms is greater in amphetamine dependent individuals who are older and who have more extensive amphetamine use disorders (McGregor 2005). Withdrawal symptoms typically present within 24 hours of the last use of amphetamine, with a withdrawal syndrome involving two general phases that can last 3 weeks or more. The first phase of this syndrome is the initial "crash" that resolves within about a week (Gossop 1982;McGregor 2005) ...
Advokat C. Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD. J. Atten. Disord. July 2007, 11 (1): 8–16. PMID 17606768. doi:10.1177/1087054706295605.
Bowyer JF, Hanig JP. Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity. Temperature (Austin). November 2014, 1 (3): 172–182. PMC 5008711 . PMID 27626044. doi:10.4161/23328940.2014.982049. Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia (≥40°C) are minimally neurotoxic. Hyperthermia likely enhances AMPH and METH neurotoxicity directly through disruption of protein function, ion channels and enhanced ROS production. ... The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier (BBB) resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals. ... In animal models that evaluate the neurotoxicity of AMPH and METH, it is quite clear that hyperthermia is one of the essential components necessary for the production of histological signs of dopamine terminal damage and neurodegeneration in cortex, striatum, thalamus and hippocampus.
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Krause J. SPECT and PET of the dopamine transporter in attention-deficit/hyperactivity disorder. Expert Rev. Neurother. April 2008, 8 (4): 611–625. PMID 18416663. doi:10.1586/14737175.8.4.611. Zinc binds at ... extracellular sites of the DAT [103], serving as a DAT inhibitor. In this context, controlled double-blind studies in children are of interest, which showed positive effects of zinc [supplementation] on symptoms of ADHD [105,106]. It should be stated that at this time [supplementation] with zinc is not integrated in any ADHD treatment algorithm.
Sulzer D. How addictive drugs disrupt presynaptic dopamine neurotransmission. Neuron. February 2011, 69 (4): 628–649. PMC 3065181 . PMID 21338876. doi:10.1016/j.neuron.2011.02.010. They did not confirm the predicted straightforward relationship between uptake and release, but rather that some compounds including AMPH were better releasers than substrates for uptake. Zinc, moreover, stimulates efflux of intracellular [3H]DA despite its concomitant inhibition of uptake (Scholze et al., 2002).
Scholze P, Nørregaard L, Singer EA, Freissmuth M, Gether U, Sitte HH. The role of zinc ions in reverse transport mediated by monoamine transporters. J. Biol. Chem. June 2002, 277 (24): 21505–21513. PMID 11940571. doi:10.1074/jbc.M112265200. The human dopamine transporter (hDAT) contains an endogenous high affinity Zn²⁺ binding site with three coordinating residues on its extracellular face (His193, His375, and Glu396). ... Although Zn²⁺ inhibited uptake, Zn²⁺ facilitated [3H]MPP+ release induced by amphetamine, MPP+, or K+-induced depolarization specifically at hDAT but not at the human serotonin and the norepinephrine transporter (hNET).
Scassellati C, Bonvicini C, Faraone SV, Gennarelli M. Biomarkers and attention-deficit/hyperactivity disorder: a systematic review and meta-analyses. J. Am. Acad. Child Adolesc. Psychiatry. October 2012, 51 (10): 1003–1019.e20. PMID 23021477. doi:10.1016/j.jaac.2012.08.015. With regard to zinc supplementation, a placebo controlled trial reported that doses up to 30 mg/day of zinc were safe for at least 8 weeks, but the clinical effect was equivocal except for the finding of a 37% reduction in amphetamine optimal dose with 30 mg per day of zinc.¹¹⁰
Eiden LE, Weihe E. VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse. Ann. N. Y. Acad. Sci. January 2011, 1216: 86–98. PMC 4183197 . PMID 21272013. doi:10.1111/j.1749-6632.2010.05906.x. VMAT2 is the CNS vesicular transporter for not only the biogenic amines DA, NE, EPI, 5-HT, and HIS, but likely also for the trace amines TYR, PEA, and thyronamine (THYR) ... [Trace aminergic] neurons in mammalian CNS would be identifiable as neurons expressing VMAT2 for storage, and the biosynthetic enzyme aromatic amino acid decarboxylase (AADC). ... AMPH release of DA from synapses requires both an action at VMAT2 to release DA to the cytoplasm and a concerted release of DA from the cytoplasm via "reverse transport" through DAT.
Borowsky B, Adham N, Jones KA, Raddatz R, Artymyshyn R, Ogozalek KL, Durkin MM, Lakhlani PP, Bonini JA, Pathirana S, Boyle N, Pu X, Kouranova E, Lichtblau H, Ochoa FY, Branchek TA, Gerald C. Trace amines: identification of a family of mammalian G protein-coupled receptors. Proc. Natl. Acad. Sci. U.S.A. July 2001, 98 (16): 8966–8971. PMC 55357 . PMID 11459929. doi:10.1073/pnas.151105198.
Underhill SM, Wheeler DS, Li M, Watts SD, Ingram SL, Amara SG. Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons. Neuron. 2014-07, 83 (2): 404–416. PMC 4159050 . PMID 25033183. doi:10.1016/j.neuron.2014.05.043. AMPH also increases intracellular calcium (Gnegy et al., 2004) that is associated with calmodulin/CamKII activation (Wei et al., 2007) and modulation and trafficking of the DAT (Fog et al., 2006; Sakrikar et al., 2012). ... For example, AMPH increases extracellular glutamate in various brain regions including the striatum, VTA and NAc (Del Arco et al., 1999; Kim et al., 1981; Mora and Porras, 1993; Xue et al., 1996), but it has not been established whether this change can be explained by increased synaptic release or by reduced clearance of glutamate. ... DHK-sensitive, EAAT2 uptake was not altered by AMPH (Figure 1A). The remaining glutamate transport in these midbrain cultures is likely mediated by EAAT3 and this component was significantly decreased by AMPH
SLC1A1 solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1 [ Homo sapiens (human) ]. NCBI Gene. United States National Library of Medicine – National Center for Biotechnology Information. [2014-11-11]. （原始内容存档于2020-10-21）. Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons. ... internalization of EAAT3 triggered by amphetamine increases glutamatergic signaling and thus contributes to the effects of amphetamine on neurotransmission.
Zhu HJ, Appel DI, Gründemann D, Markowitz JS. Interaction of organic cation transporter 3 (SLC22A3) and amphetamine. J. Neurochem. 2010-07, 114 (1): 142–149. PMC 3775896 . PMID 20402963. doi:10.1111/j.1471-4159.2010.06738.x.
Rytting E, Audus KL. Novel organic cation transporter 2-mediated carnitine uptake in placental choriocarcinoma (BeWo) cells. J. Pharmacol. Exp. Ther. January 2005, 312 (1): 192–198. PMID 15316089. doi:10.1124/jpet.104.072363.
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Vicentic A, Jones DC. The CART (cocaine- and amphetamine-regulated transcript) system in appetite and drug addiction. J. Pharmacol. Exp. Ther. February 2007, 320 (2): 499–506. PMID 16840648. doi:10.1124/jpet.105.091512. The physiological importance of CART was further substantiated in numerous human studies demonstrating a role of CART in both feeding and psychostimulant addiction. ... Colocalization studies also support a role for CART in the actions of psychostimulants. ... CART and DA receptor transcripts colocalize (Beaudry et al., 2004). Second, dopaminergic nerve terminals in the NAc synapse on CART-containing neurons (Koylu et al., 1999), hence providing the proximity required for neurotransmitter signaling. These studies suggest that DA plays a role in regulating CART gene expression possibly via the activation of CREB.
Zhang M, Han L, Xu Y. Roles of cocaine- and amphetamine-regulated transcript in the central nervous system. Clin. Exp. Pharmacol. Physiol. June 2012, 39 (6): 586–592. PMID 22077697. doi:10.1111/j.1440-1681.2011.05642.x. Recently, it was demonstrated that CART, as a neurotrophic peptide, had a cerebroprotective against focal ischaemic stroke and inhibited the neurotoxicity of β-amyloid protein, which focused attention on the role of CART in the central nervous system (CNS) and neurological diseases. ... The literature indicates that there are many factors, such as regulation of the immunological system and protection against energy failure, that may be involved in the cerebroprotection afforded by CART
Rogge G, Jones D, Hubert GW, Lin Y, Kuhar MJ. CART peptides: regulators of body weight, reward and other functions. Nat. Rev. Neurosci. October 2008, 9 (10): 747–758. PMC 4418456 . PMID 18802445. doi:10.1038/nrn2493. Several studies on CART (cocaine- and amphetamine-regulated transcript)-peptide-induced cell signalling have demonstrated that CART peptides activate at least three signalling mechanisms. First, CART 55–102 inhibited voltage-gated L-type Ca2+ channels ...
Lin Y, Hall RA, Kuhar MJ. CART peptide stimulation of G protein-mediated signaling in differentiated PC12 cells: identification of PACAP 6–38 as a CART receptor antagonist. Neuropeptides. October 2011, 45 (5): 351–358. PMC 3170513 . PMID 21855138. doi:10.1016/j.npep.2011.07.006.
Finnema SJ, Scheinin M, Shahid M, Lehto J, Borroni E, Bang-Andersen B, Sallinen J, Wong E, Farde L, Halldin C, Grimwood S. Application of cross-species PET imaging to assess neurotransmitter release in brain. Psychopharmacology. November 2015, 232 (21–22): 4129–4157. PMC 4600473 . PMID 25921033. doi:10.1007/s00213-015-3938-6. More recently, Colasanti and colleagues reported that a pharmacologically induced elevation in endogenous opioid release reduced [¹¹C]carfentanil binding in several regions of the human brain, including the basal ganglia, frontal cortex, and thalamus (Colasanti et al. 2012). Oral administration of d-amphetamine, 0.5 mg/kg, 3 h before [¹¹C]carfentanil injection, reduced BPND values by 2–10 %. The results were confirmed in another group of subjects (Mick et al. 2014). However, Guterstam and colleagues observed no change in [¹¹C]carfentanil binding when d-amphetamine, 0.3 mg/kg, was administered intravenously directly before injection of [¹¹C]carfentanil (Guterstam et al. 2013). It has been hypothesized that this discrepancy may be related to delayed increases in extracellular opioid peptide concentrations following amphetamine-evoked monoamine release (Colasanti et al. 2012; Mick et al. 2014).
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Colasanti A, Searle GE, Long CJ, Hill SP, Reiley RR, Quelch D, Erritzoe D, Tziortzi AC, Reed LJ, Lingford-Hughes AR, Waldman AD, Schruers KR, Matthews PM, Gunn RN, Nutt DJ, Rabiner EA. Endogenous opioid release in the human brain reward system induced by acute amphetamine administration. Biol. Psychiatry. September 2012, 72 (5): 371–377. PMID 22386378. doi:10.1016/j.biopsych.2012.01.027.
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DOSAGE FORMS AND STRENGTHS
Extended-release oral suspension contains 2.5 mg amphetamine base per mL.

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"Table 5: N-containing drugs and xenobiotics oxygenated by FMO （页面存档备份，存于互联网档案馆）"
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DOSAGE FORMS AND STRENGTHS
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who.int

apps.who.int

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wikipedia.org

en.wikipedia.org

NMDA接受器們為與電壓相關的ligand-gated ion channels（英语：ligand-gated ion channels）。ligand-gated ion channels（英语：ligand-gated ion channels）這個通道需要glutamate 以及一個共同促進劑（co-agonist ）：(D-serine 或大豆屬glycine)的同時連接才能被開啟。
^[139]
該篇回顧表示magnesium L-aspartate（英语：magnesium aspartate）及氯化鎂能大幅改善成癮行為。
The human dopamine transporter contains a high affinity extracellular zinc binding site（英语：binding site） which, upon zinc binding, inhibits dopamine reuptake（英语：reuptake） and amplifies amphetamine-induced dopamine efflux（英语：neurotransmitter efflux） in vitro.^[157]^[158]^[159]The human serotonin transporter and norepinephrine transporter do not contain zinc binding sites.^[159]
a G_s-coupled（英语：Gs alpha subunit） and G_q-coupled（英语：Gq alpha subunit） G protein-coupled receptor (GPCR) discovered in 2001, which is important for regulation of brain monoamines.

worldcat.org

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Nestler, Eric J.; Malenka, Robert C. Chapter 15: Reinforcement and Addictive Disorders. Molecular neuropharmacology : a foundation for clinical neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 364–375. ISBN 978-0-07-164119-7. OCLC 273018757.
Nestler, Eric J. Cellular basis of memory for addiction. Dialogues in Clinical Neuroscience. 2013-12, 15 (4): 431–443. ISSN 1294-8322. PMC 3898681 . PMID 24459410. doi:10.31887/DCNS.2013.15.4/enestler.
Volkow, Nora D.; Koob, George F.; McLellan, A. Thomas. Longo, Dan L. , 编. Neurobiologic Advances from the Brain Disease Model of Addiction. New England Journal of Medicine. 2016-01-28, 374 (4): 363–371. ISSN 0028-4793. PMC 6135257 . PMID 26816013. doi:10.1056/NEJMra1511480 （英语）.