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↑  Montgomery KA. . Psychiatry (Edgmont). 2008-06, 5 (6): 50–55. PMC 2695750 . PMID 19727285.
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1 2 3 4  Shoptaw SJ, Kao U, Ling W. Shoptaw SJ, Ali R , 编. . 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.
1 2  Greydanus D.  (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）.
1 2  Childs E, de Wit H. . 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.
1 2  Nestler, Eric J.; Malenka, Robert C. .  2nd. New York: McGraw-Hill Medical. 2009: 364–375. ISBN 978-0-07-164119-7. OCLC 273018757.
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1 2  Spiller HA, Hays HL, Aleguas A. . 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.  (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)
↑  Kanehisa Laboratories. . KEGG Pathway. 2014-10-10  [2014-10-31]. （原始内容存档于2020-08-08）.
1 2 3 4 5  Nechifor M. . Magnes. Res. March 2008, 21 (1): 5–15. PMID 18557129.
1 2 3 4 5  Ruffle JK. . 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.
1 2 3 4 5  Nestler, Eric J. . 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.
↑  Robison AJ, Nestler EJ. . Nat. Rev. Neurosci. November 2011, 12 (11): 623–637. PMC 3272277 . PMID 21989194. doi:10.1038/nrn3111. ΔFosB serves as one of the master control proteins governing this structural plasticity.
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22  Olsen CM. . 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).
1 2 3 4  Lynch WJ, Peterson AB, Sanchez V, Abel J, Smith MA. . 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.
1 2 3  Zhou Y, Zhao M, Zhou C, Li R. . 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.
1 2 3  Linke SE, Ussher M. . 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.
1 2  Malenka RC, Nestler EJ, Hyman SE. . Sydor A, Brown RY  (编).  2nd. New York, USA: McGraw-Hill Medical. 2009: 386. ISBN 9780071481274. Currently, cognitive–behavioral therapies are the most successful treatment available for preventing the relapse of psychostimulant use.
↑  Greene SL, Kerr F, Braitberg G. . Emerg. Med. Australas. 2008-10, 20 (5): 391–402. PMID 18973636. doi:10.1111/j.1742-6723.2008.01114.x.
↑  Albertson TE. . Olson KR, Anderson IB, Benowitz NL, Blanc PD, Kearney TE, Kim-Katz SY, Wu AH  (编).  6th. New York: McGraw-Hill Medical. 2011: 77–79. ISBN 9780071668330.
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↑  Volkow, Nora D.; Koob, George F.; McLellan, A. Thomas. Longo, Dan L. , 编. . 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）.
↑  Malenka RC, Nestler EJ, Hyman SE. . Sydor A, Brown RY  (编).  2nd. New York: McGraw-Hill Medical. 2009: 368. ISBN 9780071481274. Such agents also have important therapeutic uses; cocaine, for example, is used as a local anesthetic (Chapter 2), and amphetamines and methylphenidate are used in low doses to treat attention deficit hyperactivity disorder and in higher doses to treat narcolepsy (Chapter 12). Despite their clinical uses, these drugs are strongly reinforcing, and their long-term use at high doses is linked with potential addiction, especially when they are rapidly administered or when high-potency forms are given.
↑  Kollins SH. . 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.
↑  Stolerman IP. Stolerman IP , 编. . Berlin, Germany; London, England: Springer. 2010: 78. ISBN 9783540686989.
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↑  Perez-Mana C, Castells X, Torrens M, Capella D, Farre M. Pérez-Mañá C , 编. . Cochrane Database Syst. Rev. September 2013, 9: CD009695. PMID 23996457. doi:10.1002/14651858.CD009695.pub2.
↑  Hyman SE, Malenka RC, Nestler EJ. . Annu. Rev. Neurosci. July 2006, 29: 565–598. PMID 16776597. doi:10.1146/annurev.neuro.29.051605.113009.
1 2 3 4 5 6 7 8  Robison AJ, Nestler EJ. . Nat. Rev. Neurosci. November 2011, 12 (11): 623–637. PMC 3272277 . PMID 21989194. doi:10.1038/nrn3111.
1 2 3 4  Steiner H, Van Waes V. . Prog. Neurobiol. January 2013, 100: 60–80. PMC 3525776 . PMID 23085425. doi:10.1016/j.pneurobio.2012.10.001.
↑  Malenka RC, Nestler EJ, Hyman SE. . Sydor A, Brown RY  (编).  2nd. New York, USA: McGraw-Hill Medical. 2009: 94. ISBN 9780071481274.
↑  Kanehisa Laboratories. . KEGG Pathway. 2014-10-29  [2014-10-31]. （原始内容存档于2019-11-12）.
↑  Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P. . Proc. Natl. Acad. Sci. U.S.A. 2009-02, 106 (8): 2915–2920. PMC 2650365 . PMID 19202072. doi:10.1073/pnas.0813179106.
↑  Nestler EJ. . Neuropharmacology. January 2014,. 76 Pt B: 259–268. PMC 3766384 . PMID 23643695. doi:10.1016/j.neuropharm.2013.04.004.
1 2  Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M. . 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. . 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. . Neuropharmacology. February 2016, 101: 154–164. PMID 26391065. doi:10.1016/j.neuropharm.2015.09.023.
↑  Stoops WW, Rush CR. . 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. . 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. . Br. J. Clin. Pharmacol. February 2014, 77 (2): 382–400. PMC 4014020 . PMID 23039267. doi:10.1111/j.1365-2125.2012.04474.x.
1 2 3 4  Grandy DK, Miller GM, Li JX. . 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.
1 2  Jing L, Li JX. . 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.
1 2  Malenka RC, Nestler EJ, Hyman SE. . Sydor A, Brown RY  (编).  2nd. New York, USA: McGraw-Hill Medical. 2009: 124–125. ISBN 9780071481274.
1 2 3  Carroll ME, Smethells JR. . 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.
1 2 3  Shoptaw SJ, Kao U, Heinzerling K, Ling W. Shoptaw SJ , 编. . 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. . Drug and Alcohol Dependence (Elsevier BV). 1998, 49 (2): 157–163  [2017-05-09]. doi:10.1016/s0376-8716(97)00160-9.
↑  . Medscape Reference. 2015-12-03  [2017-05-09]. （原始内容存档于2020-08-10）.
↑   (PDF). United States Food and Drug Administration. Teva Pharmaceuticals USA, Inc. October 2015  [2016-05-18]. （原始内容存档 (PDF)于2018-09-15）.
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↑  Advokat C. . J. Atten. Disord. July 2007, 11 (1): 8–16. PMID 17606768. doi:10.1177/1087054706295605.
1 2 3 4  Bowyer JF, Hanig JP. . 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.
↑  . Hazardous Substances Data Bank. United States National Library of Medicine – Toxicology Data Network.   [2014-02-26]. （原始内容存档于2017-10-02）. Direct toxic damage to vessels seems unlikely because of the dilution that occurs before the drug reaches the cerebral circulation.
↑  Malenka RC, Nestler EJ, Hyman SE. . Sydor A, Brown RY  (编).  2nd. New York, USA: McGraw-Hill Medical. 2009: 370. ISBN 9780071481274. Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons.
↑  Sulzer D, Zecca L. . Neurotox. Res. February 2000, 1 (3): 181–195. PMID 12835101. doi:10.1007/BF03033289.
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1 2  Neal R. Swerdlow. Savita G. Bhakta , Jo Talledo, Lindsay Benster, Juliana Kotz, Maria Lavadia and Gregory A. Light. . Neurophsychopharmacology. 2019.
↑  Hofmann FG.  2nd. New York, USA: Oxford University Press. 1983: 329. ISBN 9780195030570.
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↑  Krause J. . 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. . 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).
1 2  Scholze P, Nørregaard L, Singer EA, Freissmuth M, Gether U, Sitte HH. . 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. . 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
↑  Richard RA. . . Treatment Improvement Protocol 33. Substance Abuse and Mental Health Services Administration. 1999. （原始内容存档于2020-11-11） 使用|archiveurl=需要含有|url= (帮助).  |section-url=被忽略 (帮助); |section=被忽略 (帮助); 使用|accessdate=需要含有|url= (帮助)
1 2 3 4   (PDF). United States Food and Drug Administration. Shire US Inc: 12–16. January 2015  [2015-02-24]. （原始内容存档 (PDF)于2015-02-25）.
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1 2  . . Technische Universität Braunschweig. （原始内容存档于2017-06-22） 使用|archiveurl=需要含有|url= (帮助).  |section-url=被忽略 (帮助); |section=被忽略 (帮助); 使用|accessdate=需要含有|url= (帮助)
1 2  . . Technische Universität Braunschweig. （原始内容存档于2017-06-23） 使用|archiveurl=需要含有|url= (帮助).  |section-url=被忽略 (帮助); |section=被忽略 (帮助); 使用|accessdate=需要含有|url= (帮助)
1 2  . . National Center for Biotechnology Information. （原始内容存档于2013-06-07） 使用|archiveurl=需要含有|url= (帮助).  |section-url=被忽略 (帮助); |section=被忽略 (帮助); 使用|accessdate=需要含有|url= (帮助)
1 2  . . National Center for Biotechnology Information. （原始内容存档于2014-10-18） 使用|archiveurl=需要含有|url= (帮助).  |section-url=被忽略 (帮助); |section=被忽略 (帮助); 使用|accessdate=需要含有|url= (帮助)
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1 2 3 4 5  Eiden LE, Weihe E. . 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.
↑  Maguire JJ, Davenport AP. . IUPHAR database. International Union of Basic and Clinical Pharmacology. 2 December 2014  [8 December 2014]. （原始内容存档于2015-06-29）.
↑  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. . Proc. Natl. Acad. Sci. U.S.A. July 2001, 98 (16): 8966–8971. PMC 55357 . PMID 11459929. doi:10.1073/pnas.151105198.
1 2  Underhill SM, Wheeler DS, Li M, Watts SD, Ingram SL, Amara SG. . 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
1 2  . IUPHAR database. International Union of Basic and Clinical Pharmacology.   [2015-11-13]. （原始内容存档于2020-10-28）.
1 2 3  . 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. . J. Neurochem. 2010-07, 114 (1): 142–149. PMC 3775896 . PMID 20402963. doi:10.1111/j.1471-4159.2010.06738.x.
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1 2 3  Vicentic A, Jones DC. . 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. . 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
1 2  Rogge G, Jones D, Hubert GW, Lin Y, Kuhar MJ. . 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. . Neuropeptides. October 2011, 45 (5): 351–358. PMC 3170513 . PMID 21855138. doi:10.1016/j.npep.2011.07.006.
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