Μεθυλφαινιδάτη (Greek Wikipedia)

Analysis of information sources in references of the Wikipedia article "Μεθυλφαινιδάτη" in Greek language version.

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archive.org

Stahl, Stephen M. (11 Απριλίου 2013). Stahl's Essential Psychopharmacology: Neuroscientific Basis and Practical Applications (4th έκδοση). Cambridge University Press. ISBN 978-1107686465.
«Stimulant medication therapy in the treatment of children with attention deficit hyperactivity disorder». Pediatr. Clin. North Am. 36 (5): 1183–97. 1989. doi:10.1016/S0031-3955(16)36764-5. PMID 2677938. https://archive.org/details/sim_pediatric-clinics-of-north-america_1989-10_36_5/page/1183.
«Does Stimulant Therapy of Attention-Deficit/Hyperactivity Disorder Beget Later Substance Abuse? A Meta-analytic Review of the Literature». Pediatrics 111 (1): 179–85. 2003. doi:10.1542/peds.111.1.179. PMID 12509574. https://archive.org/details/sim_pediatrics_2003-01_111_1/page/179.
Neinstein, Lawrence (2009). Handbook of adolescent health care. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-0-7817-9020-8.
«Methylphenidate: a review of its neuropharmacological, neuropsychological and adverse clinical effects». Hum Psychopharmacol 19 (3): 151–80. 2004. doi:10.1002/hup.579. PMID 15079851. https://archive.org/details/sim_human-psychopharmacology_2004-04_19_3/page/151.
«Methylphenidate hydrochloride as an antidepressant: controversy, case studies, and review». South. Med. J. 85 (10): 985–91. 1992. doi:10.1097/00007611-199210000-00012. PMID 1411740. https://archive.org/details/sim_southern-medical-journal_1992-10_85_10/page/985.
«Stimulants in the treatment of depression: a critical overview». J Clin Psychiatry 50 (7): 241–9. 1989. PMID 2567730. https://archive.org/details/sim_journal-of-clinical-psychiatry_1989-07_50_7/page/241.
«Chapter 13: Higher Cognitive Function and Behavioral Control». Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd έκδοση). New York: McGraw-Hill Medical. 2009. σελ. 318. ISBN 9780071481274. Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD. Positron emission tomography (PET) demonstrates that methylphenidate decreases regional cerebral blood flow in the doroslateral prefrontal cortex and posterior parietal cortex while improving performance of a spatial working memory task. This suggests that cortical networks that normally process spatial working memory become more efficient in response to the drug. ... [It] is now believed that dopamine and norepinephrine, but not serotonin, produce the beneficial effects of stimulants on working memory. At abused (relatively high) doses, stimulants can interfere with working memory and cognitive control ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors.
«Non-specific effects of Methylphenidate (Ritalin) on cognitive ability and decision-making of ADHD and healthy adult». Psychopharmacology 210 (4): 511–519. 2010. doi:10.1007/s00213-010-1853-4. PMID 20424828. https://archive.org/details/sim_psychopharmacology_2010-07_210_4/page/511.
«Illicit use of specific prescription stimulants among college students: prevalence, motives, and routes of administration». Pharmacotherapy 26 (10): 1501–1510. October 2006. doi:10.1592/phco.26.10.1501. PMID 16999660. PMC 1794223. https://archive.org/details/sim_pharmacotherapy_2006-10_26_10/page/1501.
«Growth on stimulant medication; clarifying the confusion: a review». Archives of Disease in Childhood 90 (8): 801–6. August 2005. doi:10.1136/adc.2004.056952. PMID 16040876. PMC 1720538. https://archive.org/details/sim_archives-of-disease-in-childhood_2005-08_90_8/page/801.
«Chapter 15: Reinforcement and Addictive Disorders». Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd έκδοση). New York: McGraw-Hill Medical. 2009. σελ. 368. ISBN 9780071481274. Cocaine, [amphetamine], and methamphetamine are the major psychostimulants of abuse. The related drug methylphenidate is also abused, although it is far less potent. These drugs elicit similar initial subjective effects ; differences generally reflect the route of administration and other pharmacokinetic factors. 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.
«Serotonin syndrome». Neurology 45 (2): 219–23. February 1995. doi:10.1212/wnl.45.2.219. PMID 7854515. https://archive.org/details/sim_neurology_1995-02_45_2/page/219.
«Influence of ethanol and gender on methylphenidate pharmacokinetics and pharmacodynamics.». Clinical Pharmacology and Therapeutics 81 (3): 346–53. March 2007. doi:10.1038/sj.clpt.6100082. PMID 17339864. PMC 3188424. https://archive.org/details/sim_clinical-pharmacology-and-therapeutics_2007-03_81_3/page/346.
«Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin». Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd έκδοση). New York: McGraw-Hill Medical. 2009. σελίδες 154–157. ISBN 9780071481274.
«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 70 (2): 185–98. February 2013. doi:10.1001/jamapsychiatry.2013.277. PMID 23247506. https://archive.org/details/sim_jama-psychiatry_2013-02_70_2/page/185.
«Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies». The Journal of Clinical Psychiatry 74 (9): 902–17. September 2013. doi:10.4088/JCP.12r08287. PMID 24107764. PMC 3801446. https://archive.org/details/sim_journal-of-clinical-psychiatry_2013-09_74_9/page/902.
«Methylphenidate hydrochloride given with or before breakfast: II. Effects on plasma concentration of methylphenidate and ritalinic acid». Pediatrics 72 (1): 56–59. 1983. PMID 6866592. https://archive.org/details/sim_pediatrics_1983-07_72_1/page/56.
«Methylphenidate is stereoselectively hydrolyzed by human carboxylesterase CES1A1». The Journal of Pharmacology and Experimental Therapeutics 310 (2): 469–76. August 2004. doi:10.1124/jpet.104.067116. PMID 15082749. https://archive.org/details/sim_journal-of-pharmacology-and-experimental-therapeutics_2004-08_310_2/page/469.
«Conformational analysis of methylphenidate and its structural relationship to other dopamine reuptake blockers such as CFT». Pharmaceutical Research 12 (10): 1430–4. October 1995. doi:10.1023/A:1016262815984. PMID 8584475. https://archive.org/details/sim_pharmaceutical-research_1995-10_12_10/page/1430.
Myers, Richard L (Αυγούστου 2007). The 100 most important chemical compounds: a reference guide. ABC-CLIO. σελ. 178. ISBN 978-0-313-33758-1. Ανακτήθηκε στις 10 Σεπτεμβρίου 2010. named ritalin after his wife.
«Paediatric methylphenidate (Ritalin) restrictive conditions of prescription in France». Br J Clin Pharmacol 57 (1): 115–6. January 2004. doi:10.1046/j.1365-2125.2003.01943.x. PMID 14678352. PMC 1884413. https://archive.org/details/sim_british-journal-of-clinical-pharmacology_2004-01_57_1/page/115.

books.google.com

Bonewit-West K, Hunt SA, Applegate E (2012). Today's Medical Assistant: Clinical and Administrative Procedures (στα Αγγλικά). Elsevier Health Sciences. σελ. 571. ISBN 9781455701506.
Preedy, Victor R. (2016). Neuropathology of Drug Addictions and Substance Misuse Volume 3: General Processes and Mechanisms, Prescription Medications, Caffeine and Areca, Polydrug Misuse, Emerging Addictions and Non-Drug Addictions (στα Αγγλικά). Academic Press. σελ. 651. ISBN 9780128006771.
Myers, Richard Leroy (1 Ιανουαρίου 2007). The 100 Most Important Chemical Compounds: A Reference Guide. ABC-CLIO. σελ. 178. ISBN 9780313337581. Ανακτήθηκε στις 24 Σεπτεμβρίου 2016.

cjcp.ca

«A randomized, controlled effectiveness trial of OROS-methylphenidate compared to usual care with immediate-release methylphenidate in attention deficit-hyperactivity disorder». Can J Clin Pharmacol 13 (1): e50–62. 2006. PMID 16456216. Αρχειοθετήθηκε από το πρωτότυπο στις 15 December 2011. http://webarchive.nationalarchives.gov.uk/20111215210932/http%3A//www.cjcp.ca/CJCP_05%2D012_e50%2Dr101628.

clincalc.com

«The Top 300 of 2020». ClinCalc. Ανακτήθηκε στις 11 Απριλίου 2020.
«Methylphenidate - Drug Usage Statistics». ClinCalc. Ανακτήθηκε στις 11 Απριλίου 2020.

comlaw.gov.au

«Poisons Standard 2012 as amended made under paragraph 52D(2)(a) of the Therapeutic Goods Act 1989». Therapeutic Goods Administration. 27 Νοεμβρίου 2014. Αρχειοθετήθηκε από το πρωτότυπο στις 1 Ιουλίου 2015. Ανακτήθηκε στις 28 Ιουνίου 2015.

crossinology.com

«Ritalin and Attention Deficit Disorder: History of its Use, Effects and Side Effects» (PDF). 1995. Αρχειοθετήθηκε από το πρωτότυπο (PDF) στις 24 Αυγούστου 2012. Ανακτήθηκε στις 22 Ιουλίου 2014.

dea.gov

Woodworth, Terrance (16 Μαΐου 2000). «DEA Congressional Testimony». Αρχειοθετήθηκε από το πρωτότυπο στις 12 Οκτωβρίου 2007. Ανακτήθηκε στις 2 Νοεμβρίου 2007.

doi.org

dx.doi.org

«Pharmacokinetics and clinical effectiveness of methylphenidate». Clinical Pharmacokinetics 37 (6): 457–70. December 1999. doi:10.2165/00003088-199937060-00002. PMID 10628897.
«Neurobiology of Executive Functions: Catecholamine Influences on Prefrontal Cortical Functions». Biological Psychiatry 57 (11): 1377–84. 2005. doi:10.1016/j.biopsych.2004.08.019. PMID 15950011.
«The history of attention deficit hyperactivity disorder». ADHD Attention Deficit and Hyperactivity Disorders 2 (4): 241–55. 2010. doi:10.1007/s12402-010-0045-8. PMID 21258430.
«Stimulants: use and abuse in the treatment of ADD». Current Opinion in Pharmacology 5 (1): 87–93. 2005. doi:10.1016/j.coph.2004.10.001. PMID 15661631.
«Methylphenidate HCl: therapy for attention deficit hyperactivity disorder». Expert Rev Neurother 5 (3): 325–31. 2005. doi:10.1586/14737175.5.3.325. PMID 15938665.
«Treatment of attention deficit hyperactivity disorder in adults». Expert Rev Neurother 5 (1): 107–21. 2005. doi:10.1586/14737175.5.1.107. PMID 15853481.
«Stimulant medication therapy in the treatment of children with attention deficit hyperactivity disorder». Pediatr. Clin. North Am. 36 (5): 1183–97. 1989. doi:10.1016/S0031-3955(16)36764-5. PMID 2677938. https://archive.org/details/sim_pediatric-clinics-of-north-america_1989-10_36_5/page/1183.
Management (1 November 2011). «ADHD: Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents». Pediatrics 128 (5): 1007–1022. doi:10.1542/peds.2011-2654. ISSN 0031-4005. PMID 22003063.
«Methylphenidate in children with hyperactivity: review and cost-utility analysis». Pharmacoepidemiol Drug Saf 10 (2): 85–94. 2001. doi:10.1002/pds.564. PMID 11499858.
«Long-term outcomes with medications for attention-deficit hyperactivity disorder: current status of knowledge». CNS Drugs 25 (7): 539–554. July 2011. doi:10.2165/11589380-000000000-00000. PMID 21699268.
«Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents – assessment of adverse events in non-randomised studies». Cochrane Database Syst Rev 5: CD012069. 2018. doi:10.1002/14651858.CD012069.pub2. PMID 29744873. «Our findings suggest that methylphenidate may be associated with a number of serious adverse events as well as a large number of non-serious adverse events in children. Concerning adverse events associated with the treatment, our systematic review of randomised clinical trials (RCTs) demonstrated no increase in serious adverse events, but a high proportion of participants suffered a range of non‐serious adverse events.».
«Methylphenidate for children and adolescents with attention deficit hyperactivity disorder (ADHD)». Cochrane Database Syst Rev 11 (11): CD009885. November 2015. doi:10.1002/14651858.CD009885.pub2. PMID 26599576. Αρχειοθετήθηκε από το πρωτότυπο στις 2021-02-28. https://web.archive.org/web/20210228063939/https://findresearcher.sdu.dk:8443/ws/files/129083195/Methylphenidate_for_children_and_adolescents_with_attention_deficit_hyperactivity_disorder_ADHD_.pdf. Ανακτήθηκε στις 2020-10-06. «the low quality of the underpinning evidence means that we cannot be certain of the magnitude of the effects.».
«Practice parameter for the use of stimulant medications in the treatment of children, adolescents, and adults». J. Am. Acad. Child Adolesc. Psychiatry 41 (2 Suppl): 26S–49S. February 2002. doi:10.1097/00004583-200202001-00003. PMID 11833633.
«Effect of stimulant medications for attention-deficit/hyperactivity disorder on later substance use and the potential for stimulant misuse, abuse, and diversion». J Clin Psychiatry 68 Suppl 11 (11): 15–22. 2007. doi:10.4088/jcp.1107e28. PMID 18307377.
«Does Stimulant Therapy of Attention-Deficit/Hyperactivity Disorder Beget Later Substance Abuse? A Meta-analytic Review of the Literature». Pediatrics 111 (1): 179–85. 2003. doi:10.1542/peds.111.1.179. PMID 12509574. https://archive.org/details/sim_pediatrics_2003-01_111_1/page/179.
«Mitigating risks of students use of study drugs through understanding motivations for use and applying harm reduction theory: a literature review». Harm Reduction Journal 14 (1): 68. October 2017. doi:10.1186/s12954-017-0194-6. PMID 28985738.
«Psychopharmacology for young children: clinical needs and research opportunities». Pediatrics 108 (4): 983–9. October 2001. doi:10.1542/peds.108.4.983. PMID 11581454. https://semanticscholar.org/paper/7b921a206155401fc089da016b94d96ceba389a3.
«Integrative neuroscience approach to predict ADHD stimulant response». Expert Review of Neurotherapeutics 6 (5): 753–63. 2006. doi:10.1586/14737175.6.5.753. PMID 16734523.
«Treatment modalities for narcolepsy». Neurology 50 (2 Suppl 1): S43-8. February 1998. doi:10.1212/WNL.50.2_Suppl_1.S43. PMID 9484423.
«Evaluation of treatment with stimulants in narcolepsy». Sleep 17 (8 Suppl): S103-6. December 1994. doi:10.1093/sleep/17.suppl_8.S103. PMID 7701190.
«Wake-promoting pharmacotherapy for psychiatric disorders». Curr Psychiatry Rep 16 (12): 524. December 2014. doi:10.1007/s11920-014-0524-2. PMID 25312027.
«Methylphenidate: a review of its neuropharmacological, neuropsychological and adverse clinical effects». Hum Psychopharmacol 19 (3): 151–80. 2004. doi:10.1002/hup.579. PMID 15079851. https://archive.org/details/sim_human-psychopharmacology_2004-04_19_3/page/151.
«Methylphenidate hydrochloride as an antidepressant: controversy, case studies, and review». South. Med. J. 85 (10): 985–91. 1992. doi:10.1097/00007611-199210000-00012. PMID 1411740. https://archive.org/details/sim_southern-medical-journal_1992-10_85_10/page/985.
«Palliative uses of methylphenidate in patients with cancer: a review». J. Clin. Oncol. 20 (1): 335–9. 2002. doi:10.1200/JCO.20.1.335. PMID 11773187.
Ruthirakuhan, Myuri T.; Herrmann, Nathan; Abraham, Eleenor H.; Chan, Sarah; Lanctôt, Krista L. (2018-05-04). «Pharmacological interventions for apathy in Alzheimer's disease». The Cochrane Database of Systematic Reviews 5: CD012197. doi:10.1002/14651858.CD012197.pub2. ISSN 1469-493X. PMID 29727467.
«The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex». Biol. Psychiatry 77 (11): 940–950. June 2015. doi:10.1016/j.biopsych.2014.09.013. PMID 25499957. «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). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation.».
«Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis». J. Cogn. Neurosci. 27 (6): 1069–1089. January 2015. doi:10.1162/jocn_a_00776. PMID 25591060. Αρχειοθετήθηκε από το πρωτότυπο στις 19 September 2018. https://web.archive.org/web/20180919111616/https://repository.upenn.edu/neuroethics_pubs/130/. Ανακτήθηκε στις 14 November 2018. «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.».
«Psychostimulants and cognition: a continuum of behavioral and cognitive activation». Pharmacol. Rev. 66 (1): 193–221. January 2014. doi:10.1124/pr.112.007054. PMID 24344115.
«Non-specific effects of Methylphenidate (Ritalin) on cognitive ability and decision-making of ADHD and healthy adult». Psychopharmacology 210 (4): 511–519. 2010. doi:10.1007/s00213-010-1853-4. PMID 20424828. https://archive.org/details/sim_psychopharmacology_2010-07_210_4/page/511.
«Illicit use of specific prescription stimulants among college students: prevalence, motives, and routes of administration». Pharmacotherapy 26 (10): 1501–1510. October 2006. doi:10.1592/phco.26.10.1501. PMID 16999660. PMC 1794223. https://archive.org/details/sim_pharmacotherapy_2006-10_26_10/page/1501.
«Neurophysiological determinants of theoretical concepts and mechanisms involved in pacing». Sports Med. 43 (5): 301–311. May 2013. doi:10.1007/s40279-013-0030-4. PMID 23456493.
Ornoy, Asher (6 February 2018). «Pharmacological Treatment of Attention Deficit Hyperactivity Disorder During Pregnancy and Lactation». Pharmaceutical Research 35 (3): 46. doi:10.1007/s11095-017-2323-z. PMID 29411149.
«Development of a rational scale to assess the harm of drugs of potential misuse». Lancet 369 (9566): 1047–53. March 2007. doi:10.1016/S0140-6736(07)60464-4. PMID 17382831.
«Practitioner review: current best practice in the management of adverse events during treatment with ADHD medications in children and adolescents». Journal of Child Psychology and Psychiatry, and Allied Disciplines 54 (3): 227–46. March 2013. doi:10.1111/jcpp.12036. PMID 23294014.
«Growth on stimulant medication; clarifying the confusion: a review». Archives of Disease in Childhood 90 (8): 801–6. August 2005. doi:10.1136/adc.2004.056952. PMID 16040876. PMC 1720538. https://archive.org/details/sim_archives-of-disease-in-childhood_2005-08_90_8/page/801.
«ADHD, Multimodal Treatment, and Longitudinal Outcome: Evidence, Paradox, and Challenge». Wiley Interdisciplinary Reviews. Cognitive Science 6 (1): 39–52. January 2015. doi:10.1002/wcs.1324. PMID 25558298.
«Transdermal therapy for attention-deficit hyperactivity disorder with the methylphenidate patch (MTS)». CNS Drugs 28 (3): 217–28. March 2014. doi:10.1007/s40263-014-0141-y. PMID 24532028.
«Methylphenidate-induced psychosis in adult attention-deficit/hyperactivity disorder: report of 3 new cases and review of the literature». Clinical Neuropharmacology 33 (4): 204–6. July 2010. doi:10.1097/WNF.0b013e3181e29174. PMID 20571380.
«FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in children and young adults». United States Food and Drug Administration. 20 Δεκεμβρίου 2011. Αρχειοθετήθηκε από το πρωτότυπο στις 30 Οκτωβρίου 2013. Ανακτήθηκε στις 4 Νοεμβρίου 2013.

• «ADHD drugs and serious cardiovascular events in children and young adults». N. Engl. J. Med. 365 (20): 1896–1904. November 2011. doi:10.1056/NEJMoa1110212. PMID 22043968.

• «FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in adults». United States Food and Drug Administration. 15 Δεκεμβρίου 2011. Αρχειοθετήθηκε από το πρωτότυπο στις 30 Οκτωβρίου 2013. Ανακτήθηκε στις 4 Νοεμβρίου 2013.

• «ADHD medications and risk of serious cardiovascular events in young and middle-aged adults». JAMA 306 (24): 2673–2683. December 2011. doi:10.1001/jama.2011.1830. PMID 22161946.
«Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents - assessment of adverse events in non-randomised studies». The Cochrane Database of Systematic Reviews 5: CD012069. May 2018. doi:10.1002/14651858.CD012069.pub2. PMID 29744873.
«Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation, mechanisms of toxicity, and management». CNS Drugs 27 (7): 531–543. June 2013. doi:10.1007/s40263-013-0084-8. PMID 23757186. «The management of amphetamine, dextroamphetamine, and methylphenidate overdose is largely supportive, with a focus on interruption of the sympathomimetic syndrome with judicious use of benzodiazepines. In cases where agitation, delirium, and movement disorders are unresponsive to benzodiazepines, second-line therapies include antipsychotics such as ziprasidone or haloperidol, central alpha-adrenoreceptor agonists such as dexmedetomidine, or propofol. ... However, fatalities are rare with appropriate care».
«Severe toxicity due to injected but not oral or nasal abuse of methylphenidate tablets». Swiss Med Wkly 141: w13267. 2011. doi:10.4414/smw.2011.13267. PMID 21984207.
«Methylphenidate Abuse and Psychiatric Side Effects». Prim Care Companion J Clin Psychiatry 2 (5): 159–164. 2000. doi:10.4088/PCC.v02n0502. PMID 15014637.
«Risks of high-dose stimulants in the treatment of disorders of excessive somnolence: a case-control study». Sleep 28 (6): 667–72. 2005. doi:10.1093/sleep/28.6.667. PMID 16477952.
«Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants». Prog. Neurobiol. 100: 60–80. January 2013. doi:10.1016/j.pneurobio.2012.10.001. PMID 23085425.
«Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens». Proc. Natl. Acad. Sci. U.S.A. 106 (8): 2915–20. 2009. doi:10.1073/pnas.0813179106. PMID 19202072. Bibcode: 2009PNAS..106.2915K. «Despite decades of clinical use of methylphenidate for ADHD, concerns have been raised that long-term treatment of children with this medication may result in subsequent drug abuse and addiction. However, meta analysis of available data suggests that treatment of ADHD with stimulant drugs may have a significant protective effect, reducing the risk for addictive substance use (36, 37). Studies with juvenile rats have also indicated that repeated exposure to methylphenidate does not necessarily lead to enhanced drug-seeking behavior in adulthood (38). However, the recent increase of methylphenidate use as a cognitive enhancer by the general public has again raised concerns because of its potential for abuse and addiction (3, 6–10). Thus, although oral administration of clinical doses of methylphenidate is not associated with euphoria or with abuse problems, nontherapeutic use of high doses or i.v. administration may lead to addiction (39, 40).».
«Pharmacotherapy of methamphetamine addiction: an update». Substance Abuse 29 (3): 31–49. 2008. doi:10.1080/08897070802218554. PMID 19042205.
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The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...
Conclusions
Πρότυπο:In5ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a molecular switch (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.».

• «Epigenetic regulation in drug addiction». Annals of Agricultural and Environmental Medicine 19 (3): 491–6. 2012. PMID 23020045. «For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription».

• «Transcriptional and epigenetic mechanisms of addiction». Nature Reviews. Neuroscience 12 (11): 623–37. October 2011. doi:10.1038/nrn3111. PMID 21989194. «ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure^14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption^14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.».
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«Practice parameter for the use of stimulant medications in the treatment of children, adolescents, and adults». J. Am. Acad. Child Adolesc. Psychiatry 41 (2 Suppl): 26S–49S. February 2002. doi:10.1097/00004583-200202001-00003. PMID 11833633.
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«Does Stimulant Therapy of Attention-Deficit/Hyperactivity Disorder Beget Later Substance Abuse? A Meta-analytic Review of the Literature». Pediatrics 111 (1): 179–85. 2003. doi:10.1542/peds.111.1.179. PMID 12509574. https://archive.org/details/sim_pediatrics_2003-01_111_1/page/179.
«Mitigating risks of students use of study drugs through understanding motivations for use and applying harm reduction theory: a literature review». Harm Reduction Journal 14 (1): 68. October 2017. doi:10.1186/s12954-017-0194-6. PMID 28985738.
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«The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex». Biol. Psychiatry 77 (11): 940–950. June 2015. doi:10.1016/j.biopsych.2014.09.013. PMID 25499957. «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). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation.».
«Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis». J. Cogn. Neurosci. 27 (6): 1069–1089. January 2015. doi:10.1162/jocn_a_00776. PMID 25591060. Αρχειοθετήθηκε από το πρωτότυπο στις 19 September 2018. https://web.archive.org/web/20180919111616/https://repository.upenn.edu/neuroethics_pubs/130/. Ανακτήθηκε στις 14 November 2018. «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.».
«Psychostimulants and cognition: a continuum of behavioral and cognitive activation». Pharmacol. Rev. 66 (1): 193–221. January 2014. doi:10.1124/pr.112.007054. PMID 24344115.
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«ADHD, Multimodal Treatment, and Longitudinal Outcome: Evidence, Paradox, and Challenge». Wiley Interdisciplinary Reviews. Cognitive Science 6 (1): 39–52. January 2015. doi:10.1002/wcs.1324. PMID 25558298.
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• «ADHD drugs and serious cardiovascular events in children and young adults». N. Engl. J. Med. 365 (20): 1896–1904. November 2011. doi:10.1056/NEJMoa1110212. PMID 22043968.

• «FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in adults». United States Food and Drug Administration. 15 Δεκεμβρίου 2011. Αρχειοθετήθηκε από το πρωτότυπο στις 30 Οκτωβρίου 2013. Ανακτήθηκε στις 4 Νοεμβρίου 2013.

• «ADHD medications and risk of serious cardiovascular events in young and middle-aged adults». JAMA 306 (24): 2673–2683. December 2011. doi:10.1001/jama.2011.1830. PMID 22161946.
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«Cellular basis of memory for addiction». Dialogues in Clinical Neuroscience 15 (4): 431–43. December 2013. PMID 24459410. «Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.⁴¹. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.4».
«Molecular neurobiology of addiction: what's all the (Δ)FosB about?». The American Journal of Drug and Alcohol Abuse 40 (6): 428–37. November 2014. doi:10.3109/00952990.2014.933840. PMID 25083822. «
The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...
Conclusions
Πρότυπο:In5ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a molecular switch (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.».

• «Epigenetic regulation in drug addiction». Annals of Agricultural and Environmental Medicine 19 (3): 491–6. 2012. PMID 23020045. «For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription».

• «Transcriptional and epigenetic mechanisms of addiction». Nature Reviews. Neuroscience 12 (11): 623–37. October 2011. doi:10.1038/nrn3111. PMID 21989194. «ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure^14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption^14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.».
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«Prevalent intravenous abuse of methylphenidate among treatment-seeking patients with substance abuse disorders: a descriptive population-based study». Journal of Addiction Medicine 9 (3): 188–94. 29 November 2016. doi:10.1097/ADM.0000000000000115. PMID 25748561.

pubmedcentral.nih.gov

«The history of attention deficit hyperactivity disorder». ADHD Attention Deficit and Hyperactivity Disorders 2 (4): 241–55. 2010. doi:10.1007/s12402-010-0045-8. PMID 21258430.
Management (1 November 2011). «ADHD: Clinical Practice Guideline for the Diagnosis, Evaluation, and Treatment of Attention-Deficit/Hyperactivity Disorder in Children and Adolescents». Pediatrics 128 (5): 1007–1022. doi:10.1542/peds.2011-2654. ISSN 0031-4005. PMID 22003063.
«Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents – assessment of adverse events in non-randomised studies». Cochrane Database Syst Rev 5: CD012069. 2018. doi:10.1002/14651858.CD012069.pub2. PMID 29744873. «Our findings suggest that methylphenidate may be associated with a number of serious adverse events as well as a large number of non-serious adverse events in children. Concerning adverse events associated with the treatment, our systematic review of randomised clinical trials (RCTs) demonstrated no increase in serious adverse events, but a high proportion of participants suffered a range of non‐serious adverse events.».
«Mitigating risks of students use of study drugs through understanding motivations for use and applying harm reduction theory: a literature review». Harm Reduction Journal 14 (1): 68. October 2017. doi:10.1186/s12954-017-0194-6. PMID 28985738.
Ruthirakuhan, Myuri T.; Herrmann, Nathan; Abraham, Eleenor H.; Chan, Sarah; Lanctôt, Krista L. (2018-05-04). «Pharmacological interventions for apathy in Alzheimer's disease». The Cochrane Database of Systematic Reviews 5: CD012197. doi:10.1002/14651858.CD012197.pub2. ISSN 1469-493X. PMID 29727467.
«The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex». Biol. Psychiatry 77 (11): 940–950. June 2015. doi:10.1016/j.biopsych.2014.09.013. PMID 25499957. «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). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attention-deficit/hyperactivity disorder and other conditions associated with PFC dysregulation.».
«Psychostimulants and cognition: a continuum of behavioral and cognitive activation». Pharmacol. Rev. 66 (1): 193–221. January 2014. doi:10.1124/pr.112.007054. PMID 24344115.
«Illicit use of specific prescription stimulants among college students: prevalence, motives, and routes of administration». Pharmacotherapy 26 (10): 1501–1510. October 2006. doi:10.1592/phco.26.10.1501. PMID 16999660. PMC 1794223. https://archive.org/details/sim_pharmacotherapy_2006-10_26_10/page/1501.
«Exposure to attention deficit hyperactivity disorder medications during pregnancy». Canadian Family Physician 53 (7): 1153–5. 2007. PMID 17872810.
«Growth on stimulant medication; clarifying the confusion: a review». Archives of Disease in Childhood 90 (8): 801–6. August 2005. doi:10.1136/adc.2004.056952. PMID 16040876. PMC 1720538. https://archive.org/details/sim_archives-of-disease-in-childhood_2005-08_90_8/page/801.
«ADHD, Multimodal Treatment, and Longitudinal Outcome: Evidence, Paradox, and Challenge». Wiley Interdisciplinary Reviews. Cognitive Science 6 (1): 39–52. January 2015. doi:10.1002/wcs.1324. PMID 25558298.
«Transdermal therapy for attention-deficit hyperactivity disorder with the methylphenidate patch (MTS)». CNS Drugs 28 (3): 217–28. March 2014. doi:10.1007/s40263-014-0141-y. PMID 24532028.
«FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in children and young adults». United States Food and Drug Administration. 20 Δεκεμβρίου 2011. Αρχειοθετήθηκε από το πρωτότυπο στις 30 Οκτωβρίου 2013. Ανακτήθηκε στις 4 Νοεμβρίου 2013.

• «ADHD drugs and serious cardiovascular events in children and young adults». N. Engl. J. Med. 365 (20): 1896–1904. November 2011. doi:10.1056/NEJMoa1110212. PMID 22043968.

• «FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in adults». United States Food and Drug Administration. 15 Δεκεμβρίου 2011. Αρχειοθετήθηκε από το πρωτότυπο στις 30 Οκτωβρίου 2013. Ανακτήθηκε στις 4 Νοεμβρίου 2013.

• «ADHD medications and risk of serious cardiovascular events in young and middle-aged adults». JAMA 306 (24): 2673–2683. December 2011. doi:10.1001/jama.2011.1830. PMID 22161946.
«Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents - assessment of adverse events in non-randomised studies». The Cochrane Database of Systematic Reviews 5: CD012069. May 2018. doi:10.1002/14651858.CD012069.pub2. PMID 29744873.
«Methylphenidate Abuse and Psychiatric Side Effects». Prim Care Companion J Clin Psychiatry 2 (5): 159–164. 2000. doi:10.4088/PCC.v02n0502. PMID 15014637.
«Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants». Prog. Neurobiol. 100: 60–80. January 2013. doi:10.1016/j.pneurobio.2012.10.001. PMID 23085425.
«Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens». Proc. Natl. Acad. Sci. U.S.A. 106 (8): 2915–20. 2009. doi:10.1073/pnas.0813179106. PMID 19202072. Bibcode: 2009PNAS..106.2915K. «Despite decades of clinical use of methylphenidate for ADHD, concerns have been raised that long-term treatment of children with this medication may result in subsequent drug abuse and addiction. However, meta analysis of available data suggests that treatment of ADHD with stimulant drugs may have a significant protective effect, reducing the risk for addictive substance use (36, 37). Studies with juvenile rats have also indicated that repeated exposure to methylphenidate does not necessarily lead to enhanced drug-seeking behavior in adulthood (38). However, the recent increase of methylphenidate use as a cognitive enhancer by the general public has again raised concerns because of its potential for abuse and addiction (3, 6–10). Thus, although oral administration of clinical doses of methylphenidate is not associated with euphoria or with abuse problems, nontherapeutic use of high doses or i.v. administration may lead to addiction (39, 40).».
«Pharmacotherapy of methamphetamine addiction: an update». Substance Abuse 29 (3): 31–49. 2008. doi:10.1080/08897070802218554. PMID 19042205.
«Cellular basis of memory for addiction». Dialogues in Clinical Neuroscience 15 (4): 431–43. December 2013. PMID 24459410. «Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.⁴¹. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.4».
«Molecular neurobiology of addiction: what's all the (Δ)FosB about?». The American Journal of Drug and Alcohol Abuse 40 (6): 428–37. November 2014. doi:10.3109/00952990.2014.933840. PMID 25083822. «
The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...
Conclusions
Πρότυπο:In5ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a molecular switch (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction.».

• «Epigenetic regulation in drug addiction». Annals of Agricultural and Environmental Medicine 19 (3): 491–6. 2012. PMID 23020045. «For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken ... In this way, the induction of CDK5 gene expression occurs together with suppression of the G9A gene coding for dimethyltransferase acting on the histone H3. A feedback mechanism can be observed in the regulation of these 2 crucial factors that determine the adaptive epigenetic response to cocaine. This depends on ΔFosB inhibiting G9a gene expression, i.e. H3K9me2 synthesis which in turn inhibits transcription factors for ΔFosB. For this reason, the observed hyper-expression of G9a, which ensures high levels of the dimethylated form of histone H3, eliminates the neuronal structural and plasticity effects caused by cocaine by means of this feedback which blocks ΔFosB transcription».

• «Transcriptional and epigenetic mechanisms of addiction». Nature Reviews. Neuroscience 12 (11): 623–37. October 2011. doi:10.1038/nrn3111. PMID 21989194. «ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure^14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption^14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.».
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«The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity». Journal of Neurochemistry 116 (2): 164–76. January 2011. doi:10.1111/j.1471-4159.2010.07109.x. PMID 21073468.
«VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse». Ann. N. Y. Acad. Sci. 1216 (1): 86–98. January 2011. doi:10.1111/j.1749-6632.2010.05906.x. PMID 21272013. Bibcode: 2011NYASA1216...86E. «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) ... 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.».
«Striatal dopamine neurotransmission: regulation of release and uptake». Basal Ganglia 6 (3): 123–148. August 2016. doi:10.1016/j.baga.2016.02.001. PMID 27141430. «Despite the challenges in determining synaptic vesicle pH, the proton gradient across the vesicle membrane is of fundamental importance for its function. Exposure of isolated catecholamine vesicles to protonophores collapses the pH gradient and rapidly redistributes transmitter from inside to outside the vesicle. ... Amphetamine and its derivatives like methamphetamine are weak base compounds that are the only widely used class of drugs known to elicit transmitter release by a non-exocytic mechanism. As substrates for both DAT and VMAT, amphetamines can be taken up to the cytosol and then sequestered in vesicles, where they act to collapse the vesicular pH gradient.».
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«Methylphenidate for children and adolescents with attention deficit hyperactivity disorder (ADHD)». Cochrane Database Syst Rev 11 (11): CD009885. November 2015. doi:10.1002/14651858.CD009885.pub2. PMID 26599576. Αρχειοθετήθηκε από το πρωτότυπο στις 2021-02-28. https://web.archive.org/web/20210228063939/https://findresearcher.sdu.dk:8443/ws/files/129083195/Methylphenidate_for_children_and_adolescents_with_attention_deficit_hyperactivity_disorder_ADHD_.pdf. Ανακτήθηκε στις 2020-10-06. «the low quality of the underpinning evidence means that we cannot be certain of the magnitude of the effects.».

semanticscholar.org

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«Prescription Stimulants' Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis». J. Cogn. Neurosci. 27 (6): 1069–1089. January 2015. doi:10.1162/jocn_a_00776. PMID 25591060. Αρχειοθετήθηκε από το πρωτότυπο στις 19 September 2018. https://web.archive.org/web/20180919111616/https://repository.upenn.edu/neuroethics_pubs/130/. Ανακτήθηκε στις 14 November 2018. «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.».

web.archive.org

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