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مراجع

↑  . DOI:10.1176/appi.ajp.2013.12060782. {{استشهاد ويب}}: الوسيط |title= غير موجود أو فارغ (من ويكي بيانات) (مساعدة) والوسيط |مسار= غير موجود أو فارع (مساعدة)
↑  Laviolette، Steven R.؛ Van Der Kooy، Derek (2001). "GABAA receptors in the ventral tegmental area control bidirectional reward signalling between dopaminergic and non-dopaminergic neural motivational systems". European Journal of Neuroscience. ج. 13 ع. 5: 1009–15. DOI:10.1046/j.1460-9568.2001.01458.x. PMID:11264674.
↑   نسخة محفوظة 05 ديسمبر 2013 على موقع واي باك مشين.
↑  Steiner H، Van Waes V (يناير 2013). "Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants". Prog. Neurobiol. ج. 100: 60–80. DOI:10.1016/j.pneurobio.2012.10.001. PMC:3525776. PMID:23085425.
↑  Malenka RC، Nestler EJ، Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ط. 2nd). New York: McGraw-Hill Medical. ص. 364–375. ISBN:9780071481274.
↑  Nestler EJ (ديسمبر 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. ج. 15 ع. 4: 431–443. PMC:3898681. PMID:24459410. Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
↑  "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. اطلع عليه بتاريخ 2015-02-09.
↑  Volkow ND، Koob GF، McLellan AT (يناير 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. ج. 374 ع. 4: 363–371. DOI:10.1056/NEJMra1511480. PMID:26816013. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
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التصنيفات الطبية:  رموز المراجعة التاسعة للتصنيف الدولي للأمراض (ICD-9): 305  رموز المراجعة العاشرة للتصنيف الدولي للأمراض (ICD-10): F19  
المعرفات الخارجية:  مكنز المعهد القومي للسرطان (NCI): C92203  أنطولوجيا الأمراض: DOID:303  PatientLikeMe condition ID: addiction-drugs  نظام اللغة الطبية الموحدة (UMLS CUI): C0236969  موقع مدلاين (MedlinePlus): 001522  
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