قالب:مسرد الإدمان
(تم التحويل من قالب:Addiction glossary)
هذه الصفحة may be too technical for most readers to understand. Please improve هذه الصفحة to make it understandable to non-experts, without removing the technical details. (February 2017) |
مسرد الإدمان والإعتياد [1][2][3][4] | |
---|---|
| |
Template documentation
This template uses the definitions for these terms from the following references (note: these have been slightly modified for brevity):
Template reflist; to expand, click the show button to the right →
|
---|
الاستخدام
- Basic usage
To transclude this glossary to another page as it appears above, simply add the following to the target page's source code:
{{مسرد الإدمان}}
Optional parameters
- Template with all optional parameters
{{مسرد الإدمان | width= | align= | collapse= | reverse citation order= }}
- Optional parameter definitions
|width=
– specify the width of the table (e.g., in pixels, 400px).|collapse=
– specify if the table is collapsed (e.g.,yes
)|align=
– specify the alignment of the table on the target page. The default alignment is|align=right
; the only alternative alignment option is|align=left
.|reverse citation order=
– reverses the order of the first 2 citations in this template if|reverse citation order=yes
. This parameter is only useful on certain pages that cite these 2 references in the opposite order as was defined in this template.
Editors can experiment in this template's sandbox (create | mirror) and testcases (create) pages. Subpages of this template. |
- ^
{{cite book}}
: Empty citation (help) - ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410.
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.
- ^ "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. Retrieved 9 February 2015.
- ^ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMID 26816013.
Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.