View source for Template:Addiction glossary

<noinclude>
{{technical|date=February 2017|set of definitions}}
</noinclude>{{Glossary infobox
| template name = Addiction glossary
| align         = {{{align|right}}}
| width         = {{{width|402px}}}
| collapse      = {{{collapse|}}}
| header        = Addiction and dependence glossary{{ifeq|{{{reverse citation order}}}|yes|<ref name="Cellular basis">{{cite journal | author = Nestler EJ | title = Cellular basis of memory for addiction | journal =  Dialogues in Clinical Neuroscience| volume = 15 | issue = 4 | pages = 431–443 |date=December 2013  | pmid = 24459410 | pmc = 3898681 | doi = | quote = 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.&nbsp;... 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&nbsp;... 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.<sup>41</sup>&nbsp;... 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.}}</ref><ref name="Addiction glossary">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 364–375| edition = 2nd | chapter = Chapter 15: Reinforcement and Addictive Disorders}}</ref><!-- Reverse citation order
-->|<!--
--><ref name="Addiction glossary">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 9780071481274 | pages = 364–375| edition = 2nd | chapter = Chapter 15: Reinforcement and Addictive Disorders}}</ref><ref name="Cellular basis">{{cite journal | author = Nestler EJ | title = Cellular basis of memory for addiction | journal =  Dialogues in Clinical Neuroscience| volume = 15 | issue = 4 | pages = 431–443 |date=December 2013  | pmid = 24459410 | pmc = 3898681 | doi = | quote = 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.&nbsp;... 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&nbsp;... 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.<sup>41</sup>.&nbsp;... 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.}}</ref>}}<ref name="Nestler Labs Glossary">{{cite web|title=Glossary of Terms|url=http://neuroscience.mssm.edu/nestler/glossary.html|website=Mount Sinai School of Medicine|publisher=Department of Neuroscience|accessdate=9 February 2015}}</ref><ref name="Brain disease">{{cite journal | vauthors = Volkow ND, Koob GF, McLellan AT | title = Neurobiologic Advances from the Brain Disease Model of Addiction | journal =  New England Journal of Medicine| volume = 374 | issue = 4 | pages = 363–371 | date = January 2016 | pmid = 26816013 | pmc = 6135257 | doi = 10.1056/NEJMra1511480 | quote = 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.<br />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.}}</ref>
| data1         =
* '''[[Medicine:Addiction|addiction]]''' – a [[brain disorder]] characterized by [[wikt:compulsive|compulsive]] engagement in rewarding [[Philosophy:Stimulus (psychology)|stimuli d]]espite adverse consequences
* '''[[addictive behavior]]''' – a behavior that is both rewarding and reinforcing
* '''[[Medicine:Addiction|addictive drug]]''' – a drug that is both rewarding and reinforcing
* '''[[Medicine:Substance dependence|dependence]]''' – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake)
* '''[[reverse tolerance|drug sensitization]]''' or '''reverse tolerance''' – the escalating effect of a drug resulting from repeated administration at a given dose
* '''[[Medicine:Drug withdrawal|drug withdrawal]]''' – symptoms that occur upon cessation of repeated drug use
* '''[[Medicine:Physical dependence|physical dependence]]''' – dependence that involves persistent physical–[[wikt:somatic|somatic]] withdrawal symptoms (e.g., fatigue and [[Medicine:Delirium tremens|delirium tremens]])
* '''[[Medicine:Psychological dependence|psychological dependence]]''' – dependence that involves emotional–motivational withdrawal symptoms (e.g., [[Medicine:Dysphoria|dysphoria]] and [[Medicine:Anhedonia|anhedonia]])
* '''[[Philosophy:Reinforcement|reinforcing]] stimuli''' – stimuli that increase the probability of repeating behaviors paired with them
* '''[[Philosophy:Reward system|rewarding]] stimuli''' – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
* '''[[Philosophy:Sensitization|sensitization]]''' – an amplified response to a stimulus resulting from repeated exposure to it
* '''[[Medicine:Substance use disorder|substance use disorder]]''' – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
* '''[[Chemistry:Drug tolerance|tolerance]]''' – the diminishing effect of a drug resulting from repeated administration at a given dose
}}<noinclude>
{{documentation|content=
This template uses the definitions for these terms from the following references (note: these have been slightly modified for brevity):
{{cot|Template reflist;&nbsp;to expand, click the show button to the right&nbsp;→|bg=white}}
{{reflist talk}}
{{cob}}

==Usage==
;Basic usage
To transclude this glossary to another page <u>as it appears above</u>, simply add the following to the target page's source code:
: {{tlx|{{BASEPAGENAME}}}}

===Optional parameters===
;Template with all optional parameters
: {{tlx|{{BASEPAGENAME}}&nbsp;|&nbsp;width{{=}}&nbsp;|&nbsp;align{{=}}&nbsp;|&nbsp;collapse{{=}}&nbsp;|&nbsp;reverse citation order{{=}}&nbsp;}}

;Optional parameter definitions
* {{para|width}} – specify the width of the table (e.g., in pixels, 400px).
* {{para|collapse}} – specify if the table is collapsed (e.g., <code>yes</code>)
* {{para|align}} – specify the alignment of the table on the target page. The default alignment is {{para|align|right}}; the only alternative alignment option is {{para|align|left}}.
* {{para|reverse citation order}} – reverses the order of the first 2 citations in this template if {{para|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.

}}
[[Category:Addiction|τ]]
[[Category:Behavioral addiction|τ]]
[[Category:Glossaries of medicine|τ]]
[[Category:Psychology templates]]
</noinclude>