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This template was considered for deletion on 2015 January 15. The result of the discussion was "keep".

This should be at the bottom as a navbox. Doc James (talk · contribs · email) 02:27, 27 November 2014 (UTC)Reply[reply]

@Doc James: I wanted this to be a pseudo-infobox/table to allow for more flexibility in its placement in different articles. This is fine as an infobox in articles specifically on addiction - the disease infobox in those articles is hardly serving any useful purpose given how minimal the content is in most of them (i.e., if applicable, a DSM link and an ICD link that should just be refs in the section on diagnostics). This really should be in the lead of addiction articles. In drug articles where the addiction section is long enough (e.g., Adderall#Addiction), this would also be a suitable/useful template to include.

Frankly, I think this template needs more visibility due to the incredible lack of consistent terminology used to describe addictions over the last few decades; I wasn't entirely clear on what exactly constituted an addiction or the characteristics/properties of addictive drugs until I looked up the definitions of these things in neuropsychology texts (excluding the diagnostic classification systems, these terms are thankfully consistently defined at the moment). The outdated/abandoned view that a dependence-withdrawal syndrome is necessary/sufficient for an addiction contributed to this problem in the past. The current problem is the retarded nomenclature/terminology (re: the preceding sentence) still used by a particular disease classification system simply because they want to avoid using the word "addiction", a decision which is both arbitrary and frequently criticized in the aforementioned neuropsychology texts. In any event, that's my reasoning for designing the template like this (this happens to be a copy of Boghog's Template:Transcription factor glossary). Seppi333 (Insert 2¢ | Maintained) 15:18, 2 December 2014 (UTC)Reply[reply]

I think this is a fair compromise Opioid_dependence#Symptoms_of_withdrawal. I am okay with it in the lead of the addiction article but not all the rest.

This is why we often have a first section called classification or terminology. If it becomes long it should be a subpage. There is confusing terminology in many many areas. Doc James (talk · contribs · email) 17:33, 2 December 2014 (UTC)Reply[reply]

• http://neuroscience.mssm.edu/nestler/glossary.html

Seppi333 (Insert 2¢ | Maintained) 06:24, 3 February 2015 (UTC)Reply[reply]

The orange background of the header has insufficient contrast with the foreground text, per WP:COLOUR. I removed it (citing WP:COLOUR in my edit summary), but have been reverted on the spurious grounds that other templates also exhibit this problem. Making our content accessible to people with disabilities is not an option; it is required by WMF policy. Andy Mabbett (Pigsonthewing); Talk to Andy; Andy's edits 22:31, 20 August 2015 (UTC)Reply[reply]

So your issue is with colorblind viewing - which form of color blindness has an issue viewing juxtaposed orange and blue objects? I'm ok with removing it if there is one. Seppi333 (Insert 2¢) 22:50, 20 August 2015 (UTC)Reply[reply]

I disagree. "Abuse" and "misuse" are highly subjective terms, but don't confuse "abuse" with "abuse liability" which is a largely reducible quality of psychoactive drugs. Abuse liability/potential is precisely a psychpharmacological quality, an evaluation of which is currently required in new drug applications to the FDA and used by the DEA to apply scheduling. The term(s) occur in current drug monographs. "Abuse liability" could be changed to "addiction liability" and would apply to the same definition. So how about this change?

Since the term "drug sensitization" is listed, there is no need for "sensitization" itself. It is not specific to drug addiction but is simply a term from behaviorism. Further, the term "stimuli" should be softened (replaced) to deal with drugs and not behaviorism. The term addictive behavior needs to be tweaked as well. (It opens the door to "addictive personality" which has the same problems as "abuse".) How could the terms noted above be tweaked?

I generally agree with your intentions but I perceive them as a tad rigid. Biologic mechanisms are essential but there is a dimension to human addiction (e.g., set) that doesn't exist in pigeons or rats. Behaviorism can't explain and generally takes no interest in the hard problem. IMO if the intention of this glossary is based in behaviorism then "behaviorism" should be included in the displayed title and the opportunity for a general glossary be created. — Box73 (talk) 21:06, 11 December 2015 (UTC)Reply[reply]

This glossary is used on pages related to behavioral addiction (e.g. gambling addiction, sex addiction) in addition to substance addiction. Hence the presence of non-drug addiction terms and general language. Sizeofint (talk) 21:19, 11 December 2015 (UTC)Reply[reply]

Sorry, didn't read the last sentence. So you want to have separate entries for substance and behavioral topics (e.g. separate entries for behavioral addiction and substance addication)? Sizeofint (talk) 21:39, 11 December 2015 (UTC)Reply[reply]

I didn't know this was dealing with non-drug addictions. If it was just drug related the definitions could be tuned to drugs and perhaps softened a bit. Others might make the same assumption I did. Yet a separate glossary would make the articles too busy, invites controversy and is probably better left in another article. Given the span, these definitions are appropriate. I misunderstood and apologize to Seppi. Box73 (talk) 11:58, 14 December 2015 (UTC)Reply[reply]

The primary reason that this template was created was to improve accessibility by juxtaposing it with sections on content which covers the biomolecular mechanisms of addiction because those sections are extremely technical by nature (e.g., ΔFosB). A secondary intended use for this template is for clarifying the distinction between "addiction" and "dependence" in the few articles (e.g., the subtopic articles listed in this template) that are directly related to those 2 concepts. The template is not intended to provide a complete glossary of any/all terms related to disorders involving drug use. The terms in that template are used in dozens of papers and several textbooks that I've read on addiction (assuming mechanisms are covered in the publication). I intentionally avoided the use of diagnostic terms because the most obvious issue with adding them is that the DSM defines dependence differently than the way it is defined in the template. There's also multiple terms from diagnostic models which are used to mean "addiction" but which use another term with the same definition as addiction instead (for god knows what reason). If you want to create a glossary that covers diagnostic terms, you'll need to confine the scope of the glossary to that terminology to avoid issues.

Thanks for explaining that. I also appreciate the distinction between addiction and dependence. It is true that cancer patients treated with opioids will typically become physically dependent but this is not addiction. The aversion to "addiction" I think is the morality issue, addiction requires an "addict". Even Wikipedia prefers "recreational use". Box73 (talk) 13:10, 14 December 2015 (UTC)Reply[reply]

Addictive behavior is correctly defined: this is most commonly used term for a non-drug stimulus which can induce an addiction. "Addictive personality" is an entirely unrelated concept. Sensitization is indeed necessary because both drugs and behaviors can induce sensitization of neural processes, like reward sensitization. Drugs and behaviors can also cross-sensitize (e.g., reward from amphetamine and sexual activity), which is outside the scope of drug (cross-)sensitization.

I better understand now. Without any criticism, I am anxious about addiction being applied so generally. Everything bad habit, lifestyle or assumed prerequisites to an illness. Everything learned is potentially an addiction. Folks taking antipsychotics frequently become compulsive smokers, probably an attempt to compensate for dopamine antagonism. Is this a dependence or addiction? Do other animals develop a liking for psilocybin? Some soldiers in Vietnam developed addictions to heroin that ended with their tour of duty; why are changes in environment not successful here? When I was an infant, my dad smoked, my mom got on him and he just stopped; is addiction a lack of will? You needn't answer; these are rhetorical thoughts of mine. Box73 (talk) 13:10, 14 December 2015 (UTC)Reply[reply]

Lastly, while it may appear that this glossary is simply a list of terms from behaviorism models (this template only includes operant conditioning; addiction is mediated through both operant and classical conditioning) that are applicable to addiction, the research involving these concepts spans molecular biology, neurology, pharmacology, and genetic engineering. This is in addition to psychology, as these conditioning models are simply used for the quantification of various addiction-related processes/behaviors; the vast majority of addiction research using these models has little to do with psychology-based research, which for example would be something like personality theories of addiction. Virtually all of the current research using these 2 conditioning models examines a biological basis, not a psychological basis, for addiction in humans. Seppi333 (Insert 2¢) 22:05, 11 December 2015 (UTC)Reply[reply]

It wasn't so much about behaviorism vs. personality as it was the abstract terms and definitions. This makes sense as they are applied across behavioral addictions. Box73 (talk) 13:10, 14 December 2015 (UTC)Reply[reply]

The addiction liability term isn't particularly relevant to any of the sections where this template is transcluded, except possibly the lead/body transclusions of the addiction article. For now, I'm removing it and noting it in the missing concepts section for the addiction article at Talk:Addiction#Missing concepts. Frankly, I would have added the conditioning terminology listed in that section to this glossary if it didn't take up so much space in articles. There have been discussions at WT:MED and my talk page involving the length of this template, which is why additional concepts need to either be defined in the main addiction article or introduced in an article-based glossary of addiction-related terms. Seppi333 (Insert 2¢) 12:55, 12 December 2015 (UTC)Reply[reply]

No problem. I was thinking about it relating to the drug boxes but it isn't necessary and I understand the issues of length as well. Thank you for taking the time to explain this. Box73 (talk) 13:10, 14 December 2015 (UTC)Reply[reply]

Dear @Seppi333:

This glossary is used in articles read by laypeople, such as Food addiction.

You dealt with the ((jargon-inline)) tags which I added to the glossary a couple of weeks ago. In your edit summary, you wrote that almost every piece of jargon which I tagged is a nontechnical word which would be defined in any half-decent dictionary. I partially agree. I do agree that "characterized", "engagement", "adaptive", and "cessation" are found in every dictionary. But I still think they're not easy words for laypeople to understand.

George Orwell has written:

• "Never use a long word where a short one will do."

• "Never use a foreign phrase, a scientific word, or a jargon word if you can think of an everyday English equivalent."

Dear all: Are there more-common words, simpler than "characterized", "engagement", "adaptive", "cessation", "stimuli", and "somatic", which we could use instead?

Kind regards, TealHill (talk) 16:47, 19 February 2017 (UTC)Reply[reply]

Resolved

@Frietjes: I'm not sure what's causing this issue. Previously, this the collapsed header for this template aligned perfectly with the width of the image beneath it in Amphetamine#Addiction. Now, the entire glossary table is shifted to the right by a few pixels and it looks awkward. The same issue is occurring in the 3 articles that transclude that section of amphetamine (Adderall#Addiction, Lisdexamfetamine#Addiction, and Dextroamphetamine#Addiction) as well as Methamphetamine#Addiction and ΔFosB.
NB: you didn't change the class parameter in ΔFosB. It displayed with broken formatting until the quotation marks were removed; please be more careful next time.

Interestingly, the alignment of this glossary with the table above it in the Reward system article isn't broken/skewed, so this appears to only be an issue with adjacent images.

The only way I can think of fixing this at the moment is reverting some of your changes to this template, which would also necessitate reverting the changes to all of the articles that transclude this template. However, I figured I'd ping you to see if we can come up with a fix to the current formatting in order to address this problem. Seppi333 (Insert 2¢) 02:41, 20 January 2018 (UTC)Reply[reply]

Expand the tab below for further details on the problem I'm referring to.

How the glossary and image appear on the above pages

Addiction and dependence glossary[1][2][3] addiction – a biopsychosocial disorder characterized by persistent use of drugs (including alcohol) despite substantial harm and adverse consequences addictive drug – psychoactive substances that with repeated use are associated with significantly higher rates of substance use disorders, due in large part to the drug's effect on brain reward systems dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated exposure to a stimulus (e.g., drug intake) drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose drug withdrawal – symptoms that occur upon cessation of repeated drug use physical dependence – dependence that involves persistent physical–somatic withdrawal symptoms (e.g., fatigue and delirium tremens) psychological dependence – dependence socially seen as being extremely mild compared to physical dependence (e.g., with enough willpower it could be overcome) reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them rewarding stimuli – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach sensitization – an amplified response to a stimulus resulting from repeated exposure to it substance use disorder – a condition in which the use of substances leads to clinically and functionally significant impairment or distress tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose v t e Signaling cascade in the nucleus accumbens that results in amphetamine addiction v t e Note: colored text contains article links. Nuclear pore Nuclear membrane Plasma membrane Cav1.2 NMDAR AMPAR DRD1 DRD5 DRD2 DRD3 DRD4 Gs Gi/o AC cAMP cAMP PKA CaM CaMKII DARPP-32 PP1 PP2B CREB ΔFosB JunD c-Fos SIRT1 HDAC1 [Color legend 1] This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methamphetamine, and phenethylamine. Following presynaptic dopamine and glutamate co-release by such psychostimulants,[4][5] postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP-dependent pathway and a calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[4][6][7] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-Fos gene with the help of corepressors;[4][8][9] c-Fos repression acts as a molecular switch that enables the accumulation of ΔFosB in the neuron.[10] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for 1–2 months, slowly accumulates following repeated high-dose exposure to stimulants through this process.[8][9] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[8][9] Notice how the right margin for the glossary is slightly further to the right than the image below it. It appears to be skewed rightward by somewhere between 2px to 5px. Consequently, the left margin of the glossary isn't aligning with the image due to the skewed right margin. Previously, the glossary and image left+right margins aligned perfectly. Reflist References ^ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY (eds.). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–375. ISBN 9780071481274. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience. 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. ^ Volkow ND, Koob GF, McLellan AT (January 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". New England Journal of Medicine. 374 (4): 363–371. doi:10.1056/NEJMra1511480. PMC 6135257. 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. ^ a b c Renthal W, Nestler EJ (September 2009). "Chromatin regulation in drug addiction and depression". Dialogues in Clinical Neuroscience. 11 (3): 257–268. doi:10.31887/DCNS.2009.11.3/wrenthal. PMC 2834246. PMID 19877494. [Psychostimulants] increase cAMP levels in striatum, which activates protein kinase A (PKA) and leads to phosphorylation of its targets. This includes the cAMP response element binding protein (CREB), the phosphorylation of which induces its association with the histone acetyltransferase, CREB binding protein (CBP) to acetylate histones and facilitate gene activation. This is known to occur on many genes including fosB and c-fos in response to psychostimulant exposure. ΔFosB is also upregulated by chronic psychostimulant treatments, and is known to activate certain genes (eg, cdk5) and repress others (eg, c-fos) where it recruits HDAC1 as a corepressor. ... Chronic exposure to psychostimulants increases glutamatergic [signaling] from the prefrontal cortex to the NAc. Glutamatergic signaling elevates Ca2+ levels in NAc postsynaptic elements where it activates CaMK (calcium/calmodulin protein kinases) signaling, which, in addition to phosphorylating CREB, also phosphorylates HDAC5. Figure 2: Psychostimulant-induced signaling events ^ Broussard JI (January 2012). "Co-transmission of dopamine and glutamate". The Journal of General Physiology. 139 (1): 93–96. doi:10.1085/jgp.201110659. PMC 3250102. PMID 22200950. Coincident and convergent input often induces plasticity on a postsynaptic neuron. The NAc integrates processed information about the environment from basolateral amygdala, hippocampus, and prefrontal cortex (PFC), as well as projections from midbrain dopamine neurons. Previous studies have demonstrated how dopamine modulates this integrative process. For example, high frequency stimulation potentiates hippocampal inputs to the NAc while simultaneously depressing PFC synapses (Goto and Grace, 2005). The converse was also shown to be true; stimulation at PFC potentiates PFC–NAc synapses but depresses hippocampal–NAc synapses. In light of the new functional evidence of midbrain dopamine/glutamate co-transmission (references above), new experiments of NAc function will have to test whether midbrain glutamatergic inputs bias or filter either limbic or cortical inputs to guide goal-directed behavior. ^ Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014. Most addictive drugs increase extracellular concentrations of dopamine (DA) in nucleus accumbens (NAc) and medial prefrontal cortex (mPFC), projection areas of mesocorticolimbic DA neurons and key components of the "brain reward circuit". Amphetamine achieves this elevation in extracellular levels of DA by promoting efflux from synaptic terminals. ... Chronic exposure to amphetamine induces a unique transcription factor delta FosB, which plays an essential role in long-term adaptive changes in the brain. ^ Cadet JL, Brannock C, Jayanthi S, Krasnova IN (2015). "Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat". Molecular Neurobiology. 51 (2): 696–717 (Figure 1). doi:10.1007/s12035-014-8776-8. PMC 4359351. PMID 24939695. ^ a b c Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nature Reviews Neuroscience. 12 (11): 623–637. doi:10.1038/nrn3111. PMC 3272277. PMID 21989194. ΔFosB serves as one of the master control proteins governing this structural plasticity. ... ΔFosB also represses G9a expression, leading to reduced repressive histone methylation at the cdk5 gene. The net result is gene activation and increased CDK5 expression. ... In contrast, ΔFosB binds to the c-fos gene and recruits several co-repressors, including HDAC1 (histone deacetylase 1) and SIRT 1 (sirtuin 1). ... The net result is c-fos gene repression. Figure 4: Epigenetic basis of drug regulation of gene expression ^ a b c Nestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clinical Psychopharmacology and Neuroscience. 10 (3): 136–143. doi:10.9758/cpn.2012.10.3.136. PMC 3569166. PMID 23430970. The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives. ... As a result of its stability, the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure. ... ΔFosB overexpression in nucleus accumbens induces NFκB ... In contrast, the ability of ΔFosB to repress the c-Fos gene occurs in concert with the recruitment of a histone deacetylase and presumably several other repressive proteins such as a repressive histone methyltransferase ^ Nestler EJ (October 2008). "Transcriptional mechanisms of addiction: Role of ΔFosB". Philosophical Transactions of the Royal Society B: Biological Sciences. 363 (1507): 3245–3255. doi:10.1098/rstb.2008.0067. PMC 2607320. PMID 18640924. Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch—from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure References ^   Ion channel   G proteins & linked receptors   (Text color) Transcription factors

Seppi333 (Insert 2¢) 02:59, 20 January 2018 (UTC)Reply[reply]

@Frietjes: Actually, nevermind. After tinkering around with the HTML settings for one of the pages in my browser, I found that setting the right margin to 2.5px fixes the problem. Setting the right margin to 2.5px in this template for right alignment when class="toccolours mw-collapsible mw-collapsed" should equalize the table/glossary margins on all of these pages. Seppi333 (Insert 2¢) 03:15, 20 January 2018 (UTC)Reply[reply]

Seppi333, it looks like when this template is placed below another box, that other box is generated by either (a) ((Infobox medical condition)) or (b) ((Annotated image 4)). do you think it would be a good idea to use the same margins for both the collapsed and uncollapsed cases? also, wouldn't it be more obvious syntax to just have |collapsed=y instead of having to say |class=toccolours mw-collapsible mw-collapsed. and, finally, how about using infobox as the basic class and actual list markup? to show what I am talking about, see Template:Addiction glossary/sandbox. Frietjes (talk) 13:40, 20 January 2018 (UTC)Reply[reply]

Seppi333, unfortunately, it looks like the sandbox version does not have the same right margin as ((Annotated image 4)). so, now I am wondering if ((Annotated image 4)) has the same right margin as a standard right-floating image. if not, then the better fix would be to change ((Annotated image 4)) to match standard thumb images and infobox. Frietjes (talk) 13:43, 20 January 2018 (UTC)Reply[reply]

You're right, it looks like this pseudo-margin was introduced by ((AI4)) when the table nesting was introduced to that template. I've explained the purpose of that markup and illustrated the issue it resolved on that template's talk page (Template talk:Annotated image 4). I'm not sure how else to resolve that issue besides nesting the entire template in a borderless wikitable though. Seppi333 (Insert 2¢) 05:16, 21 January 2018 (UTC)Reply[reply]

now that AI4 has been fixed, I have updated this template to use list markup, standard infobox classes, etc. hopefully everything looks okay. Frietjes (talk) 18:42, 23 January 2018 (UTC)Reply[reply]

@Frietjes: You might want to reformat Template:Transcription factor glossary for consistency; this template was designed to mirror the format/layout of that one. Perhaps a better idea would be to create a glossary skeleton template for glossaries that are intended to appear in articles as a list in a table. That way, the glossary entries in the table could be defined in a template like this one, but the formatting could be standardized and uniformly modified in a single glossary skeleton template. Seppi333 (Insert 2¢) 06:55, 24 January 2018 (UTC)Reply[reply]

Based upon Category:Definition list templates and Category:Glossary templates, there are currently no templates which serve that purpose. Seppi333 (Insert 2¢) 07:00, 24 January 2018 (UTC)Reply[reply]

okay, I will take a look. from a preliminary search, I only found this one and the other one that matched the pattern 'class\|tocolours' when I did an insource search. but, there are probably others (just using different internal syntax). Frietjes (talk) 15:59, 24 January 2018 (UTC)Reply[reply]

@Frietjes: Do you have any objections to me creating Template:Glossary infobox^† as a glossary skeleton template which uses the infobox layout for this template? If I created that template, I would update ((Addiction glossary)) and ((Transcription factor glossary)) so that they both use/transclude that template for setting their layout (note: see the two collapse tabs below for further details). I'm sure other editors will create similar table-based glossaries for articles at some point in the future, so I think that creating a template for standardizing the layout of those glossaries now is a good idea.

^†The reason I'm proposing the title "Template:Glossary infobox" for the template instead of "Template:Infobox glossary" is that I think it's much more likely that people will search for "Template:Glossary ..." in the search box when looking for glossary templates; if the template was located at Template:Infobox glossary, it wouldn't appear in the results from the search box when searching for "Template:Glossary ..."; however, "Template:Infobox glossary" probably would appear in the extended search results from Special:Search/Template:Glossary though. Seppi333 (Insert 2¢) 11:15, 14 February 2018 (UTC)Reply[reply]

((infobox
| bodyclass = ((#if:((yesno|(({collapse|))))}|mw-collapsible mw-collapsed))
| bodystyle = width:(({width|400px))}; ((#switch:(({align|right))}
 | left = float:left; clear:left; margin-left:0; margin-right:1em;
 )); border-collapse:collapse;
| datastyle = text-align:left; padding-left:0;
| abovestyle = font-size:100%; background:#FFCC66; ((box-shadow border|a|#fafafa|3px)); padding:5px;
| above = (({above|(({header|))))))
| data1 = (({data1|(({definitions|))))))
| belowstyle = text-align:right; padding-top:0; padding-right:5px;
| below = ((#if:((yesno|(({1|(({template name|))))))))|((navbar|(({1|(({template name|))))))|mini=y))|))
))

((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 Clin. Neurosci. | 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. ... 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.<sup>41</sup>. ... 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 Clin. Neurosci. | 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. ... 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.<sup>41</sup>. ... 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 = N. Engl. J. Med. | volume = 374 | issue = 4 | pages = 363–371 | date = January 2016 | pmid = 26816013 | 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         =
* '''[[addiction]]''' – a [[brain disorder]] characterized by [[wikt:compulsive|compulsive]] engagement in rewarding [[Stimulus (psychology)|stimuli]] despite adverse consequences
* '''[[addictive behavior]]''' – a behavior that is both rewarding and reinforcing
* '''[[addiction|addictive drug]]''' – a drug that is both rewarding and reinforcing
* '''[[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
* '''[[drug withdrawal]]''' – symptoms that occur upon cessation of repeated drug use
* '''[[physical dependence]]''' – dependence that involves persistent physical–[[wikt:somatic|somatic]] withdrawal symptoms (e.g., fatigue and [[delirium tremens]])
* '''[[psychological dependence]]''' – dependence that involves emotional–motivational withdrawal symptoms (e.g., [[dysphoria]] and [[anhedonia]])
* '''[[reinforcement|reinforcing]] stimuli''' – stimuli that increase the probability of repeating behaviors paired with them
* '''[[reward system|rewarding]] stimuli''' – stimuli that the brain interprets as intrinsically positive and desirable or as something to approach
* '''[[sensitization]]''' – an amplified response to a stimulus resulting from repeated exposure to it
* '''[[substance use disorder]]''' – a condition in which the use of substances leads to clinically and functionally significant impairment or distress
* '''[[drug tolerance|tolerance]]''' – the diminishing effect of a drug resulting from repeated administration at a given dose
))

FWIW, I've already tested my proposed code for ((Glossary infobox)) and the proposed changes to ((Addiction glossary)) in two of my sandboxes, so I know my proposed template code works as expected. Seppi333 (Insert 2¢) 11:16, 14 February 2018 (UTC)Reply[reply]

User:Seppi333, I don't see any problem with creating a backend template for these infoboxes. if there is a common pattern, it makes sense to template it. Frietjes (talk) 14:57, 14 February 2018 (UTC)Reply[reply]

 Done – I also created redirects for Template:Infobox glossary & Template talk:Infobox glossary. Seppi333 (Insert 2¢) 03:39, 16 February 2018 (UTC)Reply[reply]