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This article was the subject of a Wiki Education Foundation-supported course assignment, between 3 September 2021 and 16 December 2021. Further details are available on the course page. Student editor(s): Paytonreiner.
Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT ( talk) 19:44, 16 January 2022 (UTC)
Sounds ok.
Daevatgl 20:35, Jun 16, 2004 (UTC)
May 6 2005 edits The Biochemical Basis of Neuropharmacolgy Oxford Press 1996 Chapter 9 Dopamine-- McDogm 17:21, 6 May 2005 (UTC)
Should add Adderall in here -- I would but couldnt figure out the proper medical name for it or where it fits in terms of dopamine release.
Isn't it the case that most phenethylamine DARIs inhibit by attaching as if they were the regular transporters, and others like the cocaine tropane-types attach or bind as a ligand to the transporter in an entirely different way? It is odd that such a tropane type ligand, if I'm not mistaken, attaches with a higher affinity? 71.34.103.210 ( talk) 00:45, 19 April 2009 (UTC)
I've corrected the following two errors:
I tagged the link to physical dependence as dubious. To my knowledge, straight DRIs such as methylphenidate don't cause a lot of "physical dependence". This is partly a language issue: These drugs do cause homeostatic changes in the brain, but philosophy of the mind notwithstanding, I think that that's not usually what is meant by "physical dependence". In my book, "physical dependence" means that there are serious peripheral symptoms upon discontinuation. Suboptimal Username ( talk) 17:15, 10 June 2010 (UTC)
There are withdrawal symptoms upon discontinuation, look at cocaine - huge withdrawal symptoms. Even methylphenidate when used at a high enough dose will give withdrawal symptoms -- Axxaer ( talk) 04:17, 27 September 2010 (UTC)
Cocaine is totally different though, according to the wiki page it is a Serotonin, Norepinephrine and Dopamine reuptake inhibitor. Methylphenidate as well is not selectively a dopamine reuptake inhibitor. I don't really get why you make the link between those two and DRIs Robinsona ( talk) 20:47, 11 December 2010 (UTC)
e.g. dextro- & levo- methamphetamine. Could there be a drug similar to cocaine for instance, that only preforms the function of the former mentioned dextro- (alone) or levo- (alone) by only inhibiting reuptake on those sort of transporters potentially at all? Nagelfar ( talk) 05:47, 8 July 2010 (UTC)
List of DRI’s and Intro: will simply be edited according to our research findings, and addition DRI’s not listed will be added, and the current list verified.
Process
This section will contain information about the biological processes induced by dopamine reuptake inhibitors. The process within the synapses will be covered, alone with any side effects, either long term or short term, as well as any effects caused by dopamine increase.
History
This section will cover the history of the discovery and use of dopamine reuptake inhibitors. The development over the last half century of the targeting of transporters as a means of concentrating levels of neurotransmitters within the synapse will be discussed, as well as a general history of the drugs and their discoverers.
Possible affects on cognition
This section will focus on the affects that DRI can have on emotion, as well as the possible side affects of DRI's. Another subject that this section will talk about is the controversy behind DRI's in drugs. This will touch on usage and abuse of DRI's. This section will also touch on the short term affects and the long term affects of DRI's.
Dopamine Reuptake Inhibitors and Depression — Preceding unsigned comment added by Nszynal-ru ( talk • contribs) 17:50, 12 November 2012 (UTC)
— Preceding daniadams9121 comment added by Narmstrong484 ( talk • contribs) 18:49, 9 October 2012 (UTC)
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Neuropsychprof ( talk) 22:00, 10 October 2012 (UTC)
Well I see that we all know that you need more sources I think its a good start though just a little more information in certain sections and more sources and I think this will be a good article, Good luck — Preceding unsigned comment added by Schandler91 ( talk • contribs) 17:47, 30 October 2012 (UTC)
This is a good start...but needs a lot of expansion/sourcing. Smallman12q ( talk) 22:38, 27 October 2012 (UTC)
It looks like there needs to be more sources that are actually contained within the article rather than just floating at the top. More sections should also be added to go into details about subjects raised in the introduction. I would agree with smallman12 that the article needs to be expanded and more effort needs to be put into finding sources.
Pmisner2009 ( talk) 16:39, 28 October 2012 (UTC)
I agree that maybe more sources would help generate a better informative article. I think what you have so far is good but maybe you could expand upon certain parts as in the dopaminergic pathway and get into more detail. R.EEGbrittry ( talk) 19:51, 29 October 2012 (UTC)
-- Rorystewart ( talk) 18:32, 30 October 2012 (UTC)
Hi everybody! I just got a message from Prof. Lu asking if I could take a look at everybody's work, and I've got a few suggestions to help make your article even better. I'm going to organize them in a bullet pointed list just for your ease of use; if you have any questions or need some help, you can either ask here (I've watchlisted this talk page) or on my talk page. I'm happy to help with anything! =]
All the best, Keilana| Parlez ici 06:09, 31 October 2012 (UTC)
Group, you have added some good info on a tough topic. I'm going to email this group some readings that may help. Remember to refer to the selective serotonine reuptake inhibitor page for the type of info to add to your article. Note this article is dopamine reuptake inhibitor, not specific dopamine reuptake inhibitor. This means that you can include info on agents that inhibit both dopamine & norepinephrine. It will also be good to compare and contrast dopamine, norepinephrine and serotonine reupake inhibitors with the aim of clarifying specific effects of dopamine reuptake inhibitors. Note dopamine should not be capitalized unless it's the first word in a sentence. Keep up the good work! Neuropsychprof ( talk) 08:12, 5 November 2012 (UTC)
Thanks to everyone who gave us suggestions to improve our article! While all of the suggestions were very helpful here is what we focused on:
Unfortunately, we were not able to get to everyone's feedback. Here are a few and the reasons why:
Thanks to everyone for all your feedback and suggestions, it was very helpful! Best wishes. Daniadams9121 ( talk) 19:24, 13 November 2012 (UTC)
I notice that one of the main sections of this article is on MDMA, and I find this peculiar. Firstly, because MDMA is primarily a releasing agent (rather than a reuptake inhibitor), and secondly because MDMA mainly acts on the serotonin system, although its effects on noradrenaline and dopamine are also important. There are much better examples of dopamine reuptake inhibitors than MDMA, such as methylphenidate, ethylphenidate, MDPV, pyrovalerone, and bupropion. If there is not a good reason to have this section, then I suggest that it should be removed. Woood ( talk) 08:24, 3 December 2012 (UTC)
I agree with the above, MDMA is a mixed action dopamine reuptake inhibitor and releasing agent. And even then is not a very potent one compared to its action at SERT and it's true magic in reversing, or breaking VMAT-2. In fact because of its status as a Schedule I we really don't know if the dopamine release is primary to its structure or if it's secondary to serotinergic activity. As an MDMA user who has also used amphetamine, methylphenidate and bupropion medicinally it seems likely to me that the after effects of MDMA on me (getting sleepy and wanting to go to bed) are not characteristic of a strongly, primary dopaminergic compound with such a long half-life. — Preceding
unsigned comment added by
208.102.254.241 (
talk) 22:36, 20 December 2012 (UTC)
I'm concerned at the ambiguity of the definition. It is my understanding that dopamine reuptake inhibitors must have a very low affinity for dopamine and norepinephrine, drugs with these characteristics are classified as SDRI and NDRI's respectively. Wiki pages exist for them.
Additionally, the introduction is confusing, contradictory, and informal.
"Many physicians disagree with the information noted above that is biased against the use of DRIs and stimulants because of some potential of abuse."
This is a perfect example, I have absolutely no idea what it is meant to mean.
"To date, we know of no abuse of drugs such as Bupropion."
Incorrect, publicly available literature is found in the first link when searching google for "Bupropion abuse potential."
" Contrary to the writers opinion above..."
I doubt its necessary to explain why this paragraph needs to be edited. The bias displayed in it is enough for me to have made my first addition to a Wikipedia page.
"...the only norepinephrine-dopamine reuptake inhibitor (NDRI) approved by the Food and Drug Administration."
Methylphenidate?
Regardless, I believe I've made my point, This article is probably not worth salvaging, perhaps it should be re-written from scratch?
124.183.98.85 ( talk) 17:17, 7 July 2013 (UTC)
The comment(s) below were originally left at Talk:Dopamine reuptake inhibitor/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.
Changed rating to "mid" for consistency within MCB project. This article needs an explanation of the pharmaceutical/biological effect of these inhibitors in simple terms; it's very technical right now. - tameeria 20:10, 22 February 2007 (UTC) |
Last edited at 20:10, 22 February 2007 (UTC). Substituted at 13:40, 29 April 2016 (UTC)
All the information I've read indicates that modafinil (or at least R-modafinil; I've not seen much written about L-modafinil) acts as a reuptake inhibitor which is selective for DAT (unlike, say, cocaine, which significantly inhibits DAT, NET and SERT, or methyl/ethylphenidate, which significantly inhibits both DAT and NET). Ignoring the difference in half-life, (R-)/modafinil's binding profile seems to be more similar to amineptine's than anything else. IMHO, this ought to be reflected in this article. I'm aware that the armodafinil article claims that it has "effects and feelings consistent with methylphenidate", but I'm skeptical of that claim; it appears to be based on a single study, whereas many other studies have found that both in vitro and in vivo the drug binds nearly solely to the DAT, and even Wikipedia's own modafinil article states that "it was found to significantly affect only the dopamine transporter". -- Mojace ( talk) 13:21, 25 April 2017 (UTC)
It is my understanding that it is the fluorenol-derivative of modafinil that is a weak DAT-inhibitor, and not fluorenol itself.
-- Mentropane ( talk) 20:52, 27 November 2019 (UTC)
This article is the subject of an educational assignment at Roosevelt University supported by the Wikipedia Ambassador Program during the 2012 Q3 term. Further details are available on the course page.
The above message was substituted from {{WAP assignment}}
by
PrimeBOT (
talk) on 15:53, 2 January 2023 (UTC)
This article is rated Start-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | ||||||||||||||||||||||||||||||||||
|
This article was the subject of a Wiki Education Foundation-supported course assignment, between 3 September 2021 and 16 December 2021. Further details are available on the course page. Student editor(s): Paytonreiner.
Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT ( talk) 19:44, 16 January 2022 (UTC)
Sounds ok.
Daevatgl 20:35, Jun 16, 2004 (UTC)
May 6 2005 edits The Biochemical Basis of Neuropharmacolgy Oxford Press 1996 Chapter 9 Dopamine-- McDogm 17:21, 6 May 2005 (UTC)
Should add Adderall in here -- I would but couldnt figure out the proper medical name for it or where it fits in terms of dopamine release.
Isn't it the case that most phenethylamine DARIs inhibit by attaching as if they were the regular transporters, and others like the cocaine tropane-types attach or bind as a ligand to the transporter in an entirely different way? It is odd that such a tropane type ligand, if I'm not mistaken, attaches with a higher affinity? 71.34.103.210 ( talk) 00:45, 19 April 2009 (UTC)
I've corrected the following two errors:
I tagged the link to physical dependence as dubious. To my knowledge, straight DRIs such as methylphenidate don't cause a lot of "physical dependence". This is partly a language issue: These drugs do cause homeostatic changes in the brain, but philosophy of the mind notwithstanding, I think that that's not usually what is meant by "physical dependence". In my book, "physical dependence" means that there are serious peripheral symptoms upon discontinuation. Suboptimal Username ( talk) 17:15, 10 June 2010 (UTC)
There are withdrawal symptoms upon discontinuation, look at cocaine - huge withdrawal symptoms. Even methylphenidate when used at a high enough dose will give withdrawal symptoms -- Axxaer ( talk) 04:17, 27 September 2010 (UTC)
Cocaine is totally different though, according to the wiki page it is a Serotonin, Norepinephrine and Dopamine reuptake inhibitor. Methylphenidate as well is not selectively a dopamine reuptake inhibitor. I don't really get why you make the link between those two and DRIs Robinsona ( talk) 20:47, 11 December 2010 (UTC)
e.g. dextro- & levo- methamphetamine. Could there be a drug similar to cocaine for instance, that only preforms the function of the former mentioned dextro- (alone) or levo- (alone) by only inhibiting reuptake on those sort of transporters potentially at all? Nagelfar ( talk) 05:47, 8 July 2010 (UTC)
List of DRI’s and Intro: will simply be edited according to our research findings, and addition DRI’s not listed will be added, and the current list verified.
Process
This section will contain information about the biological processes induced by dopamine reuptake inhibitors. The process within the synapses will be covered, alone with any side effects, either long term or short term, as well as any effects caused by dopamine increase.
History
This section will cover the history of the discovery and use of dopamine reuptake inhibitors. The development over the last half century of the targeting of transporters as a means of concentrating levels of neurotransmitters within the synapse will be discussed, as well as a general history of the drugs and their discoverers.
Possible affects on cognition
This section will focus on the affects that DRI can have on emotion, as well as the possible side affects of DRI's. Another subject that this section will talk about is the controversy behind DRI's in drugs. This will touch on usage and abuse of DRI's. This section will also touch on the short term affects and the long term affects of DRI's.
Dopamine Reuptake Inhibitors and Depression — Preceding unsigned comment added by Nszynal-ru ( talk • contribs) 17:50, 12 November 2012 (UTC)
— Preceding daniadams9121 comment added by Narmstrong484 ( talk • contribs) 18:49, 9 October 2012 (UTC)
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cite journal}}
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Neuropsychprof ( talk) 22:00, 10 October 2012 (UTC)
Well I see that we all know that you need more sources I think its a good start though just a little more information in certain sections and more sources and I think this will be a good article, Good luck — Preceding unsigned comment added by Schandler91 ( talk • contribs) 17:47, 30 October 2012 (UTC)
This is a good start...but needs a lot of expansion/sourcing. Smallman12q ( talk) 22:38, 27 October 2012 (UTC)
It looks like there needs to be more sources that are actually contained within the article rather than just floating at the top. More sections should also be added to go into details about subjects raised in the introduction. I would agree with smallman12 that the article needs to be expanded and more effort needs to be put into finding sources.
Pmisner2009 ( talk) 16:39, 28 October 2012 (UTC)
I agree that maybe more sources would help generate a better informative article. I think what you have so far is good but maybe you could expand upon certain parts as in the dopaminergic pathway and get into more detail. R.EEGbrittry ( talk) 19:51, 29 October 2012 (UTC)
-- Rorystewart ( talk) 18:32, 30 October 2012 (UTC)
Hi everybody! I just got a message from Prof. Lu asking if I could take a look at everybody's work, and I've got a few suggestions to help make your article even better. I'm going to organize them in a bullet pointed list just for your ease of use; if you have any questions or need some help, you can either ask here (I've watchlisted this talk page) or on my talk page. I'm happy to help with anything! =]
All the best, Keilana| Parlez ici 06:09, 31 October 2012 (UTC)
Group, you have added some good info on a tough topic. I'm going to email this group some readings that may help. Remember to refer to the selective serotonine reuptake inhibitor page for the type of info to add to your article. Note this article is dopamine reuptake inhibitor, not specific dopamine reuptake inhibitor. This means that you can include info on agents that inhibit both dopamine & norepinephrine. It will also be good to compare and contrast dopamine, norepinephrine and serotonine reupake inhibitors with the aim of clarifying specific effects of dopamine reuptake inhibitors. Note dopamine should not be capitalized unless it's the first word in a sentence. Keep up the good work! Neuropsychprof ( talk) 08:12, 5 November 2012 (UTC)
Thanks to everyone who gave us suggestions to improve our article! While all of the suggestions were very helpful here is what we focused on:
Unfortunately, we were not able to get to everyone's feedback. Here are a few and the reasons why:
Thanks to everyone for all your feedback and suggestions, it was very helpful! Best wishes. Daniadams9121 ( talk) 19:24, 13 November 2012 (UTC)
I notice that one of the main sections of this article is on MDMA, and I find this peculiar. Firstly, because MDMA is primarily a releasing agent (rather than a reuptake inhibitor), and secondly because MDMA mainly acts on the serotonin system, although its effects on noradrenaline and dopamine are also important. There are much better examples of dopamine reuptake inhibitors than MDMA, such as methylphenidate, ethylphenidate, MDPV, pyrovalerone, and bupropion. If there is not a good reason to have this section, then I suggest that it should be removed. Woood ( talk) 08:24, 3 December 2012 (UTC)
I agree with the above, MDMA is a mixed action dopamine reuptake inhibitor and releasing agent. And even then is not a very potent one compared to its action at SERT and it's true magic in reversing, or breaking VMAT-2. In fact because of its status as a Schedule I we really don't know if the dopamine release is primary to its structure or if it's secondary to serotinergic activity. As an MDMA user who has also used amphetamine, methylphenidate and bupropion medicinally it seems likely to me that the after effects of MDMA on me (getting sleepy and wanting to go to bed) are not characteristic of a strongly, primary dopaminergic compound with such a long half-life. — Preceding
unsigned comment added by
208.102.254.241 (
talk) 22:36, 20 December 2012 (UTC)
I'm concerned at the ambiguity of the definition. It is my understanding that dopamine reuptake inhibitors must have a very low affinity for dopamine and norepinephrine, drugs with these characteristics are classified as SDRI and NDRI's respectively. Wiki pages exist for them.
Additionally, the introduction is confusing, contradictory, and informal.
"Many physicians disagree with the information noted above that is biased against the use of DRIs and stimulants because of some potential of abuse."
This is a perfect example, I have absolutely no idea what it is meant to mean.
"To date, we know of no abuse of drugs such as Bupropion."
Incorrect, publicly available literature is found in the first link when searching google for "Bupropion abuse potential."
" Contrary to the writers opinion above..."
I doubt its necessary to explain why this paragraph needs to be edited. The bias displayed in it is enough for me to have made my first addition to a Wikipedia page.
"...the only norepinephrine-dopamine reuptake inhibitor (NDRI) approved by the Food and Drug Administration."
Methylphenidate?
Regardless, I believe I've made my point, This article is probably not worth salvaging, perhaps it should be re-written from scratch?
124.183.98.85 ( talk) 17:17, 7 July 2013 (UTC)
The comment(s) below were originally left at Talk:Dopamine reuptake inhibitor/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.
Changed rating to "mid" for consistency within MCB project. This article needs an explanation of the pharmaceutical/biological effect of these inhibitors in simple terms; it's very technical right now. - tameeria 20:10, 22 February 2007 (UTC) |
Last edited at 20:10, 22 February 2007 (UTC). Substituted at 13:40, 29 April 2016 (UTC)
All the information I've read indicates that modafinil (or at least R-modafinil; I've not seen much written about L-modafinil) acts as a reuptake inhibitor which is selective for DAT (unlike, say, cocaine, which significantly inhibits DAT, NET and SERT, or methyl/ethylphenidate, which significantly inhibits both DAT and NET). Ignoring the difference in half-life, (R-)/modafinil's binding profile seems to be more similar to amineptine's than anything else. IMHO, this ought to be reflected in this article. I'm aware that the armodafinil article claims that it has "effects and feelings consistent with methylphenidate", but I'm skeptical of that claim; it appears to be based on a single study, whereas many other studies have found that both in vitro and in vivo the drug binds nearly solely to the DAT, and even Wikipedia's own modafinil article states that "it was found to significantly affect only the dopamine transporter". -- Mojace ( talk) 13:21, 25 April 2017 (UTC)
It is my understanding that it is the fluorenol-derivative of modafinil that is a weak DAT-inhibitor, and not fluorenol itself.
-- Mentropane ( talk) 20:52, 27 November 2019 (UTC)
This article is the subject of an educational assignment at Roosevelt University supported by the Wikipedia Ambassador Program during the 2012 Q3 term. Further details are available on the course page.
The above message was substituted from {{WAP assignment}}
by
PrimeBOT (
talk) on 15:53, 2 January 2023 (UTC)