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This is an old revision of this page, as edited by Nvarade (talk | contribs) at 01:42, 4 February 2014. The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Layout

This page has been a stub for a very long time.--Kintaro 06:47, 30 Apr 2005 (UTC)

maybe we ought to take out the headings of each type of receptor for now, since they all say the same thing, and just have a sentence about the types. Then we can put them back in when we have more to add. It looks kinda weird now. What do you think?--Delldot 05:52, 8 October 2005 (UTC)[reply]

Personally I find the current layout to be ideal. Leaving it room to grow doesn't mishape it to much and welcomes in additions. Imo it should stay as is.Foolishben 08:16, 9 August 2007 (UTC)[reply]

merge subtypes

I think the separate articles on the D1 to D5 receptors are too small to merit their own page. It is probably better to merge all these pages into one article. When the information on a particular receptors grows sufficiently large, it can then be specified as a main article Kpmiyapuram (talk) 16:30, 2 April 2008 (UTC)[reply]

You know...it's been on my "to do" list for a while to expand each of these. Hopefully I can muster the spare time & energy to finally get crackin' on that... — Scientizzle 16:44, 2 April 2008 (UTC)[reply]
There is already sufficient information in the literature, especially related to pharmacology of dopamine receptor subtypes to justify a separate article on each. In fact some of this information has recently been added (e.g., subtype selective ligands). These receptors are of high interest as therapeutic targets to the pharmaceutical industry and the development of subtype selective ligands is a very promising way of dissociating desirable therapeutic from undesirable side effects, so the amount of information will only grow over time. Therefore I strongly oppose merging these articles. Cheers. Boghog2 (talk) 18:20, 2 April 2008 (UTC)[reply]
I added a bunch of studies on the DRD4.7 polymorphism all found off of the NCBI gene entry for DRD4. There is a wealth of information on this one polymorphism in relation to behavior. Given the amount of information, I would also agree with Boghog2. On a completely unrelated note, someone might want to go back and format the refs I listed, they may not be wikipedia standard as I just copied the citations from the NCBI database. I understand the importance of correct citation but it's a pain in the butt... StephenPCook (talk) 12:57, 16 November 2009 (UTC)[reply]
Thanks for your support and contribution to the DR article. Per your request, I have reformatted the citations that you have added using the cite journal template. If you haven't seen this yet, check out User:Diberri's Wikipedia template filling tool. Given a PubMed ID, one can quickly produce a formatted citation that can be copied and pasted into a Wikipedia article. Cheers. Boghog (talk) 06:46, 17 November 2009 (UTC)[reply]
In my attempts to remove the needs citations banner, I wonder if anyone can tell me which parts in the DRD2 subheading needs citations; the fact that the isoforms exist or that they pre or post-synaptically situated? Or both? NCBI lists a variety of studies where the sequence of the proteins were identified. I'm thinking the subtypes should be named here and their specific properties can be discussed on the DRD2 wiki. If that is the case then the comments on this page should satisfy the need of citations for both isoforms. I figured I'd seek some feedback before I edit, so thanks. StephenPCook (talk) 22:00, 2 December 2009 (UTC)[reply]

Awkward sentence

" i.e., keep going on the neurotransmission (excitatory or inhibitory) once blocked by a receptor antagonist or stimulated by the endogenous neurotransmitter itself or a synthetic full or partial agonist." Syntax is confusing... Can someone clarify please? Thanks! Horus (talk) 05:43, 28 July 2008 (UTC)[reply]

Done.—argumzio 03:31, 26 July 2009 (UTC)[reply]

More about DRD4

DRD4 also has a long list of SNP that can also be found on the NCBI website. I submit that naming each polymorphism does little to explain anything about this gene and that all that information can be summed up in a sentence. I think any other information can be retrieved from the actual database. If there is precedent for listing vntr polymorphisms on wikipedia, please feel free to revert. StephenPCook (talk) 19:49, 18 November 2009 (UTC)[reply]

Yes, that's fine. The list was rather long. --Tryptofish (talk) 19:57, 18 November 2009 (UTC)[reply]

additional receptors

Hi, I had a quick look, but couldn't see the extra 90% increase in receptors in the Science article. But I don't doubt that it's there. Another study [25] showed in a living subject, dopamine 2 receptors had increased approximately 90% after neuroleptic treatment. Notpayingthepsychiatrist (talk) 02:45, 7 February 2010 (UTC)[reply]

DA and reward

See articles (pubmed PMIDs): 6438676 and 16341013

excitatory or inhibitory?

I know that either D1 or D2 is excitatory and the other is inhibitory, but not which is which. This is something that should be in this article. —Preceding unsigned comment added by 129.64.209.130 (talk) 16:38, 16 May 2011 (UTC)[reply]

Actually, it isn't that simple, and the literature is contradictory. --Tryptofish (talk) 21:47, 16 May 2011 (UTC)[reply]
Can a discussion of the contradictory literature on this topic be added? 129.64.209.130 (talk) 19:45, 17 May 2011 (UTC)[reply]
Yes, I suppose so (but I personally would be reluctant to write it, because I have a WP:COI). --Tryptofish (talk) 00:14, 18 May 2011 (UTC)[reply]

The conventional wisdom about D1 & D2 is that D1 is Gs-coupled and post-synaptic (therefore dopamine release enhances firing of the post-synaptic neuron) and that D2 is Gi-coupled and a pre-synaptic autoreceptor (therefore dopamine release inhibits further release of dopamine from the pre-synaptic neuron). If one defines "excitatory" & "inhibitory" based solely on this model of an idealized dopamine synapse, then D1=excitatory & D2=inhibitory. Nature, however, is far more complicated...

  • Pre- and post-synaptic localization has not been conclusively characterized for each receptor in each type of synapse. Therefore, these generalities almost surely don't apply in many cases. In particular, D2short & D2long are quite different in localization (Dopamine receptor D2 needs more information on this!)
  • D3, D4 & D5 have expression patterns and signaling functionalities unique from D1 or D2
  • Dopamine receptors can be found on opposite-acting neurons (e.g., glutamatergic pyramidal neurons neurons & GABAergic interneurons), so even simple circuit models with only a handful of neurons can have complicated dopamine signaling outputs. As an example, activation of GABAergic interneurons inhibits the local circuit's glutamatergic output.
  • Zooming out even further, different brain regions can "activate" or "suppress" the firing in another region, thus dopamine signaling can have very complicated behavioral effects.

As for clearly discussing these complicated signaling effects within this article...it will take some time to develop the proper prose & citations that can convey the present models without becoming overly complicated. — Scientizzle 15:07, 18 May 2011 (UTC)[reply]

And, further, there's tons of evidence for postsynaptic D2 receptors (maybe some evidence that D3 is presynaptic). And there's also the issue of receptors that have mixed actions, such as modulating both ion channels and signaling cascades, in such a way that the ionic and the cascade-mediated effects may be opposite with respect to excitation. Indeed, it may be a case where it would just be "too much information" to go into it in this page. --Tryptofish (talk) 19:51, 18 May 2011 (UTC)[reply]
I also totally forgot to include receptor heteromers in my list above...Heteromerize a Gs-coupled GPCR with a Gi-coupled GPCR and sometimes the complex activates Gq instead! While some of the basics of these signaling complexities can and probably should be touched on in this article (or better at the individual receptor articles), it could be far too easy to overload this page with minutiae. — Scientizzle 20:11, 18 May 2011 (UTC)[reply]

What ref 25 really says

Someone seems to have misread the conclusion of the study. It is that "clinically effective doses of chemically distinct neuroleptic drugs result in 85 to 90 percent occupancy of D2 dopamine receptors". Nothing to do with increases in binding potential: that was only established in a much newer study, "for the first time", as it says there. So anyway, I'm deleting the relevant bit from the article as it is a clear misreading. Firrtree (talk) 11:32, 30 October 2012 (UTC)[reply]

More on D2 receptor family

It would be nice for the section to elaborate on the bi-phasic ability of D2 receptors to certain agonist (such as quinpirole).