Talk:Glutamate receptor

Suggestions for BI481 course

Hi,

You guys have made a great start on updating this article. I have a couple of suggestions:

• Citations. If you haven't seen this yet, please 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. This will save you an enormous amount of work and insures that the citations are displayed in a consistent manor.
• Introduction and conclusion sections are not normally included in Wikipedia articles. I have taken the liberty of merging the introduction into the lead section. The conclusion section should be integrated with the rest of the article.
• Organization. It appears that the sections of this article were written independently and then merged together. This is understable given the requirements of your course but the end result is that the article is not as cohesive as it should be. The section entitled "Types" contains a list of the mGluR subtypes while "Genetics" contains a list of the iGluR subtypes. These two sections should be merged. The "Pathology" and "Current research" sections contain the same type of information and probably should be merged together. The focus should be kept on the receptor and not research about the receptor.

Again, good work. Cheers. Boghog (talk) 10:54, 31 October 2009 (UTC)

Thanks for the organizational suggestions. We hopefully have it all set now so our sections aren't convoluted or repeated. And awesome link for the citations page! (Wangtron (talk) 18:50, 7 December 2009 (UTC))

Removed GA nomination

I want to note that I have removed the GA nomination for this article, because it was made without any discussion by an editor who has not responded to queries. If nobody is prepared to respond to issues, the GA process is a waste of a reviewer's time. If anybody is in fact prepared to make requested improvements, the article can be renominated at will. Looie496 (talk) 01:29, 12 November 2009 (UTC)

Sorry, a lot of things have come up and we are now more prepared to respond to any suggestions and comments.

GA Review

This review is transcluded from Talk:Glutamate receptor/GA1. The edit link for this section can be used to add comments to the review.

I'm pleased to review such an important article. My initial impression is that the article contains a lot of useful information but needs work in some important respects. Details will follow, but here are some initial points:

• The article needs to explain briefly, perhaps even in the lead, that glutamate is one of the 20 essential amino acids used to build protein, and therefore is found in large quantities in every part of the body.

• I don't think the Function section is accurate. As I understand it, most neuroscientists consider AMPA receptors to be the "primary" glutamate receptors. This may be disputable, but in any case I don't think they should be portrayed as secondary to NMDA receptors.

• It's very important to have an explanation of the features of the NMDA receptor that make it play a key role in neural plasticity -- i.e., the fact that the receptor depends on simultaneous pre- and postsynaptic activity. Details can be left to the subarticle, but the importance of this requires that an overview be given here.

• Current ideas about the role of glutamate receptors in schizophrenia need some coverage. (Glutamate antagonists as possible antipsychotic drugs have been getting a lot of attention recently.)

Reviewer: Looie496 (talk) 18:28, 29 November 2009 (UTC)

thank you for your feedback! we will go over these comments and do research on the issues raised. Justindchien (talk) 20:09, 29 November 2009 (UTC)

thanks so much! I think you are correct about function, I've changed "function" to a general overview of glutamate receptor's role in the nervous system, and left detailed explanation for the "structure/mechanism" where it is now noted that NMDA relies on AMPA to be activated. Philipthegreat88 (talk) 19:38, 7 December 2009 (UTC)

Starting real review

I didn't want to get into the middle of all the action that was going on in the article, but I'll start a real review now.

• Function: This section has improved but is still short of what it ought to be. Basically there are four types of receptors commonly encountered: AMPA, NMDA, metabotropic, and kainate. Metabotropic receptors operate via a second messenger system; the others are ionotropic. The primary function of AMPA and kainate receptors is fast excitation: the receptors activate in a fraction of a millisecond, and only stay active for a few milliseconds. NMDA receptors seem to have two functions. In some situations they play a simple excitatory role, but they activate and inactivate a lot slower than AMPA receptors. In other situations their role is to control synaptic plasticity. Metabotropic receptors have a long-lasting modulatory effect. Looie496 (talk) 18:46, 14 December 2009 (UTC)

• Types: I don't understand either of these two sentences: "This is due to the usage of many different messengers to carry out the signal but since there is a cascade, just one activation of a G-protein can lead to multiple activations. Glutamate receptors are usually not specifically geared towards glutamate exclusively as the ligand and sometimes even requires another agonist.". The second one requires a reference at the very least. Looie496 (talk) 18:53, 14 December 2009 (UTC)

• Excitotoxicity / Ischemia: The article should explain that stroke is one of the most common causes of death and debility, and that much of the brain damage produced by stroke is due to excitotoxicity: brain cells that are not killed immediately by loss of blood supply often die hours or days later as a consequence of excitotoxicity. Thus, treatments for excitotoxicity are very important medically, but they must be applied quickly to have any effect. Looie496 (talk) 19:01, 14 December 2009 (UTC)

• Ampakines: The article should include a brief overview of the use of ampakines as nootropic drugs. Looie496 (talk) 19:06, 14 December 2009 (UTC)

More to come.

Terminating review

I am going to terminate this GA review due to lack of responses. Please feel free to nominate the article again if it reaches a point where you feel it is ready. Looie496 (talk) 16:45, 5 January 2010 (UTC)

Peer review from BI481 Classmates

Comment 1

Potential Revision

First, you should revaluate the organization of subtopics beneath main headings, particularly in the “Clinical significance” section. It seems that the “Excitotoxicity” subtopic does not belong—make it its own heading, or, if appropriate, clarify its relevance to the clinical significance of glutamate receptors within the article.

In addition, I suggest you consider discussing in greater detail the role of glutamate receptors in EAE and Multiple Sclerosis pathogenesis under the “Potential therapeutic applications” section. Drugs that interact with ionotropic glutamate receptors to suppress EAE have emerged over the last decade, and use of receptor antagonists to control EAE with the possibility of therapeutic application in MS has also been investigated. You can find this information at:

• Bolton C, Paul C (2006). "Glutamate receptors in neuroinflammatory demyelinating disease". Mediators Inflamm. 2006 (2): 93684. doi:10.1155/MI/2006/93684. PMC 1592583. PMID 16883070.{{cite journal}}: CS1 maint: unflagged free DOI (link)

You list MS under “Neurogenerative diseases” (which should be changed to “Neurodegenerative diseases”)—perhaps consider combining the “Clinical Significance” and “Potential therapeutic applications” sections.

Bergaa7 (talk) 02:11, 24 November 2009 (UTC)

thank you for your suggestion, we are currently undergoing more research on your suggestion and may see a viable application to our article. —Preceding unsigned comment added by Justindchien (talk • contribs) 01:28, 26 November 2009 (UTC)

we have now added a MS section to potential therapeutic applications. Justindchien (talk) 21:47, 6 December 2009 (UTC)

We're going to keep the excitotoxicity subtopic because it sets up the basic mechanism to how GluR is so important in neurodegenerative diseases. I'll clarify this a little more, but the organization of the clinical significance section was set up to build on each other, from excitotoxicity to neurodegeneration to neurodegen. diseases. (Wangtron (talk) 16:48, 7 December 2009 (UTC))

Comment 2

Potential Additions

Hey guys I have a few things I suggest you include in your article. First, I think you should not only describe glutamate receptor function in neurons, but also describe their function in glial cells. Here are a couple articles I found on this subject:

• Teichberg VI (1991). "Glial glutamate receptors: likely actors in brain signaling". FASEB J. 5 (15): 3086–91. PMID 1660422. {{cite journal}}: Unknown parameter |month= ignored (help) and
• Steinhäuser C, Gallo V (1996). "News on glutamate receptors in glial cells". Trends Neurosci. 19 (8): 339–45. PMID 8843603. {{cite journal}}: Unknown parameter |month= ignored (help)

Finally, it would be more informative to describe the NMDA receptor in more detail including serine/glycine coagonists, the antagonist binding sites (Zn site, Mg blocker, MK801/PCP binding site), and also NMDA’s role in silent synapses.

Pat Bolan(talk) 2:28, 24 November 2009 (UTC)

Hi, we have linked to the other wikipedia article which talkes about NMDA receptors specifically. We are providing an overview for Glutamate Receptors, not specific information on certain glutamate receptors. There was already an NMDA receptor wikipedia article. if we include it here, then there would be no use for the NMDA receptor article. —Preceding unsigned comment added by Justindchien (talk • contribs) 01:22, 26 November 2009 (UTC)

Hey, I think you are right that the activity of glial glutamate receptors is important for the nervous system, I have included information from your papers. However, I think the information on NMDA is a bit too detailed for the general glutamate receptor page. Thanks! Philipthegreat88 (talk) 19:39, 7 December 2009 (UTC)

Comment 3

Hi, I found an article specifically discussing when the glutamate receptor was first cloned in 1989. Perhaps you may want to cite some of the implications of this research and some of the questions that were raised from the data. It may provide a better background as to where research is going and what is still left to be answered about the glutamate receptor.

• Hollmann M, Heinemann S (1994). "Cloned glutamate receptors". Annu. Rev. Neurosci. 17: 31–108. doi:10.1146/annurev.ne.17.030194.000335. PMID 8210177.

neurosoltisk (talk) 10:11, 27 November 2009 —Preceding unsigned comment added by 76.6.35.35 (talk)

thank you for your feedback, but it doesn't seem that we have access to this article. Justindchien (talk) 19:39, 29 November 2009 (UTC)

Comment 4

Hi guys,

I think you all have done a great job, I just had a couple of suggestions/comments that might be helpful. I would include some pictures/diagrams in your article; these figures will help the reader understand the content better. I think our textbook has a couple of good ones. I would also go into a little more detail about how AMPA and NMDA receptors work, especially how NMDA receptors rely on AMPA receptors to depolarize the cell. In addition, I would also explain how Glutamate transport is affected by energy deficiency in your ischemia section.

Great job!

chengkd (talk) 28 November 2009 —Preceding unsigned comment added by 99.22.12.185 (talk) 23:45, 28 November 2009 (UTC)

thanks for your suggestions. many images are subject to copyright laws and require permission from the copyright holders so that is why we have not uploaded any images yet. Also, NMDA and AMPA receptors have their own wikipedia articles that we have linked to. we may provide a brief overview though. Justindchien (talk) 05:43, 5 December 2009 (UTC)

Oops! Good call, the glu transporter system is pretty essential to neurodegeneration. Shall throw it in there! Like monkeys throwing coconuts! (Wangtron (talk) 17:45, 7 December 2009 (UTC))

Comment 5

Hi!

Overall, I think the article does a great job of providing some basic knowledge about glutamate receptors. I just had a little trouble with the organization of the topics. For example, the discussion of ionotropic and metabotropic receptors in the "Function" section precedes the more detailed explanation in subsequent section. Also, you do a good job of talking about receptors in the PNS but I think a section of receptors in glial cells might be helpful. You might also be able to mention the link to oxidative stress. (cystine xCt transporter).

Rabihgeha (talk) 19:25, 29 November 2009 (UTC)Rabihgeha

we wrote this article before we went over that part in class. perhaps you are right but we need to find sources to back up that information. Justindchien (talk) 05:46, 5 December 2009 (UTC)

Yeah, we'll get the oxidative stress part under excitotoxicity. Thanks for bringing that up, especially cuz we recently learned that in class. (Wangtron (talk) 03:21, 7 December 2009 (UTC))

great suggestion, thanks! I've changed around the "function" and "structure/mechanism" sections a bit to make it flow a bit easier, as I mentioned above. Philipthegreat88 (talk) 19:41, 7 December 2009 (UTC)

Comment 6

Great job on the article and congrats on the Good Article nomination. I noticed that suggestions to gain GA status included a need for more information linking glutamate receptors to schizophrenia. I took the liberty of researching the topic a little further and found a very informative article published November 16, 2009 titled "Glutamatergic deficits and parvalbumin-containing inhibitory neurons in the prefrontal cortex in schizophrenia." It can be found through PubMed, http://www.ncbi.nlm.nih.gov/pubmed/19917116?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=1. The article discusses how expression of mRNA for the NR2A subunit of the NMDA receptors was decreased in a subset of inhibitory interneurons in the cerebral cortex in schizophrenia and how this pathophysiology contributes to the disease. In terms of cleaning up the already existing sections of the article, I also agree with previous sections that the "Function" section can use some elaboration regarding the mechanism of both the AMPA and NMDA receptors. I understand that additional Wiki pages exist for these topics, but do feel that as the first section in your article, it is important to effectively explain how these receptors function, especially in terms of HOW this functioning leads to plasticity. Currently, you just mention that it does lead to plasticity. Otherwise, this is a very impressive article!

Naweston (talk) 19:38, 29 November 2009 (UTC)

thanks for your suggestion! we definitely will use this article Justindchien (talk) 05:44, 5 December 2009 (UTC)

Thanks for the article and the suggestion. Sounds gooood. (Wangtron (talk) 03:23, 7 December 2009 (UTC))

Comment 7

First off, well written article, I found it overall easy to follow and I think it covered the subject very well. In the section labeled "Function" I noticed that your explanation included information regarding the binding of NMDA to NMDA receptors that, while correct, may be a little bit confusing when considering the article is covering the glutamate binding to these specific receptors. I think that you should make a point of stating that, while NMDA is the specific agonist for the receptor, the receptor is more important for its binding of glutamate in the CNS. Additionally, when you mention that the receptor causes an action potential it can be misleading. Perhaps it would be more clear if you said that the receptor opened as a result of the agonist binding, and the resulting ion flow, when combined with the flow of many receptors, leads to an excitation and perhaps an action potential. There is a mention in the article telling the reader "as mentioned in the pathology section" but I noticed there is no specific section in the article. Finally, you did a good job of mentioning glutamate receptors in the PNS, but when you talk about their role in diabetes it is merely hinted at. If there is more information, perhaps the role of glutamate receptors in diabetes would be a good topic to expand upon. Rueltnj (talk) 02:16, 30 November 2009 (UTC)

thank you for your comments. we will try to clear this up when we go through the final editing process. Justindchien (talk) 05:46, 5 December 2009 (UTC)

Thank you, these are very useful suggestions, I've noted in the "Function" section that the receptors are activated by glutamate, and differentiated between the EPSC and the AP. Hopefully this makes it more clear. Philipthegreat88 (talk) 17:11, 7 December 2009 (UTC)

So, I changed "function" around in response to some other suggestions, but I still have that information included in the "structure/mechanism" section. Thanks again! Philipthegreat88 (talk) 19:42, 7 December 2009 (UTC)

Comment 8

In the table for types of glutamate receptors, metabotropic is misspelled as “imetabotropic”.

In the “Effects outside the central nervous system” section, the sentence describing immunohistochemistry should have the pronoun “them” replaced with “iGluRs” to clarify the sentence.

In the Clinical Significance section, under the Excitotoxicity subheading, it is mentioned that excitotoxicity can be induced, but the significance of this phenomenon is not stated. Mentioning that neurodegenerative diseases, such as Alzeheimer’s and Parkinson’s may result will lead to a better transition for the next two subheadings.

Regarding the Ischemia subsection in Potential therapeutic applications, the role of calcium in relation to glutamate receptors and ischemia should be discussed.

In the seizures subsection, the sentence “Using rodent models, labs have found that the introduction of antagonists to these glutamate receptors help counteract the epileptic symptoms” should be reworked. The mention of “labs” is inappropriate and should be rephrased.

Overall, the article is very informative and the use of tables helps to organize information. Meidenbauer (talk) 02:47, 30 November 2009 (UTC)

thank you for pointing out the technical errors. they have now been corrected. Justindchien (talk) 05:48, 5 December 2009 (UTC)

The excitotoxicity section explains the different mechanisms that causes cell death, specifically excessive calcium and oxidative stress. This is all classified under glutamate excitotoxicity. Neurodegeneration and neurodegen. diseases have excitotoxicity as their underlying cause of cell death. I'll try to clarrify a lil more. Chyeah. (Wangtron (talk) 17:51, 7 December 2009 (UTC))

Comment 9

This article should endeavour to make consistent use of the agreed IUPAC nomenclature for ligand gated ion channels i.e. AMPA receptor subunits should be referred to as GluA1 rather than GluR1 etc. cf. Collingridge et al. Neuropharmacology 2009 vol. 56 issue 1 pp 2-5 — Preceding unsigned comment added by 78.144.77.91 (talk) 12:00, 26 March 2012 (UTC)

Uncertain statement

"Almost all diseases involving glutamate receptors have very similar, if not identical, pathways, differing slightly only in the area in the brain where the issue occurs"

Is the statement confirmed or a guess? James James 173 (talk) 08:07, 12 September 2012 (UTC)

I can't even understand what it means. If you want to remove it, you have my support. Since glutamate receptors are ubiquitous in the brain, it's hard to imagine any interpretation that could possibly be valid. Looie496 (talk) 18:37, 12 September 2012 (UTC)

External links modified

Hello fellow Wikipedians,

I have just modified one external link on Glutamate receptor. Please take a moment to review my edit. If you have any questions, or need the bot to ignore the links, or the page altogether, please visit this simple FaQ for additional information. I made the following changes:

• Added archive https://web.archive.org/web/20070915085831/http://www.bris.ac.uk/Depts/Synaptic/info/glutamate.html to http://www.bris.ac.uk/Depts/Synaptic/info/glutamate.html

When you have finished reviewing my changes, you may follow the instructions on the template below to fix any issues with the URLs.

This message was posted before February 2018. After February 2018, "External links modified" talk page sections are no longer generated or monitored by InternetArchiveBot. No special action is required regarding these talk page notices, other than regular verification using the archive tool instructions below. Editors have permission to delete these "External links modified" talk page sections if they want to de-clutter talk pages, but see the RfC before doing mass systematic removals. This message is updated dynamically through the template {{source check}} (last update: 5 June 2024).

• If you have discovered URLs which were erroneously considered dead by the bot, you can report them with this tool.
• If you found an error with any archives or the URLs themselves, you can fix them with this tool.

Cheers.—InternetArchiveBot (Report bug) 03:27, 20 October 2017 (UTC)

Establishment of glutamate as a neurotransmitter

In the section function of glutamate it is stated that it was established as a neurotransmitter in the 1960s. However in the well cited paper of Watkins et al. it is described how it took until the 1980s to fully establish the function of glutamate as a neurotransmitter. Please check the following ressource for further verification. WATKINS, Jeffrey C.; JANE, David E. The glutamate story. British journal of pharmacology, 2006, 147. Jg., Nr. S1, S. S100-S108. 77.119.220.68 (talk) 23:57, 30 April 2023 (UTC)