Talk:Glutamate receptor

Glutamate receptor is currently a Biology and medicine good article nominee. Nominated by Justindchien (talk) at 01:25, 26 November 2009 (UTC)

An editor has indicated a willingness to review the article in accordance with the good article criteria and will decide whether or not to list it as a good article. Comments are welcome from any editor who has not nominated or contributed significantly to this article. This review will be closed by the first reviewer. To add comments to this review, click discuss review and edit the page.

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)[reply]

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)[reply]

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

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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)[reply]

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

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)[reply]

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[reply]

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)[reply]