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This is an old revision of this page, as edited by Justindchien (talk | contribs) at 01:04, 29 November 2009 (Removed GA nomination). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Comments from BI481 Classmates

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]

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.

Potential Revisions

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 the url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592583/. 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 (talkcontribs) 01:28, 26 November 2009 (UTC)[reply]

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 (talkcontribs) 01:22, 26 November 2009 (UTC)[reply]

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.

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