Talk:NMDA receptor

message: I added some detail to the gating of the receptor, since the implication was that the NMDAR was primarily a voltage-gated channel.  It is ligand gated, of course, with there being some voltage-dependence of that gating - and the primary apparent voltage-dependence (of the current flow, not the gating) coming from the open-channel block by divalent cations.  I wanted to add a reference to the voltage-dependence of gating, but I don't yet know how to edit the reference list.  Sorry - I used to edit a lot under a different user name (Synaptidude), but I can't remember the password, and the email account I used is long-dead - so I can't recover it - hence the new user name.  Sorry also that I have not done any editing in WP for years, so I don't remember all the protocols for labelling this comment - so sorry if I mess it up.  Neuromanncer (talk) 01:22, 2 March 2016 (UTC)
thread_title: Gating

message: I don't have time to do this now, but someone should change all of the NR1/NR2 to GluN1/GluN2. This is now the preferred denotation that is used in the literature. It keeps the format of the subunit name consistent with other glutamate receptors(for example AMPA subunits are GluA1/2 (which used to be GluR1/2) and Kinate subunits are GluK...) 18 February 2012  — Preceding unsigned comment added by 140.160.61.201 (talk) 20:49, 18 February 2013 (UTC)
replies: text: I suggest that more about the Ca++ that comes through the NMDA receptor and how it regulates calmodulin-dependent protein kinase II Rincrate (talk) 04:24, 29 September 2015 (UTC)
thread_title: Untitled

message: I don't have time to do this now, but someone should change all of the NR1/NR2 to GluN1/GluN2. This is now the preferred denotation that is used in the literature. It keeps the format of the subunit name consistent with other glutamate receptors(for example AMPA subunits are GluA1/2 (which used to be GluR1/2) and Kinate subunits are GluK...) 18 February 2012  — Preceding unsigned comment added by 140.160.61.201 (talk) 20:49, 18 February 2013 (UTC)
replies: text: I suggest that more about the Ca++ that comes through the NMDA receptor and how it regulates calmodulin-dependent protein kinase II Rincrate (talk) 04:24, 29 September 2015 (UTC)

text: I would like to see more about the AMPA receptor in reference to the Mg++ ligand that blocks the NMDA receptor until the cell sufficiently depolarizes. Reading this article leaves me wondering why and how the cell depolarizes sufficiently, especially considering that it cannot depolarize through the NMDA receptor due to the Mg++ ligand. Trb9 (talk) 01:58, 27 September 2016 (UTC)
thread_title: Untitled

message: I plan on updating this page with information specific to the role of NMDA receptors to excitotoxicity. Right now I find only a mention of it under the subunit section. I also realize this will have some overlap with the page on excitotoxicity itself. I have gone back and forth on the location of some of this information but since my research has been exclusively on the role of NMDA receptors in toxicity/plasticity I will be uploading it here when I finnish. Any suggestions from those who also have experience in this field will be appreciated. Cpm827 (talk) 04:58, 29 November 2016 (UTC)
thread_title: Excitotoxicity

message: Hello fellow Wikipedians,
I have just modified 4 external links on NMDA 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/20140427010101/http://www.cmj.org/Periodical/LinkIn.asp?journal=Chinese+Medical+Journal&linkintype=pubmed&year=2000&vol=113&issue=10&beginpage=948 to http://www.cmj.org/Periodical/LinkIn.asp?journal=Chinese%20Medical%20Journal&linkintype=pubmed&year=2000&vol=113&issue=10&beginpage=948
*Added archive https://web.archive.org/web/20110927082419/http://www.sinauer.com/neuroscience4e/ to http://www.sinauer.com/neuroscience4e
*Added archive https://web.archive.org/web/20110927082419/http://www.sinauer.com/neuroscience4e/ to http://www.sinauer.com/neuroscience4e
*Added archive https://web.archive.org/web/20041213040240/http://www.bris.ac.uk/Depts/Synaptic/info/pharmacology/NMDA.html to http://www.bris.ac.uk/Depts/Synaptic/info/pharmacology/NMDA.html
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thread_title:  External links modified (February 2018) 

message: A better picture is needed than figure 1. The picture looks like a child's drawing. A digitally created image is required.  — Preceding unsigned comment added by 86.129.178.168 (talk) 19:37, 17 August 2018 (UTC)
thread_title:  Figure 1 

message: Perhaps I am reading the subsection on neural plasticity wrong but it seems to suggest that the opening of NMDA receptors leads to LTD, not LTP?  Purves et al. write in the 5th edition of Neuroscience (p173) that "The NMDA receptor behaves like a molecular coincidence detector: The channel of this receptor opens (to induce LTP) only when two events occur simultaneously: glutamate is bound to the receptor, and the post-synaptic cell is depolarized to relieve the Mg2+ block of the channel pore."
Am I reading this section wrong or should I change it? — Preceding unsigned comment added by SK8RBOI (talk • contribs)  03:25, 29 July 2019 (UTC)
thread_title:  NMDA & LTP inhibition 

message: This article is of poor quality because mostly outdated (e.g. the idea that NMDAR inhibition is supposed to be beneficial has been attributed to different subunit compositions) and should be revised by neuroscientists (please share your knowledge!).  — Preceding unsigned comment added by 195.176.238.195 (talk) 14:22, 9 March 2021 (UTC)
thread_title:  poor quality