Talk:SK channel

Untitled
Edits have been created by Bethany Chaves, Matt White, and Ryan Burns as a part of a Wikipedia article project. My group topic is the SK channel at Boston College. These changes were major, though much of the original information on this page was left 'as is.' Additional edits and criticism are welcome. All three group members contributed equally to the new page seen. The image added was created on Photoshop by Ryan Burns.

Ryburns83 (talk) 23:09, 1 November 2012 (UTC)

Revised Edition
We have tweaked the page a bit. We have updated the language in both sections regarding blockers and modulators so as to imply specificity to small SK subtypes. We have also revised vague and confusing language about NMDA and AMPA receptors in the LTP-related material. Finally, we added the missing citations to the Parkinson's section and clarified information regarding what TH+ and TH- mean, phenotypically. Ryburns83 (talk) 19:17, 30 November 2012 (UTC)

In regard to the statement that “SK channels are coupled to NMDA receptors, which, in turn, are coupled with AMPA receptors, another ligand-gated channel that permisses cation influx” in the Synaptic Plasticity section, this sentence was added by another editor. It was changed back to its original wording which excluded AMPA receptors because the information about AMPA receptors is inherent to the function of NMDA receptors in LTP. Therefore, this information was not necessary in the article as a reader could click on the NMDA receptor Wikilink if they need more detailed information on how NMDA receptors function. Additionally, the introduction paragraph was edited to make some of the previously vague language more clear. Whitenp (talk) 18:05, 3 December 2012 (UTC)

In response to those comments which inquired about other important amino acid residues: the structure section will remain as is, for SK channels are highly conserved in structure with other potassium channels (this is mentioned multiple times throughout the article), and all important residues to which subunits or attached or selectivity occurs are included in the article. Furthermore, the blockers section now includes more direct language encompassing the nature by which antagonists bind: directly to the pore region. Specific residues can vary per antagonist, so this information was left out on purpose for clarity or organizational purposes. Information on cations mimicking potassium to block the channel was included due to the consistency by which they antagonize the pore. Ryburns83 (talk) 23:39, 3 December 2012 (UTC)

Review
Good article! I have a few suggestions. In the “Blockers” and “Modulators” sections, you often say “all three types of SK channels,” but above you describe four types of SK channels. Is SK4 an SK channel? In the “Synaptic plasticity and long term potentiation” section, you write that: “SK channels are coupled to NMDA receptors, which, in turn, are coupled with AMPA receptors, another ligand-gated channel that permisses cation influx.” I think you should change the wording of this sentence so that it doesn’t seem like you mean that NMDA receptors and AMPA receptors bind each other at the postsynaptic density. Also, you need to include citations in your “Role in Parkinson’s Disease” section; so far there are none. Overall, good job! Reedich (talk) 16:03, 29 November 2012 (UTC)

Peer review

 * Hi SK Channel group! Great layout of your article overall - it matches many of the other wiki site on proteins to make a cohesive site. The images are also great and impressive considering the process needed to put them up on this site, well done. I think you should think about adding some images in the blockers section, as this would show how structure dictates function in this sense. I also recommend beefing up the function section, especially how Ca-activated potassium channels contribute to repolarization, and how presence can be detected by raising intracellular calcium (info from our book), as well as add in function how they are distinguishable from other Ca-activated K channels. As far as the LTP section, find some sources on details of how SK channels are coupled to NMDA receptors and add a bit more to this section. Also, make sure to tag some of the other “lingo” that has a link to another wiki page (you did a pretty good job of this throughout the article, just don't miss any). Lastly, you have a good amount of sources. Good work! Ritterlb (talk) 21:15, 19 November 2012 (UTC)


 * Hey guys. First off, I really like your illustrations. They make the article easy to understand, and it breaks up the paragraphs well. Great layout and effort into making the design of your site attractive. I agree with the comment below mine that you guys need to elaborate more on the structure section of the article. Including amino acid sequences can never hurt, especially when you are talking about loops and transmembrane sections. Are these loops caused by a Proline or is there another unique secondary structure within these tail domains which cause these loops? This may explain more about the pore and the P-loop. In addition, I don't really like how you have a mix of paragraphs and bullet points in the Parkinson's disease section. You should pick a layout type and stick to it. Overall, this is a good article, and a lot of my comments are covered below by the other students. Take what they and myself say into consideration, and your article can be even better. Great job! Nucerop (talk) 22:12, 19 November 2012 (UTC)

Hey Guys. To start off, I really thought this article was well done. I thought it was great that you highlighted specific inhibitors and modulators of the SK channel as well as its role in long term potentiation and in Parkinson's disease so great job! As for my suggestions, I was thinking including more to the structure section of the article. You guys did a good job on it, but my suggestion for that section is that maybe, if possible, you can include specific amino acid residues that play an important role in the SK channel function. I saw that you included the GYGD amino acid sequence for the selectivity filter, but are there other important residues? Maybe there's not, but if there are, this would add to the structure section of your article. In addition, maybe obtaining a crystal structure of the channel will help as well. Also on the section of modulators, where (which residues) do each type of modulator interact with or do they all interact with the same residues? What is the action of the modulator exactly (mechanistically)? If possible, this would be great to show in this section. Overall, this is a really well done article. Keep up the good work! Agajulapalli (talk) 22:18, 16 November 2012 (UTC)

Hey guys, your article is very informative and has great diagrams. I think you could clarify a few things to make it easier to read for someone not as familiar with neuroscience. In the lead section you say “central neurons and other types of electrically excitable cells.” Do you mean neurons in the central nervous system? I think you should be clear if these are channels found in nervous tissue or whether they are found in just any cell membrane. You do a good job explaining this in the function section, maybe make the lead section more general. Also you say SK channels are involved in the mAHP but then don’t really explain what that is or why it's important. Later you mention the “production of m-AHP” in the Parkinson’s section and I wasn't sure if you were referring to the same thing. In the gating mechanism section you could add links to “voltage activated calcium channels” and “NMDA receptors.” In the function section you could introduce links to the different types of neurons that have SK channels. The gating mechanism and the structure sections also seem to cover some of the same information about the role of calmodulin binding the channel, maybe you could combine these since the structure section got pretty detailed on this while the gating section seemed to describe it generally. The discussion of experiments where the SK channels were blocked were interesting and informative and definitely helped me to understand their function better. That was good to do after identifying specific molecules that block the channels. Lastly I was a little confused in the Parkinson’s section about the SNc neurons. Maybe if you added a sentence that summarized what those are and sort of describe which symptoms of PD their degeneration leads to. Overall great job guys this is a very detailed and specific channel and your article covered it well.User:Dfarrell007 Dfarrell007 (talk) 22:17, 17 November 2012 (UTC)

Hi guys. I think you are off to a great start with this article. There are, however, a few minor changes and additions which you may want to consider. Like another commenter said, I would abbreviate and simplify your introductory paragraph. I think one of the strengths of Wikipedia is the brief description of each topic provided in the short introduction, and for this reason it might not be a bad idea to make the introduction section far less detailed. I would also recommend expanding the Function section. It seemed pretty vague and I found myself asking a few questions. How it the structural conservation important in terms of it function? How do SK channels affect excitability? These answers can, at least to some extent, be pretty straightforward to someone who has some background knowledge of neuroscience, but explicitly addressing these questions will surely make your article more comprehensive and robust. Lastly, I might consider expand upon the protein information box found in the top right corner of the article. Maybe add a crystal structure, ortholog information, or expression data, if any is available. All things considered, I think you guys did a great job. depaloj (talk) 17:49, 18 November 2012 (UTC)

Hey fellas, I thought your article was really well written. The sections talking about Structure and Gating Mechanisms especially were really specific and well-done. I thought the Blockers section too was really thorough and did well to highlight some of the (even minor) compounds that play a role in blocking the SK channels. It was good that you named the main players in the body of the paragraph, described them, and then proceeded to use bullet points to highlight the others; it really focused the attention of the reader on the main compounds while still making them aware of more minor ones. I have a few suggestions-- In the Parkinson's Disease section, you mention that dopamine excess in the synapse leads to mitochondrial damage involving free radical production. it might be helpful to include a sentence or two describing how this happens, since it isn't intuitive to know how the mechanism works and it may not be explicitly known by the reader. Also, in the few sentences after that, you describe TH+ and TH- phenotypes of the substantia nigra neurons. What do these phenotypes mean? This part of your article doesnt describe the phenotypes and isn't cited. The substantia nigra wikipedia page also doesnt mention these phenotypes. It might help to throw in a sentence or two describing what they mean. Overall, great work and I'm sure your final product will be excellent! Liber.mark (talk) 20:34, 19 November 2012 (UTC)

Peer Review - Marko
Excellent detail and organization overall. However, I feel that some more information regarding the discovery of this channel would be helpful. Was there a particular drug or other chemical compound whose mechanism and/or effects became the impetus for studies on structure and function of the channel, for example?

Also, does the SK channel play a role in long-term depression? (Long-term potentiation is mentioned; if there is a role in long-term depression, it would be interesting to see how the roles of the channel relate.)

Progress looks good! Marko Tkach (talk) 05:33, 19 November 2012 (UTC)