User talk:Kitra101

Wow, thanks for the thorough info, sorry for the mistake! Guess I forgot scientists have a sense of humor sometimes ;) Anyways, thanks for correcting the article and being kind about the error, where others might have gotten offended. Peace, delldot talk 19:41, 12 May 2007 (UTC)[reply]

Well, all I have is an undergrad, and I did my undergrad thesis on excitotoxicity, which is only vaguely related, so I can't claim to be an expert by a long shot. But judging from vaguely-recalled neurobio and cognitive psych classes, I think you're on the right track. I't s sort of the "use it or lose it" principle. The more a given path is used, the stronger it gets. Here's what Principles of Neural Science has to say about it:

activation of the NMDA receptor leads to activation of calcium-dependent enzymes and certain second messenger-dependent protein kinases in the postsynaptic cell... These biochemical reactions are important for triggering signal transduction pathways that contribute to certain long-lasting modifications in the synapse that are thought to be important for learning and memory... Because NMDA receptors require a significant level of presynaptic activity before they can function maximally, long-term synaptic modification mediated by the NMDA receptor is often referred to as activity-dependent synaptic modification.

Sort of frustratingly vague. As for the question "what does the strength of a synapse have to do with storing data," I'm not really sure, I had always just assumed that the firing of the neuron is directly linked to the retrieval of the info, so the stronger you make the synapse the more accessible the info is. You probably know everything in Hebbian theory but you may want to give it a look. I was skimming Chapter 63 in Principles of Neural Science, which is about the subject, to try and get a clue, but so far no direct answer to your question. I'll let you know if I stumble across something or if I run into my old neurobio professor. Peace, delldot talk 20:19, 12 May 2007 (UTC)[reply]

Ah hah! Ground I'm firmer on.

1. In ischemia, cells run low on O₂ and thus the ability to produce ATP (plus other processes are going crazy using up ATP), so the ATP-dependent Na and K pumps fail (they're either directly ATP-dependent or they're dependent on a gradient that's dependent on ATP). Since the pumps that maintain the membrane potential fail, the cell's flooded with Na⁺, and it depolarizes. This opens the VGCC's. Ca²⁺ rushes in, depolarizes the membrane further, and it's all downhill from there.

2. Mitochondria in neurons undergoing excitotoxicty are disturbed for a number of reasons. For one, they're charged with bufferring a lot of that excess Ca²⁺ in the cell, and that depolarizes them and kicks off a lot of processes within them. One result is mitochondrial permeability transition, which can lead to release of cytochrome c and possibly apoptosis in a process that I think looks a lot like the intrinsically mediated pathway (Some think mitochondria swell and rupture, while others think cyt c is released through some pathway). Whether the classic form of intrinsic apoptosis takes place too i'm not sure. In an insult like ischemia or TBI, cells that are less injured (e.g. those in the ischemic penumbra in the case of stroke) tend to die by apoptosis, while the more severely injured (e.g. those in the ischemic core in stroke or at the site of injury in TBI) tend to die by necrosis.

3. When you say negative feedback, do you mean some compensatory mechanism that's naturally in the cell? Or treatments? As for the cell, all I know of is positive feedback, which is why everything goes so haywire (Ca rushes in, VGCC's open, repeat). Here's what I know about treatment: In the '90's everyone was really excited about neuroprotective drugs that might block excitotoxicity by blocking glutamate receptors, and they worked well in animal and cell culture models, but that ended up being a pretty catastrophic failure when they got to clinical trials, since most patients ended up the same or worse off on the drugs. The thing seems to be that since glu receptors are so ubiquitous and (as you brought up) important for normal function like memory, you can't just block them without serious (e.g. psychotomimetic) side effects. There are also tons of other strategies that are being considered or tried for treating excitotoxicity: canabinoid agonists, calpain blockers, AMPA inhibitors, GABA agonists, preventing glu release, hypothermia, pretty much anything you can imagine. With varying levels of success, nothing mind-blowing yet. IMHO, they should refine clinical trials and try drugs that gently modulate NMDARs, rather than blocking them completely.

By the way, when I was working on my thesis, I found that if I emailed the author of a paper I liked, I got an answer to my question about 1/2 or 2/3 of the time, so you might try that with some of these questions. But that was fun! Give me more! Peace, delldot talk 21:16, 12 May 2007 (UTC)[reply]

Well aspartate also stimulates NMDARs, the big culprit behind excitotoxicity. According to Aspartame controversy, "approximately 40% of aspartame (by mass) is broken down into aspartic acid." (Though you can never trust that wikipedia, did you know any random person can edit that? ;) ) That could explain why it would induce excitotoxicity if you injected it directly into the brain, but I'm not so sure about the question of whether it's a danger in food, since I've never seen a satisfying explanation as to how the stuff would get across the blood brain barrier (same with MSG) except in infants and children whose BBB's aren't as fully formed, or maybe someone with an infection or injury that compromised the BBB. Good luck on the exam! Peace, delldot talk 03:30, 14 May 2007 (UTC)[reply]

Not as strongly as glu, but yes it stimulates them. See for example [1]. Maybe I better go add that little fact to those articles! How'd you do on your exam? Peace, delldot talk 04:15, 16 May 2007 (UTC)[reply]

Unfortunately, I don't know the answer to any of those questions. Yeah, the hippocampus is very very NMDAR dense, hence its sensitivity to TBI and other insults, but I don't recall hearing anything either way about cholinergic neurons. And I know next to nothing about the anterior cingulate gyrus.

The way talk page posting usually works on WP is you create a new section for a new topic, but to continue posting in the old section for the same topic. I actually like people to post new comments at the bottom of my page, because I'm paranoid that if I get two messages in a row, I'll only notice the last one if the second-to-last one is not near the bottom of the page. But it's up to you. By the way, I'd suggest not removing old comments but rather posting below them; that way others can follow the conversation and it's easier to find old info if you need to look back through it. I frequently find myself needing to follow up on old posts or whatnot and it's helpful to have them there in the talk page or its archives. Anyway, sorry I can't be more help with this round of questions! Did you try looking at anterior cingulate gyrus? (Though frequently with more obscure medical and neurobio topics, WP is less than optimally helpful...) Peace, delldot talk 16:52, 17 May 2007 (UTC)[reply]

Re Question

I think the edits I do should speak for themself. So, no need to post it. If you're just curious look at the things I've edited and you can figure it out quite easily. Nephron T|C 06:20, 28 May 2007 (UTC)[reply]

Ipecac/Family guy

Hi there, I did watch the clip and I agree it was funny (like most family guy episodes), however, it's a bit pop culture/triva and therefore probably not really very encyclopedic which is why I removed it. Cheers Mr Bungle 01:05, 31 May 2007 (UTC)[reply]

Featured article candidate: Black Death

I appreciate you're acting in good faith but it really is best if featured articles are nominated by people who have worked closely on them. This way they can give reasoned replies to reviewers and be familiar with the sources to make any suggested improvements. Someone who hasn't worked on the article can't provide this input, so the FAC rumbles on until the opposes become so overwhelming that the article is failed, taking a lot of reviewers' time. We are desperately short of reviewers and it's a disheartening process for nominator and reviewer alike to see the "opposes" pile on. In the meantime, I strongly recommend that you withdraw the article from the featured article process. This is quick and easy: you merely type "withdraw" on the article's FAC nomination page and sign. All the best, --ROGER DAVIES ^talk 21:26, 1 June 2008 (UTC)[reply]

WikiProject Medicine/Dermatology task force

I wanted to know if you (or any friends of yours) are interested in dermatology, and would be willing to help me with the WikiProject Medicine/Dermatology task force? Kilbad (talk) 03:00, 18 October 2008 (UTC)[reply]

So what field of medicine are you going into? kilbad (talk) 20:44, 4 November 2008 (UTC)[reply]

Help with dermatology-related content

I am looking for more help at the dermatology task force, particularly with our new Bolognia push 2009!, history of dermatology, or list of dermatologists pages? Perhaps you would you be able to help us? I could send you the login information for the Bolognia push if you are interested? ---kilbad (talk) 16:57, 26 November 2009 (UTC)[reply]

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