Talk:Long-term potentiation/Archive 1

message: I was reading some information on drugs used to increase the learning inside of animals that has to do with LTP. I don't exactly know too much about this subject since it seems somewhat brand new to me on a biochemical level. 
:Does anyone have information relating to the withdrawal effects on subjects that had taken in the drug? Did they show a lack of an ability to learn afterwards? What side effects did such a drug have? --Cyberman 17:56, 10 October 2005 (UTC)
thread_title:  Drug usage to stimulate and increase learning 

message: What is plasticity-related proteins? --Daxue | Talk 04:20, 8 Jan 2005 (UTC)
thread_title:  One question 

message: Hi there, I'm new to Wikipedia and stumbled across this article just the other day.  Are regular folks such as myself welcome to edit the main text of articles posted on the Wikipedia website?  If that is the case, what is the safegaurd against fraudulent information being posted?  As far as citing sources goes: How do we do it?  Forgive me if these questions are answered somewhere else on the Wikipedia website, it's just that an open source encyclopedia database is such a revolutionary concept that I am a little taken aback.
::Hey there!  And welcome to Wikipedia.  Yes yes yes!!!!!  You are not only welcome, but encouraged to edit the text of articles.  Go for it.  Be bold  The system is self-policing.  If someone vandalizes, writes fraudulent stuff, nonesense, factually incorrect statements, bad grammar  etc., someone else will edit it.
So have at it!  Synaptidude 00:23, 15 July 2005 (UTC)
thread_title:  Wikipedia???? 

message: I have several questions regarding the deliniation of LTP into two distinct phases:
1)  I understand that Early Phase LTP is the protein synthesis independent phase of LTP, meaning that the necessary components of synaptic plasticity are already present inside the cell.  Are the various receptor subunits already assembled into functional receptors that are awaiting shipment to the dendritic branches, or do they have to undergo some level of processing before shipment?
::LTP is expressed via the insertion of AMPA receptors into the extrasynaptic membrane and their subsequent diffusion into the postsynaptic membrane.  This happens too fast for synthesis, assembly or transport to be involved.  The receptors are preassembled in the ER, consitutively shipped to the dendritic spines where they are contained in recycling endosomes.  Upon the induction of LTP, they are simply translocated into the membrane.
2)  In reference to the aforementioned receptors/unassembled receptor subunits:  Where are these units stored in the cell?  What mechanism governs the release/transport of these units?  I understand that CaMK II and PKA facilitate the insertion of these new receptors into the membrane.  What I would like to know is how these receptors end up at the membrane in the first place?  
::This topic is still the subject of scientific investigation so the answers are not all known.  But what appears to happen is that the receptors are moved from intracellular recycling endosomes into the plasma membrane via a vesicle-dependent exocytosis (kind of like transmitter release, but this time, the cargo is receptors, and they are in the membrane of the vesicle, rather than in the lumen.
3)  Late Phase LTP is the protein synthesis dependent phase of LTP.  After receiving the necessary signals, transcription occurs and is immeadiately followed by translation and thusly protein synthesis.  Is it fair then to say that Late LTP serves mainly or perhaps solely to restock the neuron with the necessary components of plasticity?  If so would it be fair to say that Late LTP is really just a homeostatic mechanism, keeping the cell stocked with the materials that it needs to performs it's duties?  Do post synaptic changes occur as a direct result of L LTP or are the components of plasticity merely synthesized and left waiting for some later signal?
This is not really known, but it is believed that the protein synthesis is actually building new synaptic structure or new synapses.  Some of us think that much of the work ::on L-LTP is BS.
4)  How is it possible to activate E LTP but not L LTP?  Doesn't the fact that L LTP cannot be induced without first inducing E LTP support the argument that L LTP is a rebuilding process and not a discrete type of LTP?
::It is reported that E-LTP is induced by "weak" tetanus and L-LTP by strong.  But IMHO it doesn't all add up.  I personally believe that E and L are just different aspects of the same inseparable process.  However, if you want the party line, read Kandel
Synaptidude 21:35, 18 July 2005 (UTC)
thread_title:  Early and Late Phase LTP 

message: After further reading, I have some questions about the coincidence detector.  How does the removal of the Mg++ ion from the NMDAR channel serve as a coincidence dector?  If Ca++ is artificially inserted into the neuron will associative learning not take place unless the magnesium ion is also removed?
The more you can tell about this process the better.
Thank you for your assistance
::coincidence detector
:::In terms of finding a neuronal substrate for learning, you need some sort of coincidence detector.  Think Pavlov's dog.  The dog learned that a bell meant food was going to be delivered because the bell was presented in coincidence with the food until the dog learned the association.  So how could such coincidences be recognized by neural circuity?.  One proposal is the the NMDA receptor serves as the coincidence detector.  To understand this, you have to understand what TVP Bliss calls "The induction rule for LTP".  The induction rule says that you need two things to happen simulataneously for LTP to be induced.  Those two things are:  1) Binding of glutamate to the NMDA receptor, and 2) sufficient depolarization of the postsynaptic cell.
::::The reason that you need these two things to happen is because glutamate opens the gate on the NMDA receptor channel.  But current can't flow through the channel because it is magnesium blocked.  You also need sufficient depolarization to allow the magnesium to leave the channel. This allows other ions, in particular calcium, to flow through the NMDA channel.  The reason that depolarization "works" is because the magnesium binding site inside the NMDAR channel is even with the plane of the plasma membrane and thus, is acted upon by the electric field of the membrane.  When the membrane is depolarized, the electric field grows weaker and magnesium is not held as firmly in the channel, allowing it to escape.
::::The critical factor that induces LTP is the calcium that enters the cell through the NMDAR channel.
:::So the reason that this provides a coincidence detector is that it means that one synapse can help another synapse to potentiate.  If you have a strong LTP inducing stimulus on one synaptic input, it not only meets the induction rule for that input, but it also depolarizes the whole postsynaptic cell.  If a "weak" (i.e. not strong enough to induce LTP on it's own) input is activated at the same time, it releases glutamate onto it's own postsynaptic NMDARs.  The channel opens, and IF BY COINCIDENCE THE CELL IS ALREADY DEPOLARIZED BY ANOTHER INPUT then the weak input will meet the induction rule, and hence will potentiate.
::Back to Pavlov's dog.  What if the infomation of "food" (known is classical pavlovian conditioning as the US (unconditioned stimulus)) is carried on the strong input, and the information on the bell (the CS or conditioned stimulus) is carried on the weak input.  The bell means nothing to the dog, so the input remains weak.  But if the food is consistantly paired with the bell, the strong and weak inputs get activated together, and the neural system is able to detect the coincidence between them because the stong input helps the weak input to potentiate.
:See?    Synaptidude 00:20, 21 July 2005 (UTC)
thread_title:  coincidence detector? 

message: Plasticity
I know that plasticity refers to the altering of connections between neurons, i just want to make sure that i understand all the different forms that plasticity can assume:
insertion of new receptors
phosphorylation or movement of old receptors to increase efficacy
increased dendritic spines and branching
did i miss anything??
Plasticity in the larger sense of biology means any change in a system that can be brought about by interaction of that system with it's environment.  Synaptic plasticity refers specifically to changes that can occur at synapses in response to the environment, usually in response to synaptic electrical activity.
new receptors, old receptors, spine morphology etc, are aspects of plastic mechanism, but the term "forms" of plasticity, it is usually taken to mean a higher level.  Forms of plasticity would be LTP, LTD, PPF, PTP, depotentiation, etc.  The things you mention are mechanisms that might underly those forms of plastcity.  For LTP, it is thought to be mainly movement of AMPARs into the membrane, while LTD is their removal.  Phosphorylation it thought to be a trigger for the receptor trafficking.  Spine and branching morphology changes are though perhaps to mediate longer slower forms of synaptic plasticity.
Synaptidude 00:41, 15 August 2005 (UTC)
thread_title:  Quick question 

message: Hi guys, great effort, great job! Just a remark I came across right now about the confusion of the terms cooperativity and associativity, both claimed to be different properties of LTP.
Well, Bruce McNaughton, an electrophysiologist who contributed largely to the field and introduced the term "cooperativity" claims that to be the source of still ongoing confusion as for: there is no difference between cooperativity and associativity. The same occurs in your description of NMDA-receptor-dependent LTP and carries on with this. I think it's worth a fusion to stop muddling. 
Have a look at the references.
PMID 12740107
Bye, Tobi.
Associativity and cooperatively with regards to LTP are usually used to denote slightly different aspects of LTP, although both have the same underlying mechanism.  Associativity is used to describe how one set of inputs can provide postsynaptic depolarization to another set of input to allow the induction of LTP in the second set. In other words, the association of a strong input and a weak one allows induction in the weak one.  Cooperativity is usually taken to mean the number of axons within a given input that must be activated to get LTP at all.  A few axons do not sufficiently depolarize the postsynaptic cell to induce LTP.  It takes the simultanous activation (the coorperative activation) of many to get LTP.
In both cases, it is sufficient depolarization of the postsynaptic membrane potential to allow the unblocking of the NMDAR (by magnesium) that is the underlying mechanism.
So, they are the same thing, but usually taken to mean different aspects of the same thing.
Synaptidude 00:36, 15 August 2005 (UTC)
thread_title:  Cooperativity vs. associativity 

message: Just wanted synaptidude and all others who contribute to wikipedia for the awesome job you guys are doing explaining some fairly complex topics....thanks
::ya'welcome! Synaptidude 18:35, 10 October 2005 (UTC)
thread_title:  Thanks 

message: I have read much of the role of CREB 1, that it is activated by the active subunits of PKA and that it goes on to regulate gene expression, my question is this:  Have researchers pinpointed which genes are transcribed or what the end product proteins do inside the neuron?  I understand that these genetic products relate to synaptic plasticity but exactly is produced?
::The answer, for the most part, is 'no'.  Experiments using gene arrays to capture and identify mRNAs produced, increased, or decreased after LTP have been failures.  This is probably because brain tissue is so heterogeneous that the number of cells that have actually undergone LTP is very small compared to the number of cells in the tissue (e.g. Glia make mRNA, but are (probably) not involved in LTP.). There are lots of gene products that increase after strong activity (the early-immediate genes), but the role of these is unclear and they don't require LTP, only activity.Synaptidude 18:24, 10 October 2005 (UTC)
thread_title:  The role of CREB 1 

message: The definition of associative LTP was dead wrong, so I corrected it. January 27, 2006.
:For the record, I think you misinterpreted that section as defining "associativity" as it pertains to LTP. Sorry for the confusion. My original intent was to distinguish between the associative LTP that occurs at CA1 synapses and the non-associative LTP that occurs in the mossy fiber pathway. I no longer see that as an important distinction that needs to be on this page, so it's since been removed. --David Iberri (talk) 17:37, 9 April 2007 (UTC)
thread_title:  Definition of Associative LTP 

message: I googled that Tim Bliss was a co-discoverer of LTP, and included him in the sentence about the discovery in 1966, but now I have doubts. If I was wrong, -revert my change. --CopperKettle 04:36, 12 August 2006 (UTC)
replies: text: Most researchers I've spoken with (which admittedly isn't many) seem to regard Bliss as a co-discoverer, but they base that on the 1973 Bliss & Lomo paper that first characterized LTP. But based on Lomo's recent paper on the discovery of LTP, I'm fairly certain that Lomo made the initial discovery by himself in 1966, with Bliss joining the Andersen lab only in 1968. I'll revert your change for now, but feel free to continue the discussion here. --David Iberri (talk) 14:03, 12 August 2006 (UTC)
thread_title:  Am I right to include Timothy Bliss as a co-discoverer? 

message: This one's just screaming to be added to the "relationship to behavioral memory" section:  --David Iberri (talk) 04:28, 15 January 2007 (UTC)
replies: text: Done, although it could use some refining. --David Iberri (talk) 19:26, 5 February 2007 (UTC)
thread_title:  Behavioral memory 

message: recently added a brief description of hippocampal connectivity. It's good, but doesn't currently relate enough to LTP, so I've removed it for the time being and copied it here:
:Located in the temporal lobe, the hippocampal formation is a specialized region of the limbic cortex. Believed by scholars to be associated with learning and memory, the hippocampal formation receives its primary input from the entorhinal cortex. The axons of these neurons then pass through the perforant pathway and go on to form synapses with granule cells located in the dentate gyrus.
I can see this being used in a section on LTP experimental design, which might describe why the hippocampus was used in early studies, why it is important to memory in general, and why it is important to LTP specifically. The answers to all these questions have to do with hippocampal function, which is so deeply tied to its anatomy that such a section would merit a description of the latter. Cheers, David Iberri (talk) 15:49, 10 April 2007 (UTC)
thread_title:  Hippocampal anatomy 

message: *The caption of the first image is too long, it is longer than the introduction!
*Reference 23 is missing.
*Adding more "Main article" links in subsections would help guide readers to other relevant articles.
Hope this helps. TimVickers 04:49, 11 April 2007 (UTC)
replies: text: Definitely helpful; thanks. I've tightened the first image caption, moving the bulk of the text to :Image:LTP exemplar.jpg. I've also fixed the oversight in ref 23 -- thanks for catching it. I agree about the main article links; I'm starting a Retrograde signaling in LTP section as a start (haven't submitted it yet, though). Any additional comments are much appreciated! Cheers, David Iberri (talk) 06:59, 11 April 2007 (UTC)
thread_title:  Comments 

message: hwo long does LTP last?
:This is covered in the introduction to the article. --David Iberri (talk) 18:59, 27 May 2007 (UTC)
thread_title:  Duration 

message: Awesome article.  Can someone craft the last paragraph in "Late Phase" to be a bit more pedestrian?  I'm a bit lost.
http://en.wikipedia.org/wiki/Long-term_potentiation#Late_phase  —Preceding unsigned comment added by 76.22.5.47 (talk) 02:13, 2 September 2007 (UTC)
replies: text: I took a look at that section and noticed that there's quite a bit on synaptic transmission mentioned there. But as the basics of transmission are covered in the background section, I'd imagine that's not too far out of the scope of this article. Are there specific points you'd like to be clarified? --David Iberri (talk) 03:45, 3 September 2007 (UTC)
thread_title:  Late Phase Clarification 

message: Other comments: on the lede. There are a couple of inconsistencies that bother me. Sentence 1 says LTP lasts minutes or hours vs. Later in same paragraph LTP has to do with long-term memory
Sentence 1 says minutes or hours vs. paragraph 2 says years. DCDuring 11:37, 6 September 2007 (UTC)
replies: text: There's a distinction drawn between LTP observed in vitro (done in hippocampal slices, cell cultures, etc.), and LTP in vivo (observed in living animals). In vitro studies have only been able to demonstrate LTP that lasts up to several hours, while in vivo studies have observed LTP lasting for many months. --David Iberri (talk) 11:50, 6 September 2007 (UTC)
thread_title:  Inconsistencies 

message: In light of the recent discussion about overcomplexity of the lead, the lack of continuity between it and the main article body, etc., I've rewritten the lead mostly from scratch. I wound up dropping the paragraph on in vitro and in vivo observations (which unfortunately was the only spot that mentioned a difference in duration between LTP in vitro and in vivo), but this will be added in elsewhere, and shortly. I took some care to be upfront about the mechanisms of enhancing synaptic strength, and what it means to improve the strength of a synapse. Hopefully this is a step in the right direction. Comments welcome. --David Iberri (talk) 02:00, 20 September 2007 (UTC)
thread_title:  Lead rewrite 

message: I've got a question about the assertion that PKMζ inhibitors cause "Retrograde Amnesia" in the paragraph about Late-LTP. Shouldn't this be anterograde amnesia? Otherwise we should be talking about an inability to recall memories with the inhibitors. TDumbarton (talk) 20:55, 18 November 2007 (UTC)
replies: text: We are talking about an inability to recall memories after adminitering the PKMz inhibitor. That's exactly what the section on L-LTP maintenance is trying to convey. The gist is that PKMz is necessary/sufficient for maintenance of L-LTP and the persistence of long-term memories. PKMz inhibition interferes with the persistence of memories resulting in loss of established long-term memory: retrograde amnesia. It's important to distinguish between the acquisition of memory and the persistence of memory. PKMz appears to have no role in the acquisition of memory, only its persistence. Inhibiting PKMz does not interrupt memory acquisition, so it does not cause anterograde amnesia. See also . --David Iberri (talk) 16:18, 21 November 2007 (UTC)
thread_title:  PKMz and retrograde amnesia 

message: This article is very well written, well referenced, and meets all of the Good Article criteria. I'm almost at a loss as to make suggestions on how to improve it, though there are a few areas that could use some additional citations (e.g. the last 2.5 paragraphs of 'Synaptic tagging' -- "There is some evidence...", and 'Relationship to behavioral memory'). Other than that, this article is excellent. Good work! Dr. Cash (talk) 17:27, 9 December 2007 (UTC)
replies: text: Sweet. Thanks so much for reviewing this, Dr. Cash. I'll see about adding some more references for the sections you mentioned. Thanks again, David Iberri (talk) 00:09, 19 December 2007 (UTC)
thread_title:  GA Review 

message: Surprised this isn't mentioned or cited:
Si, K. et al. (December 26, 2003). A neuronal isoform of CPEB Regulates local protein synthesis and stabilizes synapse-specific long-term facilitation in Aplysia. Cell, Vol. 115, 893-904.
Quick review:
http://psychologyreview.blogspot.com/2008/02/neuronal-cpeb-stabilizes-synapse.html
--128.208.35.237 (talk) 21:52, 12 February 2008 (UTC)
thread_title:  Recommended addition of synapse-specific LTF topic 

message: I don't agree with the first property of Rapid induction. There are no references and the description sounds very much like Posttetanic Potentiation (PTP). PTP is distinctly different from LTP (please refer to Principles of Neural Science, Kandel and Jessel). PTP can last up to about an hour but is not LTP since though it is Ca2+ mediated, it does not involve phoshorylations or Kinases. As is my understanding, firing a high frequency volley through a neuron cannot IMMEDIATELY set up a LTP. It takes a couple of seconds for the cascades to work... at the bare minimum. PTP however is immediate, since it functions on residula Ca2+ from the last stimulation. 
User: Mubinchoudhury  —Preceding unsigned comment added by Mubinchoudhury (talk • contribs) 11:19, 6 May 2008 (UTC)
replies: text: Thanks for the input. By all means, be bold and correct the article (providing relevant references, of course) as you see necessary. Much thanks, David Iberri (talk) 23:32, 6 May 2008 (UTC)
thread_title:  Properties of LTP 

message: I'm doing my PhD on LTP, and even I can't get my head around this section. The intro is supposed to be the easiest to read, but right away it lists 6 different stages of LTP. And it goes into painful detail on the chemical processes. First off you can't expect to describe both Schaffer collateral LTP and mossy fiber LTP in one section. it's too complicated. Secondly, The Early Phase: Induction sections jumps right into the calcium concentration. Perhaps some insight into the NMDA receptor as a coincidence detector should be given. A good way to start would be something like this "There are two types of receptors on the postsynaptic dendrite: AMPA receptors and NMDA receptors. Both are activated by neurotransmitters, but the NMDA receptor is blocked by a magnesium blockade. This can, however, be disloged if the dendrite is sufficiently depolarised (made more positive). The dendrite can be depolarised by this, that and the other thing. Once this, that, and/or the other thing removes the magnesium blockade, the neurotransmitters can can finally activate the NMDA receptor. This will allow a huge amount of calcium in. This calcium influx is what is principally involved in bringing about LTP". Something like that should be in the intro, so the reader has at least the foggiest idea of what is going on :-) Paskari (talk) 18:26, 1 July 2008 (UTC)
thread_title:  Mechanism section poorly worded 

message: I have never fully understood this because of the loose wording of most scientists. I can't tell if, once the magnesium blockade is dislodged (due to membrane depolarization because the AMPA receptors allowed sodium in), the NMDA receptor automatically lets calcium in (since it is voltage activated), or if once the magnesium is dislodged, glutamate must still bind to the NMDA receptor to allow it to open and let calcium in. I think it's the latter for two reasons. First of all, what is the purpose of making the NMDA receptor ligand activated, if the threshold which dislodges its magnesium blockade also activates it (is the NMDA receptor actually voltage activated, or is it loosely referred to as such since increases in voltage dislodge its magnesium blockade?). Secondly, for the purposes of LTP, it would conflict with input specificity, since neighbouring regions might depolarize the spine and remove its blockade. If calcium immediately flowed in, then that spine would undergo LTP, even if it received no neurotransmitters. This line from the section on induction of E-LTP is equally as vague "Sufficient depolarization through the summation of EPSPs relieves the magnesium blockade of the NMDAR, allowing calcium influx." Paskari (talk) 18:36, 1 July 2008 (UTC)
replies: text: I found an answer to my question, and I'm going to go ahead and include it. As it turns out, glutamate must still bind to the NMDA receptor, even after the magnesium has been dislodged. Paskari (talk) 15:29, 6 July 2008 (UTC)
replies: text: I updated the section, but I didn't cite my sources (because it seems like a headache to do). I am trying to learn how to do it, please don't delete anything yet. Also there is some confusing terminology I used, so for example, in one sentence I said "...AMPA receptors and NMDARs", I personally don't like the terminology NMDARs, but I definitely wasn't going to go back and change all the "AMPA receptors" to "AMPARs", or "NMDARs" to "NMDA receptors". I'll leave that to someone else ;-) Paskari (talk) 15:56, 6 July 2008 (UTC)
thread_title:  Property of NMDA receptors 

message: Another issue scientists are notorious on is downplaying the permeability of AMPA receptors towards calcium, but making a big deal out of NMDA permeability to calcium. For example, on page 130 of Neuroscience (Purves et. al. 2008) it reads
all ionotropic glutamate receptors [NMDA, AMPA, and Kainate] are non selective cation channels...allowing the passage of Na and K, and in some cases small amounts of Ca.
Then two sentances later it says
NMDA receptors have especially interesting properties...[their] ion channels allow the entry of Ca in addition to monovalent cations such as Na and K.
It seems as if it's reiterating the previous statement at best, and down playing the role of AMPA and Kainate receptors at worst. Paskari (talk) 18:49, 2 July 2008 (UTC)
replies: text: Turns out, the AMPA receptors are parmeable to calcium, but their contributions to the calcium concentration are negligable. Paskari (talk) 15:44, 6 July 2008 (UTC)
thread_title:  Permeability of NMDA Receptor 

message: Although silent synapses are not included in this section, they prove my point that NMDA receptors are never properly described. Basically silent synapses are post synaptic spines covered in both NMDA receptors and AMPA receptors, however the AMPA receptors are inactive. Therefore, only the NMDA receptors can let ions in. But NMDA receptors are blocked at rest (by magnesium), so they can't allow ions in, until the AMPA receptors let ions in so as to depolarize the membrane potential (and dislodge the magnesium). See the Catch 22? The only other scenario is if the surrounding synapses contribute to depolarizing the said synapse. This is what I really want to see addressed in this article, an air tight explanation of how LTP works. Thanks Paskari (talk) 14:29, 3 July 2008 (UTC)
replies: text: I agree that silent synapses may deserve passing mention here, but why do you think they must be invoked to explain LTP? Also, there is no self-respecting, legitimate neuroscientist who could claim to have an "air tight" explanation for LTP's mechanism. --David Iberri (talk) 11:45, 8 July 2008 (UTC)
thread_title:  Silent Synapses 

message: As far as I'm aware LTP has been shown to work both inside an animal and inside a lab, but has it ever been proven to be naturally occuring, or is an artifical tettanus always applied? Basically is LTP a mechanism synapses are capable of exploiting or has it been proven that synapses do in fact exploit LTP in vivo? Paskari (talk) 17:05, 6 July 2008 (UTC)
replies: text: This is mentioned in the article, specifically under the Relationship to behavioral memory section. --David Iberri (talk) 11:46, 8 July 2008 (UTC)

text: I agree, and have made the following changes: . --David Iberri (talk) 14:54, 3 October 2008 (UTC)
thread_title:  in vivo vs. in vitro 

message: Here's a nice article discussing LTP in the context of addiction:
*
--David Iberri (talk) 12:37, 7 November 2008 (UTC)
thread_title:  Addiction 

message: Is this why rapid flashes of light appear in TV ads?
:This phenomenon, whereby a high-frequency stimulus could produce a long-lived enhancement in the postsynaptic cells' response to subsequent single-pulse stimuli, was initially called "long-lasting potentiation"
-75.145.87.233 (talk) 02:45, 29 July 2009 (UTC)
replies: text: See Subliminal message for a possible correlation with your idea. --Ancheta Wis (talk) 03:04, 29 July 2009 (UTC)
replies: text: As far as I know, that has nothing to do with LTP, though. Looie496 (talk) 15:30, 29 July 2009 (UTC)

text: Subliminal is a one-shot image. Rapid flashes seems to resemble "high-frequency stimulus". Why would that have "nothing to do with LTP"? - 75.145.87.233 (talk) 04:43, 30 July 2009 (UTC)
replies: text: The reason for using a high-frequency train of pulses in LTP is that a single pulse, however strong, would only activate synapses one time.  To get LTP, it's necessary to have multiple activations within a short time window.  A continuous visual stimulus produces as much activation in most brain areas as a flashing stimulus, so flashing wouldn't be associated with greater LTP except in change-sensitive parts of the brain.  In short, the resemblance of the two situations is only superficial. Looie496 (talk) 15:37, 31 July 2009 (UTC)
replies: text: I don't perceive the distinction. Rapid flashes of light would seem to qualify as "multiple activations within a short time window". What is "a continuous visual stimulus"? Must it be moving? A painting may be a continuous visual stimulus. It doesn't move, yet it may provoke an emotional response. But in general, paintings don't have such an effect. PBS often shows old photos by zooming and panning them while making them flicker. Why do that? What are the "change-sensitive parts of the brain"? Wouldn't advertisers want to target them? Isn't that the point of advertising, to change behavior; as permanently as possible? Wouldn't LTP be a helpful tool for advertisers? Might they not achieve it with rapid flashed of light? - 75.145.87.233 (talk) 00:47, 1 August 2009 (UTC)
replies: text: LTP is only "helpful for advertisers" insofar as it appears to underlie learning, memory, and other cognitive domains. It probably gives rise to all sorts of phenomena, including associative learning, habituation, classical conditioning, etc. One can certainly capitalize on these traits to change human behavior, but this is not done by directly accessing LTP. This may be difficult to grasp, and understandably so. The crucial bit is that LTP is a phenomenon observed at a cellular and synaptic level, not a behavioral one. --David Iberri (talk) 23:51, 2 August 2009 (UTC)
thread_title:  (ab)use by advertisers? 

message: I am not happy about the use of "nonHebbian". I would prefer to use the term "Hebbian" for any learning rule that alters strengths as a function of both pre-and post-synaptic activity. Thus your "antiHebbian" would still be Hebbian. One would then use "nonHebbian" for cases where learning depended on just the presynaptic, or just the postsynaptic, signal. ab is the product of a and b, but -ab is not the "antiproduct" of a and b - it's still a product, albeit of a and -b
Possibly one could say that the classical Hebbian rule is pre before post strengthens, and if it weakens instead it is still Hebbian, but in a more generalised sense. 129.49.104.32 (talk) 20:43, 25 November 2009 (UTC)
replies: text: Regarding your first point, the usage of anti-Hebbian for synapses that weaken is universal in the literature as far as I know, so I don't see how we can depart from it.  Regarding your second point, I think that you should feel free to fix the problems you see in the article, if you think you can. Looie496 (talk) 22:49, 25 November 2009 (UTC)
thread_title:  Hebbian vs. anti-Hebbian 

message: Is it possible for anyone to add the relationship between STDP and LTP to the article? I'm no expert (yet!) but I'd try to help out.. thanks --The.Filsouf (talk) 23:47, 1 January 2010 (UTC)
thread_title:  Spike timing-dependent plasticity? 

message: The article presents contradictory information about the role of protein kinase Mz (PKMz). It states:
# PKMz underlies the maintenance of E-LTP, even though there is no mention of PKMz being activated in the induction phase of E-LTP
# PKMz underlies the maintenance of L-LTP and is not required for E-LTP.
It seems most likely that PKMz is active in L-LTP and not in E-LTP, especially since the cited article makes no mention of PKMz. If that is the case, what is the mechanism for maintenance of E-LTP?
140.180.35.44 (talk) 16:37, 10 October 2010 (UTC)
replies: text: According to this review, you are right that it is involved in late but not early LTP.  I'm not sure that early LTP needs to be maintained, as by definition it decays if not consolidated into late LTP. Looie496 (talk) 17:25, 10 October 2010 (UTC)
thread_title:  Contradictory information about PKMz 

message: Is the inclusion of Cajal necessary in this article?  There are several inaccuracies in the characterization of his contribution.  Notably he did not predict or theorize about information flow or memory storage at synapses, indeed the term synapse had not even been coined at the time of his Croonian lecture. Cajal did muse about the elaboration of the dendritic tree with time.  This should be taken in context of Forel's and Cajal's work in developing animal where connections are comparatively sparse relative to the adult.  Cajal was not speculating about learning in the adult animal, he was commenting on the increasing complexity of dendritic trees during development.  Cajal also never recognized the spines as sites of contact between neurons.  —Preceding unsigned comment added by 99.240.130.52 (talk) 04:25, 17 October 2010 (UTC)
replies: text: Please feel free to make improvements in the article, which is not being very actively maintained. Looie496 (talk) 05:24, 17 October 2010 (UTC)
thread_title:  Inclusion of Ramon y Cajal