Talk:Long-term potentiation
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[edit] Hebbian vs. anti-Hebbian
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)
I would also like to comment on the statement above: "it should be explained that input specificity arises from the narrow spine 'neck' which enables the bulbous compartment to act independently by preventing CamKII from spreading to neighbouring dendrites". I thin it would be better to drop the specific reference to CaMKII : the narrow neck does ensure high specificity, but by reducing the spread of ANY second messengers, not just CaMKII. In fact, my guess is that preventing the spread dof Ca is far more important than preventing the spread of CaMKII (which does not mean this does not spread.
More generally, it must be a real headache for the authors of this vital article to be simultaneously clear, succinct and correct, and on the whole they do an admirable job. Different experts will differ on which aspect is really important, and only time will tell. But insofar as details may not be highly relevent, they should be eliminated. 129.49.104.32 (talk) 20:54, 25 November 2009 (UTC)
- 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)
[edit] Spike timing-dependent plasticity?
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)
[edit] Contradictory information about PKMz
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)
- 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)
[edit] Inclusion of Ramon y Cajal
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)
- Please feel free to make improvements in the article, which is not being very actively maintained. Looie496 (talk) 05:24, 17 October 2010 (UTC)
[edit] about Inhibitory avoidance section
can i remind whoever wrote that, or an experienced editor, that the majority (i assume all from this article) of research on LTP has been done on the hippocampus. is it a coincidence that the results were all about memory and spatial navigation and memory? what would happen if we would investigate it elsewhere? it seems like LTP however much sense it makes as physical components of memory, could have implications elsewhere. if anyone could help enlighten me on this topic please do. 161.76.137.146 (talk) 05:51, 23 November 2011 (UTC)
- LTP has been suggested as the mechanism behind certain chronic pain conditions, but I'm not sure how far advanced that theory is. --Anthonyhcole (talk) 08:44, 23 November 2011 (UTC)
