Talk:Long-term potentiation

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Wiki Education Foundation-supported course assignment

File:Sciences humaines.svg This article was the subject of a Wiki Education Foundation-supported course assignment, between 20 April 2020 and 20 July 2020. Further details are available on the course page. Student editor(s): Lowt2.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 02:49, 17 January 2022 (UTC)

Should CILTEP redirect here?

Should CILTEP redirect here? — Preceding unsigned comment added by Ocdcntx (talk • contribs) 22:33, 26 January 2015 (UTC)

LTP loss in Alzheimer's

Human cellular prion protein (PrPC) is able to bind up to 5 Cu2+ ions at [fentamolar] via its octapeptide repeats, inducing a dramatic conformational change that permits the binding of PrPC to the GluN1 subunit of NMDA receptors (NMDARs). This interaction reduces NMDAR affinity for the co-activators Gly and D-serine. Gly/D-serine inordinately retard the desensitisation kinetics of NMDARs in a concentration-dependent fashion, leading to overactivation and excitotoxicity via excessive Ca2+ influx. By reducing Gly affinity, Cu2+ bound PrPC ameliorates NMDAR overactivation by reducing Gly-induced non-desensitising currents, permitting normal receptor desensitisation following bouts of activity. In Alzheimer's, the cytotoxic amyloid-beta oligomers produced from the incorrect cleavage of the APP protein bind to PrPC, preventing its interaction with Cu2+ and subsequent association with NMDARs. The loss of NMDAR modulation through this mechanism may be one of the primary reasons why LTP is hampered in Alzheimer's disease. NMDAR overactivation results in Ca2+-mediated excitotoxicity due to a complete loss of homeostasis regarding calcineurin, CaMKII, calpain, caspase, protease, lipase and endonuclease activity, resulting in cellular necrosis. The loss of LTP explains the poor short-term memory function of AD sufferers, while the neuronal death from excitotoxicity explains the eventual failure of their long-term memory as strengthened synapses are obliterated, both of which can be explained by amyloid-beta dependent inhibition of PrPC. Of course, other factors do play a part in Alzheimer's, but this one seems to link NMDARs, synaptic dysfunction, short-term/long-term memory loss and glutamatergic cellular death within the cerebral cortex and hippocampus. I've been doing a lot of research into AD, Parkinson's and other neurodegenerative diseases, from a proteomics, as well as the memory dysfunctions aspects of the diseases. Just thought you might be interested in this given your interest in LTP and, presumably, memory. Spcroft (talk) 13:21, 21 July 2013 (UTC) Shaun

Citation for Associativity

Here is an exact source for the quote about Associativity. In fact it is directly copied-and-pasted from this textbook. I would add it myself, but the page is semi-locked, and so I can't. Also, I don't know how to properly cite references. Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. Long-Term Synaptic Potentiation. Available from: https://www.ncbi.nlm.nih.gov/books/NBK10878/ — Preceding unsigned comment added by Jordandc428 (talk • contribs) 00:01, 14 December 2016 (UTC)

GA concerns

After reviewing the article, I am concerned that it no longer meets the GA criteria because much of the article is uncited. Is anyone willing to address this, or should this go to WP:GAR? Z1720 (talk) 19:25, 5 July 2024 (UTC)

GA Reassessment

{{Wikipedia:Good article reassessment/Long-term potentiation/1}}