Talk:Synaptic plasticity

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One more Kandel praise page

The section "Biochemical mechanisms" starts - once again - with praise to Eric Kandel. Granted, he has contributed a lot and won a Nobel price for the field, but studying synaptic plasticity is - like almost all science - still a group effort. This is demonstrated e.g. by the fact that the cited paper doesn't even list him as a co-author! (Btw. he also has only one and not several "laboratories" as implied in the text). Many neuroscience related articles on Wikipeadia sound like he invented the field - which he didn't. I sometimes wonder what the other 39999 members of the Society for Neuroscience do all day long and can't help but wonder WHY his name comes up so frequently. —Preceding unsigned comment added by 146.203.21.90 (talk) 21:02, 18 October 2010 (UTC)[reply]

I agree with this comment - it's something that jumped right out me. Kandel has made major contributions to the field, but not very much to the roles of the AMPA and NMDA receptors. Much more important here were Ascher et al, Mayer and Westbrook, who showed the voltage dependent open channel Mg block of the NMDAR, which Bliss and Collingridge later popularized. Paulhummerman (talk) 02:49, 10 November 2011 (UTC)[reply]

Please feel free to edit the article to fix the problem. If there is any way I can be helpful, please say so. Looie496 (talk) 03:01, 10 November 2011 (UTC)[reply]

Too technical

This summary is aweful. Misses the key points and focuses individual achievements that are irrelevant such as changes in ion channels. Even that is not explained well. Sure LTP protocols *can* result in more than just LTP of the synaptic strength, called EPSP-to-spike potentiation (an increase in the probability that a spike will be triggered for the same input strength). That indeed relies on ion channel plasticity amongst other things.

Please someone, fix this!

I agree. This article seems overly technical. JohnJohn 18:56, 23 January 2006 (UTC)[reply]

This article is very basic: Brain Basics Synaptic Plasticity Synaptic transmission is plastic SriMesh | talk 02:08, 26 December 2008 (UTC)[reply]

Exo vs endo

I think this article also got exocytosis and endocytosis swapped. According to what I read on the endocytosis and exocytosis articles on wikipedia, exocytosis is the process of a cell removing contents out from itself, whereas endocytosis is absorbing contents into itself.

As far as I know, the article is currently factual. AMDARs are taken to the cell membrane by EXOcytosis (to move out from the cell body) and are reabsorbed back into the cell body by ENDOcytosis. They never actually leave the cell. SamuelRiv (talk) 08:40, 21 November 2007 (UTC)[reply]

Regardless of that, the use of exocytosis (used almost exclusively to describe vesicle fusion with membrane and neurotransmitter difusion across synaptic cleft) and endocytosis (vesicle recycling after exocytosis) is very misleading. I have never seen either used in the context of plasticity. Paskari (talk) 17:37, 2 July 2008 (UTC)[reply]

Utterly terrible

This is just useless! I can't imagine it getting worse. A well structured page would list the 6 main types of plasticity

facilitation
depression
augmentation
potentiation (PTP)
LTP
LTD

Instead, everything after the second sentance tells me next to nothing about plasticity. Permission to rewrite this page? Paskari (talk) 17:40, 2 July 2008 (UTC)[reply]

I would suggest first classifying plasticity into two main classes: short-term (less than a few seconds) and long-term (minutes to hours). LTD and LTP are long-term. Post-tetanic potentiation (PTP) is short-term as are other types such as paired pulse facilitation and paired-pulse depression are all short-term. I'm not sure what you mean by augmentation? Xargque (talk) 01:09, 4 July 2008 (UTC)[reply]

Yes, it would be best to label them as short term and long term. There generally 4 forms of short term plasticity:

Facilitation arises from a few APs per second and lasts for 10-100 ms
Augmentation arises from a few hundred APs per second(s) and lasts for ~10 s
Potentiation arises from a few thousand APs per minute(s) and lasts for ~5 min
Depression, on the other hand, arises from excessive use of the synapse.

These numbers are not set in stone, rather they are meant to give you a rough idea of how augmentation fits into this. I got these numbers from NEUROBIOLOGY, MOLECULES, CELLS AND SYSTEMS (GG Mathews), but you can find them in FROM NEURON TO BRAIN, and NEUROSCIENCE (D PURVES et. al.). Paskari (talk) 15:06, 6 July 2008 (UTC)[reply]

Looks good to me, I don't know if I have the authority to say so, but I would be wholeheartedly in favor of you rewriting this article along those lines. Best, Xargque (talk) 16:37, 6 July 2008 (UTC)[reply]

One other point, depression can happen at some synapses even after a single pulse. Generally, it is believed that a synapse with a high probability of release will depress after just one pulse (it's released its vesicle(s)), while at lower release probability synapses calcium buildup is a bigger factor. Here are PubMed references for relevant articles on the matter. http://www.ncbi.nlm.nih.gov/sites/entrez

1: Zucker RS, Regehr WG. Short-term synaptic plasticity. Annu Rev Physiol. 2002;64:355-405. Review. PMID: 11826273 [PubMed - indexed for MEDLINE]

An oft-cited review on short-term plasticity

2: Dobrunz LE, Stevens CF. Heterogeneity of release probability, facilitation, and depletion at central synapses. Neuron. 1997 Jun;18(6):995-1008. PMID: 9208866 [PubMed - indexed for MEDLINE]

The original, and most cited, research paper on the matter.

3: Sun HY, Lyons SA, Dobrunz LE. Mechanisms of target-cell specific short-term plasticity at Schaffer collateral synapses onto interneurones versus pyramidal cells in juvenile rats. J Physiol. 2005 Nov 1;568(Pt 3):815-40. Epub 2005 Aug 18. PMID: 16109728 [PubMed - indexed for MEDLINE]

A new paper which mathematically models short-term plasticity

4: Murphy GJ, Glickfeld LL, Balsen Z, Isaacson JS. Sensory neuron signaling to the brain: properties of transmitter release from olfactory nerve terminals. J Neurosci. 2004 Mar 24;24(12):3023-30. PMID: 15044541 [PubMed - indexed for MEDLINE]

An example of a particular CNS synapse with a very high release probability. The authors confirmed their paired-pulse ratio measurements with several other clever experimental techniques which are becoming standard for investigating release probability in a quantitative way.

5: Sun HY, Dobrunz LE. Presynaptic kainate receptor activation is a novel mechanism for target cell-specific short-term facilitation at Schaffer collateral synapses. J Neurosci. 2006 Oct 18;26(42):10796-807. PMID: 17050718 [PubMed - indexed for MEDLINE]

A case of an exception to the rule, wherein a neurotransmitter receptor on the presynaptic terminal senses the release of neurotransmitter in an autocrine fashion and thereby causes an unexpected dissociation between release probability and short-term plasticity.

In my own thesis work, I studied short-term plasticity, and I would be happy to help you in any way I can to overhaul this article. It's up to you, just let me know how much, if any, help you would like. Xargque (talk) 16:50, 6 July 2008 (UTC)[reply]

I have reviewed three text books on short term plasticity (facilitation, depression, augmentation, and potentiation) and they are near unanimous in that they have not the foggiest clue what causes augmentation and/or potentiation. With facilitation and depression they more or less agree that it has to do with accumulation of calcium (increase in p) and depletion of vesicles (decrease in N). As for reading papers, I will try to get to reading the ones you cited (once I get through all these LTP papers). What is the protocol for updating a site on wikipedia? Should I go ahead and rewrite it, then if there are objections we revert it to the old version? Or should I make a temporary page, then vote to have it copied over? Cheers Paskari (talk) 11:23, 7 July 2008 (UTC)[reply]

Your guess is at least as good as mine. I have asked this question of another user who seems to know a lot about WP. See: http://en.wikipedia.org/wiki/User_talk:Wwwwolf#Rewriting_pages

I will also be creating an article called Short term synaptic plasticity sometime in the next couple months. I'll let you know when I do, and any feedback would be greatly appreciated. Best, Xargque (talk) 17:30, 7 July 2008 (UTC)[reply]

I was going over the Help pages, and we can either create a new page and merge it into this one, or create a new page, and then worry about the renaming. But in all fairness, this is such a terrible article, I think we can literally delete most of it. However, we should discuss the structure before hand. I'm busy until Thursday, so I can't begin work on it until then anyways. Paskari (talk) 18:47, 7 July 2008 (UTC)[reply]

I cannot agree with "Utterly Terrible" and I think including all these short term effects (facilitation etc) under the rubric "plasticity" is confusing. I suggest restricting "plasticity" to long term changes (say, greater than 1 min) as in LTP and LTD. Much facilitaiton and depression is an inevitable consequence of the release machinery (e.g. vesicle depletion, calcium accumulation) and may not be even be functionally relevant. I suggest confining the whole article to long term changes, and then referring to other articles on short-lived changes in synaptic strength. Paulhummerman (talk) 02:59, 10 November 2011 (UTC)[reply]

Properties of synapses

Well I will be coming back shortly to rewrite this section, just too busy at the moment. But so far I think there should be 5 parameters used when describing synaptic strength

number of vesicles (N)
probability of vesicle release (p)
postsynaptic response (q)
synaptic delay (which corresponds to total axonal delay)
synaptic duration (which corresponds to the time the receptor remains in the open state, see Neuroscience Purves et. al. 2007, p131)

Did I miss anything? Paskari (talk) 18:23, 2 September 2008 (UTC)[reply]

Theoretical mechanisms

The theoretical mechanisms section is a little misleading. It should list

the probability of neurotransmitter release (p)
the number of vesicles of neurotransmitters (N)
the postsynaptic sensitivity to released neurotransmitters (q)

furthermore, the equation only seems to deal with q Paskari (talk) 17:02, 2 February 2009 (UTC)[reply]

That whole section should perhaps be removed. As you say, it doesn't even deal with LTP/LTD correctly, and there are many other types of synaptic plasticity that work in completely different ways. Looie496 (talk) 03:50, 3 February 2009 (UTC)[reply]

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