Talk:Long-term depression

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Suggestions from BI481 Classmates

Synaptic depression

There is a very useful and interesting article by P. G. Montarolo, E. R. Kandel and S. Schacher that examines the gill withdrawal reflex in Aplysia, which you may consider including in the article due to the model nature of the organism and its critical importance in discoverying the underlying mechanisms of this process. The paper explores the short term and long term synaptic depression caused by FMRFamide and compares it to dopamine and low-frequency stimulation. It also demonstrates that the mechanisms of long term depression result from gene products when the administer the FMRFamide in the presence of an inhibitor of protein synthesis, anisoymcin, resulting in the absence of the previously observed long term depression.

  • Montarolo PG, Kandel ER, Schacher S (1988). "Long-term heterosynaptic inhibition in Aplysia". Nature. 333 (6169): 171–4. doi:10.1038/333171a0. PMID 3367986. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

Hassan.zayn (talk) 03:07, 25 November 2009 (UTC)[reply]

Thank you for your help - I agree, an interesting article, but I am hesitant to include it. Although it could possible be referenced in the discussion of general forms of LTD, I believe the research was geared towards gaining insight in the cellular mechanisms of long term habituation. I think a discussion on the use of Aplysia as a model system would be a great addition to the Aplysia wiki page. Patrick Raab 05:41, 7 December 2009 (UTC) —Preceding unsigned comment added by Patrick.Raab.1 (talk • contribs)

AMPA receptors

Hey guys, good job so far. This is an interesting topic and I'm sure that there is a lot of external information on it so it may be hard to decide what you want to include or not. I think that it would be good to talk a little about the role of some important neurotransmitters like Serotonin in facilitating long-term depression by inducing internalization of AMPA receptors. There is an article that you'll find helpful in the journal of Physiology titled: Serotonin facilitates long-term depression induction in prefrontal cortex via p38 MAPK/Rab5-mediated enhancement of AMPA receptor internalization, by Z.Yan etc. I'll let you know if I find other information.

Kristaqkoci (talk) 05:51, 28 November 2009 (UTC)[reply]

Thanks for providing the article. It was helpful and I included a short section about it. Bergaa7 (talk) 07:35, 3 December 2009 (UTC)[reply]

EPSPs, calcium, Hebbian model, etc

  • In the Hippocampus section, be sure to refer to EPSPs with the full name the first time they are mentioned.
  • You mention that LTD in the visual cortex is homosynaptic. How do the types of LTD function in the hippocampus and the cerebellum?
  • In organizing your article, you may want to talk about the role and importance of calcium before you go into the section of STDP.
I agree - I reorganized the topics and integrated the subject matter from calcium influx section into the mechanism sections where it was pertinent. Patrick Raab 21:50, 4 December 2009 (UTC) —Preceding unsigned comment added by Patrick.Raab.1 (talk • contribs)
  • You could include a section concerning the Hebbian model of learning and how LTD is involved in this process. I found a paper by Mark Bear called Bidirectional Synaptic Plasticity: from Theory to Reality that discusses the Hebbian model and the BCM model. It goes into a detail about the visual cortex and LTD. It does mention some interesting research about visual deprivation and retinal inactivity.
Thank you for taking the time to find and suggest this paper! Although the Hebbian model is structured around LTP, it sparked further research that resulted in the development of the BCM model, which includes the following 3 assumptions – 1. active synapses are bidirectionally modifiable; 2. the sign or polarity of the modification (LTD or LTP) depends on the level of post-synaptic response relative to a modification threshold; and (iii) the value of the modification threshold varies with the history of cortical activity. Since the BCM model is a theory developed in 1982 that is being confirmed by present research, as demonstrated by the paper you provided, I felt it was best to include how present data is confirming theories in the field. Therefore, I removed the The Lisman model section and integrated findings from research papers into approppiate sub-categories under the mechanism section. This paper is a great resource and I will use it to help elaborate on Bear's previous research on the mechanism behind sliding synaptic modification threshold. Patrick Raab 02:39, 5 December 2009 (UTC) —Preceding unsigned comment added by Patrick.Raab.1 (talk • contribs)

Katie1341 (talk) 04:46, 29 November 2009 (UTC)[reply]

I changed EPSP, and no one type of LTD is specific to the cerebellum or hippocampus. Both heterosynaptic and homosynaptic forms of LTD occur in these regions. Bergaa7 (talk) 21:30, 6 December 2009 (UTC)[reply]

Comment 4

You might consider merging the "Types" heading and the "Mechanisms that weaken synapses" heading into one "Mechanisms" heading. This would be cleaner and more concise. It would also be interesting, in light of the Kauer and Malenka "Synaptic plasticity and addiction" review paper, to mention the effect of amphetamine use on LTD. The paper in the journal Science by Brebner et al,:

  • Brebner K, Wong TP, Liu L, Liu Y, Campsall P, Gray S, Phelps L, Phillips AG, Wang YT (2005). "Nucleus accumbens long-term depression and the expression of behavioral sensitization". Science. 310 (5752): 1340–3. doi:10.1126/science.1116894. PMID 16311338. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

might be useful in this area. Finally, since memory is such an important area of LTD, it would probably be good if that section was expanded to include more sources of information. Matthew Cedar Warman (talk) 17:55, 29 November 2009 (UTC)[reply]

Thank you for your suggestion about merging the two headings, but I wanted to first identify the general types of LTD before I went into detail about mechanisms in specific parts of the brain. I have restructured the "Types," section, however-let me know if the change adds clarity or if you have further suggestions. Bergaa7 (talk) 03:58, 3 December 2009 (UTC)[reply]
Thanks for the comment, I have just added a section on LTD and addiction based "Synaptic plasticity and addiction." After reading the paper I found it would be more informational to explain LTD that results from cocaine rather than amphetamine.Pat Bolan (talk) 04:20, 6 December 2009 (UTC)[reply]

Comment 5

In the mechanisms that weaken synapses, you may consider adding a visual that shows the presynaptic and postsynaptic membranes showing the respective postsynaptic receptors. A visual of the pathway may be of aid to the reader in understanding the distinction between AMPA and NMDA receptors and what each receptor does. An image of second messenger pathways may also be of help.

One section you may consider adding is one which discusses depressive disorders. Nobuo Kato (2009) discusses the mechanisms of electroconvulsive therapy on depression disorders, which may be interesting to add. Although the mechanisms for this therapy is not thoroughly understood, it might be interesting to include recent theories on how ECT impacts GABAergic dysfunction as addressed in Kato’s paper, "Neurophysiological mechanisms of electroconvulsive therapy for depression". Daigleal (talk) 23:40, 29 November 2009 (UTC)[reply]

Your second point is thoughtful, but I believe you are confusing the mental disorder "depression" with long-term synaptic depression. Bergaa7 (talk) 01:45, 3 December 2009 (UTC)[reply]
I am also working on putting up an image. Bergaa7 (talk) 07:37, 3 December 2009 (UTC)[reply]
I am not able to find an image showing the LTD mechanism that is appropriate for use, but I agree that an image would be helpful. Bergaa7 (talk) 20:47, 6 December 2009 (UTC)[reply]
It was very difficult to find an image showing LTD mechanism that coincided with copyright regulations, but I was able to find the image that was added. It demonstrates de novo LTD and depotentiation, which highlights the addition or removal of AMPAR, for LTP or LTD, respectively. Patrick Raab 03:30, 7 December 2009 (UTC) —Preceding unsigned comment added by Patrick.Raab.1 (talk • contribs)

Comment 6

Great article overall. Just a few things, you may want to make internal wiki links for NMDA receptors, mGluR receptors, and endocannabinoids in your opening in case people are unfamiliar with them. Also, the Types section could be changed, either by expanding on each subtype a little bit or by merging them into one section and just making them separate paragraphs. In the first line of the spike-timing dependent plasticity section, the link for neuroplasticity should probably be one word since that's how it is on the page it points to. It also might be interesting to include some diseases or disorders associated with LTD. Pmcb97 (talk) 00:42, 30 November 2009 (UTC)[reply]

Thank you for noting the need for internal wiki links-I took care of that point. I will also consider either integrating the descriptions of types of LTD into the mechanisms section or merging them into a single paragraph. In regard to your last point, I have been researching the role of LTD in Alzheimer's and Parkinson's disease. Any specific articles you believe I should consider would be appreciated. Bergaa7 (talk) 01:41, 3 December 2009 (UTC)[reply]
Thanks, took care of the typo for neuroplasticity Patrick Raab 22:30, 4 December 2009 (UTC)

Comment 7

I liked the page. The information you presented gelled well with what we learned in class about LTD and allowed me to gain a deeper understanding of the mechanism. I have to agree with some of the above comments that you could use a little beefing up of the 'Motor Learning and Memory' section. Here are some links that may help you add more to that section: [[1]], [[2]], [[3]]. Maybe talk about the signal-to-noise ratio and LTDs role in helping to assign importance to data. Perhaps you can reference Kim Peek as an example of someone who can remember everything but is unable to make sense/assign importance to all the data he has accumulated.Rickxicity (talk) 22:32, 29 November 2009 (UTC)[reply]

Thank you - I added information on signal-to-noise ratio in the STDP section.Patrick Raab 03:45, 7 December 2009 (UTC)
Although Kim Peek was able to remember everything and this very well may be contributed to the lack of LTD, I have been unable to locate any specific research that demonstrates this possible correlation. Research that I have found pertains to understanding Peek's brain abnormalities that include - an absent corpus callosum, missing anterior and posterior commissures, and abnormal cerebellum. To refrain from speculation, I chose to remain from referencing him.Patrick Raab 18:29, 6 December 2009 (UTC) —Preceding unsigned comment added by Patrick.Raab.1 (talk • contribs)
Thanks for the suggestion. The first link you provided was already one used for the Motor Learning and Memory section, but the second and third contain new information that I have now included into the section. Pat Bolan (talk) 11:39, 6 December 2009 (UTC)[reply]

Comment 8

I think this article is very well written, probably the best I've read so far. I found the section about LTD in the visual cortex to be particularly interesting and I think you could discuss it in more depth. Also, I liked how you talked about the experiments concerning LTD and memory in rats, but I think it would benefit your page to discuss the relationship between LTD and human memory disorders. You should explore the consequences of LTD impairment in humans and the inability to forget anything previously learned. I think you should also consider LTD and its role in disorders including Alzheimer's disease, and what further research of LTD could mean for better understanding human memory disorders. These articles might be helpful:

  • Vintém AP, Henriques AG, da Cruz E Silva OA, da Cruz E Silva EF (2009). "PP1 inhibition by Abeta peptide as a potential pathological mechanism in Alzheimer's disease". Neurotoxicol Teratol. 31 (2): 85–8. doi:10.1016/j.ntt.2008.11.001. PMID 19028567.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • Min SS, Quan HY, Ma J, Lee KH, Back SK, Na HS, Han SH, Yee JY, Kim C, Han JS, Seol GH (2009). "Impairment of long-term depression induced by chronic brain inflammation in rats". Biochem. Biophys. Res. Commun. 383 (1): 93–7. doi:10.1016/j.bbrc.2009.03.133. PMID 19341708. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

Overall, I wouldn't change much about the content or setup of your article, but would consider adding a discussion relating LTD and human memory disorders including what is already known and what needs to be studied in the future. Brikathleen (talk) —Preceding unsigned comment added by 136.167.247.48 (talk) 04:34, 30 November 2009 (UTC)[reply]

We really appreciate the positive feedback. The article you listed was a helpful starting point in researching Alzheimer's. A section has been added in the "Current research" section on the subject. Bergaa7 (talk) 07:40, 3 December 2009 (UTC)[reply]
I have recently expanded the Visual Cortex LTD mechanism section. Pat Bolan (talk) 06:06, 4 December 2009 (UTC) —Preceding unsigned comment added by 136.167.189.162 (talk) [reply]

Neurotransmitters involved in LTD, and LTP.

I think it would be particularly interesting to compare LTP and LTD on the neurotransmitter level. Although there is some description of neurotransmitters involved in LTD such as serotonin, I'd like to know if different neurotransmitters are involved in LTP. If it is the case, is there any evidence that this could be the cause of the difference between LTP and LTD in spatial learning? Sparkletts514 (talk) 20:15, 7 October 2012 (UTC)[reply]

I'm not sure there is such a thing as "the" cause. The distinction between LTP and LTD can be determined by differences in activity patterns of the two cells, but LTP can also be changed to LTD by certain types of neurotransmitter input, and LTD can be changed to LTP by other types. I haven't really kept up with the literature on this topic, but the last time I looked at it the story was pretty confusing. Looie496 (talk) 01:05, 8 October 2012 (UTC)[reply]

Caspase-3 Activation

I was thinking of adding some information about the caspase-3 activation through the mitochondria which is required for both LTP and LTD. In the synapses rather than cell death occurring, long term depression occurs which is surprising considering the activation of caspase-3 which is part of the apoptotic pathway. The article I found discusses the link between the molecular mechanisms of apoptosis and LTD.Some good articles I found that have current, exciting research:

1. "Long-Term Depression in the CNS" by Collingridge et al, 201 2. "Caspase-3 activation via Mitochondria is required for long-term depression and AMPA receptor internalization" Li et al,2010 3. "For Synapses, its Depression not Death" Bateup and Sabatini 2010 Neurosci21 (talk) 18:56, 17 October 2012 (UTC)[reply]

To assess the reliability of these sources, we need the full citations. Wadewitz (talk) 22:18, 22 October 2012 (UTC)[reply]
Can you give a bit more detail about your planned changes? — Preceding unsigned comment added by Clevwiki (talk • contribs) 23:20, 2 November 2012 (UTC)[reply]

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