Talk:Hippocampus

message: I would like to add the following after reference 31 in the section Role in Memory because I believe it contributes our understanding of the involvement of the hippocampus in memory:
Experiments using intrahippocampal transplantation of hippocampal cells in primates with neurotoxic lesions of the hippocampus have shown that the hippocampus is required for the formation and recall, but not the storage, of memories.
<Virley, D., Ridley, R.M., Sinden, J.D., Harland, S., Williams, C., Rashid, T., Gray, J.A., Lantos, P.L. and Hodges, H. (1999) Primary CA1 and conditionally immortal MHP36 cell grafts restore conditional discrimination learning and recall in marmosets after excitotoxic lesions of the hippocampal CA1 field. Brain, 122, 2321-2335.> Mountain9 (talk) 19:42, 3 December 2016 (UTC)
thread_title:  Role in memory 

message: While the page refers to the Hippocampus as sub-cortical (and indeed the hippocampal formation is technically located below the cortex), I believe there is wide consensus in the field that due to 1) the laminar structure of this brain region and 2) its tight coupling to the parahippocampal cortex, the hippocampus is considered allocortical (or possibly even cortical). In any case it is certainly not subcortical as a recent revision suggests There are any number of references to support this claim:
Wills, T. J.; Cacucci, F.; Burgess, N.; O'Keefe, J. (2010). "Development of the Hippocampal Cognitive Map in Preweanling Rats". Science. 328 (5985): 1573–1576
This is the source cited in the appropriate section of the Wikipedia Allocortex article.
Swenson RS. (2006). Review of clinical and functional neuroscience.
This source repeatedly points this difference out in the chapters on the limbic system and the cortex.
Perhaps this discussion is best summarized by the classic text "The Hippocampus Book" in the chapter "Hippocampal Neuroanatomy" by David Amaral and Lavenex Pierre:
"The reader who ventures from the relative safety of this book into the primary hippocampal literature should be aware that our usage of the term “hippocampal formation” is widely, though not universally, accepted. Some authors include only the allocortical (a term applied to cortical regions having fewer than six layers) regions as parts of the hippocampal formation. Three-layered cortical regions typically have a single neuronal cell layer with fiber-rich plexiform layers above and below the cell layer. In articles employing this usage, the hippocampal formation comprises the dentate gyrus, hippocampus, and subiculum. The remaining fields—presubiculum, parasubiculum, and entorhinal cortex—are then typically grouped together on the basis of their multilaminate structure under the term retrohippocampal (retro = behind) or parahippocampal (para = alongside or near) cortex."
A previous revision to this effect was reverted, so I hope moving this question to the talk page helps clarify this issue.
I would also point out that the reference cited for subcortical does not make any claims about the structural identity of the hippocampus. The word "subcortical" only pops up once when the chapter states the limbic system is at the border of the neocortex and subcortical structures.  — Preceding unsigned comment added by Syntaxapse (talk • contribs) 19:25, 12 January 2017 (UTC)
replies: text: Hello Syntaxapse - I cannot find any reference on the page that states that the hippoacampus is subcortical - 'subcortical' is only mentioned three times,  referring to input to the hippocampus and output and not staying that the hippocampus is subcortical. --Iztwoz (talk) 20:09, 12 January 2017 (UTC)
replies: text: Hey Iztwoz - yeah sorry for any confusion, I have since gone ahead and changed subcortical to allocortical, it seemed more specific and correct. I agree that in some literature there is some confusion regarding the nomenclature (the hippocampus is after all below the cortex), but I think most primary respected texts in the field that take great care with their language would not refer to it as subcortical. Happy to talk about this more if you feel this is important or debatable - otherwise thanks for your other work cleaning up this page! Syntaxapse (talk) 20:54, 12 January 2017 (UTC)
replies: text: Thanks for the comments. i agree with your edit. As for editing generally - anybody can make edits to any page, and if they are helpful they are very welcome. Best-- Iztwoz (talk) 21:04, 12 January 2017 (UTC)
thread_title:  Subcortical vs. Allocortical 

message: I found the first sentence not well-phrased and attempted to recast it. This then lead to questions as to what was actually being claimed, so I checked Buzsaki and was unable to find the specific claim that the hippocampus generates some of the largest EEG singals (as theta waves?) I did find something like it here, though https://www.ncbi.nlm.nih.gov/pubmed/16149083 Vertes, RP, 2005.  I come at this from the perspective of trying to make the article more readable, not any great knowledge of the subject matter.  — Preceding unsigned comment added by OmneBonum (talk • contribs) 08:25, 25 March 2017 (UTC)
thread_title:  Theta Rhythm 

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thread_title:  External links modified 

message: I propose editing the epilepsy and effects of cortisol sections to reflect findings in how stress changes the hippocampus such that it can induce seizures, or somehow integrating this information into the page: 
Corticosteroid Effects on the Hippocampus
Exposure to stress results in the release of corticosteroids in the brain. Cortisol is the most common stress hormone in humans, and corticosterone the most common in mice and rats. They virtually act on every organ in the body, but in seizures the most important region is the hippocampus. The hippocampus contains mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) that have different affinities for corticosteroids. Rapid effects of stress are mediated through membrane associated MRs. This results in an array of effects within minutes of binding including increased frequency of small excitatory postsynaptic potentials and decreased frequency of spontaneous inhibitory postsynaptic potentials. Together these could cause hyper-excitability of the hippocampus and induce a seizure. Slow effects of stress take place on a level involving DNA or genomic level. When nuclear MRs and GRs are bound by corticosteroids they alter gene expression, the process that converts DNA to RNA to proteins. Changes induced include increased amplitude of spontaneous excitatory postsynaptic potentials, and slowing the increase in number of calcium channels. By preventing the increase in number of calcium channels, it results in increased length of hyperpolarization which works to reduce the rate at which neurons can fire, which somewhat minimizes the effects of stress. These changes alter the responsiveness of the body to stress in order to maintain homeostasis. Chronic exposure to stress, however, results in disruption of these compensating mechanisms and drastic structural changes in the brain.
Corticotropin-Releasing Hormone Effects on the Hippocampus
Corticotropin-Releasing hormone (CRH) is released following stress. Immediate effects include shortening of the hyperpolarization time which increases the frequency at which neurons can fire leading to an increased risk for seizures. Chronic exposure to CRH causes more complicated and less understood changes, but studies show it can cause decreased dendritic spines on neurons in the hippocampus.
Neurosteroid Effects on the Hippocampus
Neurosteroids have been shown to reduce excitability in the hippocampus and reduce seizure occurrence. With stress, endogenous neurosteroid concentrations increase such that a product of deoxycorticosterone breakdown binds to GABA-A receptors which then raises the threshold for seizures making them harder to generate. Seizures themselves have also been shown in studies to promote neurosteroid production in the brain, creating protective effects against subsequent seizures immediately following a seizure for a few hours. Exposure to chronic stress is associated with decreased concentrations of neurosteroids in the brain, suggesting higher susceptibility to seizures during periods of chronic stress.
Gnada14 (talk) 02:07, 13 December 2017 (UTC)
thread_title:  Addition of stress effects on hippocampus in relation to seizures  

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thread_title:  External links modified 

message: I have removed a very long section on this topic. Given the breadth of this article, the sources may justify a brief mention of this topic, but certainly not more than that -- and I have doubts that even a paragraph would constitute appropriate weighting. The basic principle is that Wikipedia must not be used to publicize ideas that have not achieved widespread attention on their own. Looie496 (talk) 15:49, 29 January 2018 (UTC)
replies: text: I already placed a final warning on the IP address talk page. Looie496 (talk) 14:54, 31 January 2018 (UTC)

text: Thanks for joining the discussion. I am totally competent in hippocampal theory -- you can find my real name on my user page and look up my publication record. The problem is not that the material you are adding is illegitimate, it is that you are misunderstanding the purpose of a Wikipedia article. Wikipedia's goal is to create an encyclopedia of the quality of Britannica, but freely accessible and broader in coverage. If you read Britannica's "hippocampus" article, would you expect to find the material you added? I doubt it -- the ideas may be legitimate, but they haven't yet drawn broad enough attention to get into an article like that. The same applies here. If you wanted to create a new article entitled Hippocampal theory of consciousness it would be much more reasonable -- although even then it would be necessary to alter the tone of the writing somewhat, as Wikipedia articles are intended to inform rather than persuade. Best regards, Looie496 (talk) 17:52, 31 January 2018 (UTC)
thread_title:  Hippocampal theory of consciousness 

message: Have just restored page to previous good version. The following removed para is posted here - Previously the page referred to three main ideas over the years - this was changed to two main ideas and the para inserted in the middle.
:A recent theory by Legéndy argues that the hippocampus only creates a unique “pointer” to each new piece of episodic memory, in the form of a large cell group in CA3.  The stored information itself mostly ends up in the neocortex rather than the hippocampus; and the pointer group only has the role of retrieving it.  The peculiar distribution of the mossy cell associational projection is consistent with a biological effort to randomize (“stir”) the newly created pointer groups over a series of theta cycles, distributing their members thoughout CA3 and achieving that they, directly or indirectly, reach all cortical neurons in the areas address.Legéndy, C. R. (April 2017) "On the 'data stirring' role of the dentate gyrus of the hippocampus". Reviews in the Neurosciences 28 (6): 599-615.  DOI: 10.1515/revneuro-2016-0080.  The “memory theory” of the hippocampus is in this way reconciled with the seemingly contradictory fact that essentially all hippocampal pyramidal cells are “place cells,” through the observation that there are far more place cells having suitable parameters than are needed to make up any one pointer group; and the combinatorial diversity of group selection is more than enough to supply a lifetime’s worth of episode IDs.  However, even in non-spatial memory retrieval, the place cell properties of the pointer group cells are often utilized indirectly, as when we retrace our steps to “jog our memory” of an event. 
This content is variously found in Circuitry,  Place cells and other sections. What is referred to as a recent theory is a review. The title of the review concerns the dentate gyrus which is not mentioned in the edit and which has material in dentate gyrus section. The ref given is not entered up properly. The last half of the paragraph is uncited and some OR. The prose is not up to the featured article status. Another major change was to upset the formatting of the three main ideas and to change this to two ? Then to enter a sentence claiming a heavy criticism and giving a completely inapt ref. As it states at top of editing page any changes to content needs to be addressed on talk page.--Iztwoz (talk) 23:43, 19 November 2018 (UTC)
thread_title: Edit revert

message: I have seen multiple paragraphs and sentences in this article that are unsourced. Could someone knowledgable about this subject please fix this issue? This is an important featured article that was even peer-reviewed in a WikiJournal. For it to lose featured status in an FA-review would be a shame. Wretchskull (talk) 20:11, 11 February 2021 (UTC)
thread_title:  Citations needed 

message: This is by no means a common term in modern neuroscience. A PubMed search for "Ammon's Horn" indicates that the term saw peak use in publication in 1993 and has reduced consistently and significantly since, with 6 results containing "Ammon's Horn" published in 2021. So while true, including the term in the first paragraph may confuse or misdirect readers rather than inform them. 
I propose moving mention of the term and associated reference below to the "name" section.
https://pubmed.ncbi.nlm.nih.gov/?term=%22Ammon%27s+horn%22
CoreyinProgress (talk) 19:19, 9 December 2021 (UTC)
thread_title:  "Ammon's Horn" 

message: I suggest removing the term CA4 from this article. This is a misnomer that was introduced by Lorente de Nó (1934) and was suggested abandoned already in 1978 by Amaral in his very thorough paper on the cell types of the dentate gyrus in rats. Lorente de No's CA4 was actually the polymorphic layer of the dentate gyrus (his second reflected blade) that he thought was a continuation of the CA-field populated by modified pyramids. It has later been established that this is not the case and that the CA4 of Lorente is not continuous with the CA but is the basal polymoprhic layer of the DG. It thus makes no sense to say that the CA4 inserts into the DG, as the CA4 is actually the polymorphic layer of the DG. Naming this layer CA4 also infers that it is part of the CA-field, which is not true. What inserts into the DG is the most proximal end of CA3 and this should also be updated in the text. This has been established amongst others by the same authors that are referred to (mistakenly) in the section where CA4 is presented at first.
For references on the misnomer CA4 see: Blackstad (1956), Amaral (1978), and more recent reviews on anatomy where the term is abandoned: van Strien et al. (2009), Cappaert et al. (2015). 
The hippocampal field is full of strange nomenclature. Since Amaral conclusion has not been proven wrong over close to five decades it is well beyond time that we implement his observations and remove this misnomer. 
Jsblacks (talk) 15:33, 7 January 2022 (UTC)
thread_title:  The misnomer CA4 

message: "Anatomy" is largely unsourced (Also mentioned one year ago). :File:Place Cell Spiking Activity Example.png is unsourced. Also: why are some images numbered ("Image 8: Example of a one-second EEG theta wave", etc.) while others aren't ("Rats and cognitive maps", "Hippocampus (lowest pink bulb)", "Hippocampus highlighted in green on coronal T1 MRI images", etc.) A455bcd9 (talk) 11:18, 9 December 2022 (UTC)
thread_title:  [[WP:URFA/2020]]