HippocampusPub Date : 2024-12-10DOI: 10.1002/hipo.23667
Elisabeth A. Murray
{"title":"Quality Controls: The Role of Self-Corrective Science in Explorations of Primate Memory Systems","authors":"Elisabeth A. Murray","doi":"10.1002/hipo.23667","DOIUrl":"10.1002/hipo.23667","url":null,"abstract":"<p>In 1978, Mort Mishkin published a landmark paper describing a monkey model of H.M.'s dense, global amnesia. It depended on a combined removal of the amygdala and hippocampus (the A + H lesion) and a memory test called delayed nonmatching-to-sample (DNMS). My first project examined whether the impairment Mishkin had found in visual memory generalized to tactual stimuli. However, to gain access to the hippocampus and amygdala with 1980s surgical methods, we had to remove the underlying cortex. When we were able to test the effects of bilateral removal of that underlying cortex (the entorhinal and perirhinal cortex, or “rhinal cortex” for short) we obtained a dramatic result. This so-called “control” lesion caused a profound impairment on the DNMS task. A few years later, excitotoxic A + H lesions, which left the rhinal cortex intact, confirmed that removal of the cortical “impediments” had caused the entire memory impairment that Mishkin had observed. These results: (1) forced a reconsideration of the monkey model of global anterograde amnesia; (2) spurred study of the independent contributions of the amygdala, hippocampus, and perirhinal cortex to cognition; and (3) led to the realization that the DNMS task did not test the kinds of memory that H.M. lost after his surgery.</p>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HippocampusPub Date : 2024-12-08DOI: 10.1002/hipo.23664
Terje Lømo
{"title":"Long-Term Potentiation: The Accidental Discovery","authors":"Terje Lømo","doi":"10.1002/hipo.23664","DOIUrl":"10.1002/hipo.23664","url":null,"abstract":"<p>Long-term potentiation (LTP), is a type of synaptic plasticity now considered essential for learning and memory. Here I tell the story of how I accidentally discovered in 1966 in the laboratory of Per Andersen in Oslo, Norway, because I was not looking for it. It just emerged. I recount how I came to work with Per and why my result was not immediately followed up. Then, in 1968 Tim Bliss joined the lab and, on his urging, from 1968 to 1969 we did the experiments that resulted in Bliss and Lømo, 1973. I explain why I think the experiments later failed in Oslo, and for a few years also in Tim's lab in London, before it became a readily observable phenomenon. I also describe how Tony Gardner-Medwin and I in 1971 failed to reproduce the results that Tim and I had obtained 2 years earlier in the same lab and the same type of anesthetized rabbit preparation. I tell how this failure caused me to leave the LTP field and, instead, continue exploring mechanisms of nerve–muscle interactions, which I had studied with much success during my postdoc period in London from 1969 to 1971. I reflect on Donald Hebb's influence on LTP studies and on my experience when after many years of neglect, I became interested in LTP and the hippocampus anew and started to write about it, though without doing lab experiments. Finally, I report briefly on the experiments I am doing now in retirement, studying how the nervous system regulates body temperature through varying amounts of muscle tone.</p>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11626224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HippocampusPub Date : 2024-12-08DOI: 10.1002/hipo.23655
Fred H. Gage
{"title":"Adult Neurogenesis in the Human Dentate Gyrus","authors":"Fred H. Gage","doi":"10.1002/hipo.23655","DOIUrl":"10.1002/hipo.23655","url":null,"abstract":"<div>\u0000 \u0000 <p>In the adult dentate gyrus of the hippocampus there are neuronal stem cells that give rise to immature neurons and subsequently to mature functional granule neurons. The rate of proliferation, differentiation, and survival is regulated intrinsically and extrinsically. For example, Wnt, BMP, TLX, and BDNF all regulate adult neurogenesis intrinsically, while exercise, environmental enrichment, stress, and epilepsy are some of the extrinsic factors that regulate adult neurogenesis. A clearer picture is emerging for the functional role of these newly born neurons in behavior, demonstrating that adult neurogenesis plays a role in recognizing events, places, objects, or people as unique when comparing options that are very similar, but that these newly born cells play little role in recognition when differences are greater. Most of the research on adult neurogenesis is conducted in experimental mammals, including mice and rats. The first evidence for adult neurogenesis in humans was reported in 1998, when postmortem brains from cancer patients injected with bromodeoxyuridine (BrdU) were examined and cells were found that had divided and differentiated into mature neurons. Subsequently, additional evidence using other techniques has confirmed human adult neurogenesis. Additional in vivo live reports will be needed to monitor the effects of changes in human adult neurogenesis with age and disease.</p>\u0000 </div>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Behavioral Consequences of Hippocampal 5-HT7 Receptors Blockade in Stressed Rats","authors":"Adriana Colsera Pereira, Júlia Lopes Gonçalez, Thalita Aparecida Riul Prado, Rodrigo Campos-Cardoso, Giovana Vieira Viais Zagatto, Pedro Guilherme Pauletti Lorenzo, Cláudia Maria Padovan","doi":"10.1002/hipo.23663","DOIUrl":"10.1002/hipo.23663","url":null,"abstract":"<div>\u0000 \u0000 <p>Serotonin (5-HT) has long been involved in response to stress and its effect may be, in part, mediated by 5-HT1a and 5-HT7 receptor subtypes in different brain structures. Both pre- and post-synaptic activation of 5-HT1a receptor, respectively, in the rat median raphe nucleus (MnRN) and hippocampus, lead to adaptation to acute inescapable stressors such as restraint and forced swim. 5-HT7 receptor (5HT7r), a stimulatory G-protein coupled receptor, has also been investigated as a possible candidate for mediating stress response. In the MnRN, activation of 5-HT7r has antidepressant effects, while in the hippocampus, 5HT7r mRNA expression is increased after exposure to restraint stress, but the functional significance of these receptors remains to be determined. Therefore, the aim of this study was to investigate whether blockade of hippocampal 5HT7r would prevent and/or attenuate the behavioral effects of stress. Male adult Wistar rats with bilateral cannulas aimed at the dorsal hippocampus were restrained for 2 h and tested in the elevated plus maze (EPM) 24 h later. SB 258741 (3 nmoles/0.5 μL/side; selective 5HT7r antagonist) was administered bilateraly into the hippocampus according to the experimental protocol: immediately before or after stress, or 24 h after it (immediately before the test). In a second experiment, rats were exposed to 15 min. of forced swim, and tested 24 h later. Intra-hippocampal treatment was performed as described for the restraint stress protocol. We found that blockade of hippocampal 5-HT7r immediately after, but not before, the exposure to restraint or forced swim attenuated stress-induced behavioral changes. Similar results were obtained when SB was administered before the test in previously stressed rats. Our data suggest that activation of hippocampal 5-HT7r is crucial for the consolidation and retrieval of aversive stimulus-related memories, such as those caused by a stressful experience, probably through mechanisms involving stress-induced changes in 5-HT7r expression.</p>\u0000 </div>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HippocampusPub Date : 2024-12-07DOI: 10.1002/hipo.23657
Daniel L. Schacter
{"title":"Explicit Memory, Implicit Memory, and the Hippocampus: Insights From Early Neuroimaging Studies","authors":"Daniel L. Schacter","doi":"10.1002/hipo.23657","DOIUrl":"10.1002/hipo.23657","url":null,"abstract":"<div>\u0000 \u0000 <p>During the 1980s and 1990s, much memory research focused on the differential role of the hippocampus in various forms of memory. My work on the distinction between explicit and implicit memory led me to become involved in several early neuroimaging studies that made use of cognitive paradigms to investigate the conditions in which hippocampal activity does and does not occur, and to address the theoretical implications of these findings. Here, I summarize two such projects and some of the personal backstory associated with them.</p>\u0000 </div>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HippocampusPub Date : 2024-12-07DOI: 10.1002/hipo.23656
Lynn Nadel
{"title":"Some Memories of Stalking the Seahorse","authors":"Lynn Nadel","doi":"10.1002/hipo.23656","DOIUrl":"10.1002/hipo.23656","url":null,"abstract":"<div>\u0000 \u0000 <p>Early influences that led to the development of the cognitive map theory of hippocampal function, and the multiple trace theory, are discussed. Some details are provided, many are left out.</p>\u0000 </div>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HippocampusPub Date : 2024-12-02DOI: 10.1002/hipo.23651
J. Quinn Lee, Matt Nielsen, Rebecca McHugh, Erik Morgan, Nancy S. Hong, Robert J. Sutherland, Robert J. McDonald
{"title":"Sparsity of Population Activity in the Hippocampus Is Task-Invariant Across the Trisynaptic Circuit and Dorsoventral Axis","authors":"J. Quinn Lee, Matt Nielsen, Rebecca McHugh, Erik Morgan, Nancy S. Hong, Robert J. Sutherland, Robert J. McDonald","doi":"10.1002/hipo.23651","DOIUrl":"https://doi.org/10.1002/hipo.23651","url":null,"abstract":"<p>Evidence from neurophysiological and genetic studies demonstrates that <i>activity sparsity</i>—the proportion of neurons that are active at a given time in a population—systematically varies across the canonical trisynaptic circuit of the hippocampus. Recent work has also shown that sparsity varies across the hippocampal dorsoventral (long) axis, wherein activity is sparser in ventral than dorsal regions. While the hippocampus has a critical role in long-term memory (LTM), whether sparsity across the trisynaptic circuit and hippocampal long axis is task-dependent or invariant remains unknown. Importantly, representational sparsity has significant implications for neural computation and theoretical models of learning and memory within and beyond the hippocampus. Here we used functional molecular imaging to quantify sparsity in the rat hippocampus during performance of the Morris water task (MWT) and contextual fear discrimination (CFD) – two popular and distinct assays of LTM. We found that activity sparsity is highly reliable across memory tasks, wherein activity increases sequentially across the trisynaptic circuit (DG < CA3 < CA1) and decreases across the long axis (ventral<dorsal). These results have important implications for models of hippocampal function and suggest that activity sparsity is a preserved property in the hippocampal system across cognitive settings.</p>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/hipo.23651","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142762106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HippocampusPub Date : 2024-11-28DOI: 10.1002/hipo.23650
Natalie J. Preveza, Gueladouan Setenet, Phillip Gwin, Yeeun Bae, Morgan B. Patrick, Adam Cummings, Jennifer R. Abraham, W. Keith Ray, Richard F. Helm, Timothy J. Jarome
{"title":"Decreases in K63 Polyubiquitination in the Hippocampus Promote the Formation of Contextual Fear Memories in Both Males and Females","authors":"Natalie J. Preveza, Gueladouan Setenet, Phillip Gwin, Yeeun Bae, Morgan B. Patrick, Adam Cummings, Jennifer R. Abraham, W. Keith Ray, Richard F. Helm, Timothy J. Jarome","doi":"10.1002/hipo.23650","DOIUrl":"https://doi.org/10.1002/hipo.23650","url":null,"abstract":"<div>\u0000 \u0000 <p>Over 90% of protein degradation in eukaryotic cells occurs through the ubiquitin-proteasome system (UPS). In this system, the ubiquitin protein can bind to a substrate on its own or it can form a chain with multiple ubiquitin molecules in a process called polyubiquitination. There are 8 different sites on ubiquitin at which polyubiquitin chains can be formed, the second most abundant of which, lysine-63 (K63), is independent of the degradation process, though this mark has rarely been studied in the brain or during learning-dependent synaptic plasticity. Recently, we found that knockdown of K63 polyubiquitination in the amygdala selectively impaired contextual fear memory formation in female, but not male, rats. It is unknown, however, whether the sex-specific requirement of K63 polyubiquitination occurs in other brain regions that are required for contextual fear memory formation, including the hippocampus. Here, we found that CRISPR-dCas13-mediated knockdown of K63 polyubiquitination in the hippocampus significantly enhanced contextual fear memory in both male and female rats, a result that is in striking contrast to what we observed in the amygdala for both sex-specificity and directionality. Using unbiased proteomics, we found that following fear conditioning K63 polyubiquitination was primarily decreased at target proteins in the hippocampus of both males and females. Importantly, the target proteins and downstream functional pathways influenced by K63 polyubiquitination changes diverged significantly by sex. Together, these data suggest that unlike what we previously reported in the amygdala, decreases in K63 polyubiquitination in the hippocampus are a critical regulator of memory formation in the hippocampus of both males and females.</p>\u0000 </div>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142748886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HippocampusPub Date : 2024-11-26DOI: 10.1002/hipo.23649
{"title":"CORRECTION to “RETRACTION: Hippocampus of Ames Dwarf Mice is Resistant to β-Amyloid-Induced Tau Hyperphosphorylation and Changes in Apoptosis-Regulatory Protein Levels”","authors":"","doi":"10.1002/hipo.23649","DOIUrl":"10.1002/hipo.23649","url":null,"abstract":"<p>M. Schrag, S. Sharma, H. Brown-Borg, and O. Ghribi, “RETRACTION: Hippocampus of Ames Dwarf Mice is Resistant to β-Amyloid-Induced Tau Hyperphosphorylation and Changes in Apoptosis-Regulatory Protein Levels,” <i>Hippocampus</i> 18, no. 3 (2007): 239–244, https://doi.org/10.1002/hipo.23626.</p><p>In the above retraction notice, it was erroneously stated that Holly Brown-Borg did not respond. Brown-Borg did respond, and was unaware of Ghribi's actions and not in any way involved. Brown-Borg agrees with this decision.</p><p>The corrected retraction notice is:</p><p>The above article, published online on November 13, 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Michael E. Hasselmo, and Wiley Periodicals LLC. The retraction has been agreed upon following an investigation by the authors' institution, the University of North Dakota, which determined that this article contains data that the corresponding author, Othman Ghribi, had fabricated. Matthew Schrag and Holly Brown-Borg were unaware of Ghribi's actions and not in any way involved, and they agree with this decision. Sunita Sharma and Othman Ghribi did not respond.</p><p>The online version of this retraction has been corrected accordingly.</p>","PeriodicalId":13171,"journal":{"name":"Hippocampus","volume":"35 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/hipo.23649","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}