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Weerasinghe-Mudiyanselage, Poornima D. E., Sohi Kang, Joong-Sun Kim, Jong-Choon Kim, Sung-Ho Kim, Hongbing Wang, Taekyun Shin, and Changjong Moon. "Transcriptome Profiling in the Hippocampi of Mice with Experimental Autoimmune Encephalomyelitis." International Journal of Molecular Sciences 23, no. 23 (November 27, 2022): 14829. http://dx.doi.org/10.3390/ijms232314829.
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Experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), approximates the key histopathological, clinical, and immunological features of MS. Hippocampal dysfunction in MS and EAE causes varying degrees of cognitive and emotional impairments and synaptic abnormalities. However, the molecular alterations underlying hippocampal dysfunctions in MS and EAE are still under investigation. The purpose of this study was to identify differentially expressed genes (DEGs) in the hippocampus of mice with EAE in order to ascertain potential genes associated with hippocampal dysfunction. Gene expression in the hippocampus was analyzed by RNA-sequencing and validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Gene expression analysis revealed 1202 DEGs; 1023 were upregulated and 179 were downregulated in the hippocampus of mice with EAE (p-value < 0.05 and fold change >1.5). Gene ontology (GO) analysis showed that the upregulated genes in the hippocampi of mice with EAE were associated with immune system processes, defense responses, immune responses, and regulation of immune responses, whereas the downregulated genes were related to learning or memory, behavior, and nervous system processes in the GO biological process. The expressions of hub genes from the search tool for the retrieval of interacting genes/proteins (STRING) analysis were validated by RT-qPCR. Additionally, gene set enrichment analysis showed that the upregulated genes in the hippocampus were associated with inflammatory responses: interferon-γ responses, allograft rejection, interferon-α responses, IL6_JAK_STAT3 signaling, inflammatory responses, complement, IL2_STAT5 signaling, TNF-α signaling via NF-κB, and apoptosis, whereas the downregulated genes were related to synaptic plasticity, dendritic development, and development of dendritic spine. This study characterized the transcriptome pattern in the hippocampi of mice with EAE and signaling pathways underpinning hippocampal dysfunction. However, further investigation is needed to determine the applicability of these findings from this rodent model to patients with MS. Collectively, these results indicate directions for further research to understand the mechanisms behind hippocampal dysfunction in EAE.
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West, Greg L., Kyoko Konishi, and Veronique D. Bohbot. "Video Games and Hippocampus-Dependent Learning." Current Directions in Psychological Science 26, no. 2 (April 2017): 152–58. http://dx.doi.org/10.1177/0963721416687342.
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Research examining the impact of video games on neural systems has largely focused on visual attention and motor control. Recent evidence now shows that video games can also impact the hippocampal memory system. Further, action and 3D-platform video-game genres are thought to have differential impacts on this system. In this review, we examine the specific design elements unique to either action or 3D-platform video games and break down how they could either favor or discourage use of the hippocampal memory system during gameplay. Analysis is based on well-established principles of hippocampus-dependent and non-hippocampus-dependent forms of learning from the human and rodent literature.
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Aggleton, John P., and Malcolm W. Brown. "Episodic memory, amnesia, and the hippocampal–anterior thalamic axis." Behavioral and Brain Sciences 22, no. 3 (June 1999): 425–44. http://dx.doi.org/10.1017/s0140525x99002034.
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By utilizing new information from both clinical and experimental (lesion, electrophysiological, and gene-activation) studies with animals, the anatomy underlying anterograde amnesia has been reformulated. The distinction between temporal lobe and diencephalic amnesia is of limited value in that a common feature of anterograde amnesia is damage to part of an “extended hippocampal system” comprising the hippocampus, the fornix, the mamillary bodies, and the anterior thalamic nuclei. This view, which can be traced back to Delay and Brion (1969), differs from other recent models in placing critical importance on the efferents from the hippocampus via the fornix to the diencephalon. These are necessary for the encoding and, hence, the effective subsequent recall of episodic memory. An additional feature of this hippocampal–anterior thalamic axis is the presence of projections back from the diencephalon to the temporal cortex and hippocampus that also support episodic memory. In contrast, this hippocampal system is not required for tests of item recognition that primarily tax familiarity judgements. Familiarity judgements reflect an independent process that depends on a distinct system involving the perirhinal cortex of the temporal lobe and the medial dorsal nucleus of the thalamus. In the large majority of amnesic cases both the hippocampal–anterior thalamic and the perirhinal–medial dorsal thalamic systems are compromised, leading to severe deficits in both recall and recognition.
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Cherenkova, S. E., E. V. Marchenko, A. M. Alexandrov, N. V. Arkhipova, A. A. Chukhlovin, K. I. Sebelev, and A. M. Alexandrov. "Pharmacoresistant temporal epilepsy: the relationship of epileptiform activity and structural changes in the hippocampus." Translational Medicine 7, no. 6 (December 18, 2020): 46–54. http://dx.doi.org/10.18705/2311-4495-2020-7-6-46-54.
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Background. Hippocampal sclerosis is one of the most common structural lesions associated with epilepsy. The standard medical care in the treatment of drug-resistant temporal lobe epilepsy associated with hippocampal sclerosis is surgery with anterior temporal lobectomy. The extent of resection depends on the involvement of hippocampal sclerosis in the epileptic system. Objective. Determine the relationship between the involvement of the hippocampus in the epileptic system (on the basis of the results of intraoperative electrocorticography (ECoG)) and the presence of structural changes in it, found on the basis of MRI data. Materials and methods. The present article presents an original retrospective study of the dependence of the signs of hippocampal sclerosis according to neuroimaging data and the formation of epileptiform activity in 36 patients treated at the Polenov Neurosurgical Institute — branch of Almazov National Medical Research Centre in 2015–2018. Results. Depending on the presence of hippocampal sclerosis and epileptiform activity, patients were divided into 4 groups: 1) patients with the presence of both hippocampal sclerosis and epileptiform activity in the mesiobasal structures (n = 15); 2) patients with identified sclerosis of the hippocampus, without registration of specific activity according to the results of ECoG (n = 8); 3) patients with epileptiform activity, while MR-negative (n = 10); 4) patients without epileptiform activity and without signs of hippocampal sclerosis according to MRI (n = 3). After a statistical check of the distribution of patients, it was found that the distribution was random. Conclusion. The fact of the presence of structural changes in the hippocampus could not be a pathognomonic sign of the inclusion of the hippocampal-entorial complex in the epileptic system.
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Pereira, D., M. Freschi, R. Frittoli, A. C. Londe, T. Amaral, S. Dertkigil, A. P. Del Rio, F. Cendes, L. Rittner, and S. Appenzeller. "AB0457 HIPPOCAMPAL SUBFIELDS VOLUMES REDUCTION IN PATIENTS WITH SYSTEMIC SCLEROSIS: A LONGITUDINAL MAGNETIC RESONANCE IMAGING (MRI) VOLUMETRIC STUDY." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1255.2–1256. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3815.
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Background:Systemic sclerosis (SSc) is a multisystem disease characterized by functional and structural abnormalities of small blood vessels, fibrosis of the skin and internal organs. In addition, volume reduction and shape abnormality of the hippocampus have been demonstrated in rheumatic and neurodegenerative diseases. However, the neuroanatomy of the hippocampus is complex and is not a uniform structure, consisting of subfields with distinct morphology: cornu ammonis (CA) subfields CA1–4, dentate gyrus (DG), fimbria, and adjacent subiculum and presubiculum [1].Objectives:To investigate the hippocampal subfields volumes reduction in SSc patients using MRI.Methods:In this study we included 37 SSc patients (33 women, mean age of 53.46, SD ± 12.29; range 30 - 78) and 37 healthy controls (HC) (31 women, mean age of 48.41, SD±12.20; range 29 - 80). Cognitive evaluation was performed using the Montreal Cognitive Assessment (MoCA), mood disorders were determined through Beck’s Depression (BDI) and Beck’s Anxiety Inventories (BAI). SSc patients were further assessed for clinical and laboratory SSc manifestations, disease activity (Valentini Activity Index), severity activity (Medsger Severity Index). MRI protocol consisted of: Sagittal T1-weighted images performed with a Philips 3.0T MRI scanner. MRI brain structure volumetric was done through volBrain [2]. After 48 months MRI acquisition were repeated in 26 SSc patients and 12 healthy volunteers. Statistics was performed according nature of the variable.Results:We observed a significant reduction in hippocampal subfields volumes in SSc patients when compared to controls: Total hippocampi (SSc: mean volume = 4.78 cm3; SD = 0.38; HC: mean volume = 5.01 cm3; SD = 0.38; p = 0.033). Reduction in volume of the total hippocampi was associated with Raynaud’s phenomenon (p = 0.006). A longitudinal study showed a reduction in volume of the hippocampus subfields volumes when compared to patient’s baseline: Total hippocampi (mean initial volume = 4.78 cm3; mean follow-up volume = 4.50 cm3, p = 0.027); Total CA1 (mean initial volume = 1.59 cm3; mean follow-up volume = 1.58 cm3, p < 0.0001); Reduction in volume of the total hippocampi was associated with presence of current use of prednisone (p = 0.008). Reduction in left CA1 left associated with current use of prednisone (p = 0.014). Reduction in total subiculum was associated with presence of calcinosis (p = 0.023). No significant changes were observed in hippocampal subfields volumes in controls over the follow-up period.Conclusion:This study provides evidence of hippocampus subfields volumes reductions in SSc patients when compared to controls and was associated with Raynaud’s phenomenon, current use of losartan and correlated with BAI scores. Also, a longitudinal study showed a reduction in volume of the hippocampus subfields volumes when compared to patient’s baseline associated with calcinosis and current use of prednisone.References:[1]Eichenbaum, Howard. “A cortical–hippocampal system for declarative memory.” Nature Reviews Neuroscience 1.1 (2000): 41-50.[2]Manjon JV, Coupe P (2016) volBrain: an online MRI brain volumetry system. Front Neuroinform 10:30.Disclosure of Interests:None declared.
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Carboni, Tatiana. "HIPPOCAMPAL NEUROGENESIS IN DEPRESSIVE DISORDER." Psych-Talk 1, no. 101 (January 2022): 33–38. http://dx.doi.org/10.53841/bpstalk.2022.1.101.33.
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RECENT RESEARCH SUGGESTS THAT A LOSS OF SYNAPTIC PLASTICITY IN SPECIFIC AREAS OF THE CENTRAL NERVOUS SYSTEM, ESPECIALLY THE HIPPOCAMPUS, CAN PLAY A ROLE IN THE PATHOPHYSIOLOGY OF DEPRESSION (MASI, 2011). GIVEN THE EVIDENCE FOR HIPPOCAMPAL VOLUME CHANGES IN DEPRESSIVE PATIENTS AND ATROPHY OF HIPPOCAMPAL NEURONS UNDER STRESS, NEUROGENESIS (THE DEVELOPMENT OF NEW NEURONS IN THE ADULT BRAIN’S DENTATE GYRUS) HAS RECEIVED A LOT OF INTEREST AS A POSSIBLE MEDIATOR OF STRESS EFFECTS ON THE HIPPOCAMPUS (ANACKER, 2014).
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Zhang, X.-D., L.-R. Zhao, J.-M. Zhou, Y.-Y. Su, J. Ke, Y. Cheng, J.-L. Li, and W. Shen. "Altered hippocampal functional connectivity in primary Sjögren syndrome: a resting-state fMRI study." Lupus 29, no. 5 (February 19, 2020): 446–54. http://dx.doi.org/10.1177/0961203320908936.
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Structural and metabolic abnormalities in the hippocampus have been associated with the pathophysiological mechanism of central nervous system involvement in primary Sjögren syndrome (pSS). Nevertheless, how hippocampal function is altered in pSS remains unknown. The purpose of our study is to investigate the alterations in hippocampal functional connectivity (FC) in pSS by using resting-state functional magnetic resonance imaging (rs-fMRI). Thirty-eight patients with pSS and 38 age- and education level-matched healthy controls (HCs) underwent magnetic resonance imaging examination. Prior to each MRI examination, neuropsychological tests were performed. Left and right hippocampal FCs were analyzed by using seed-based whole-brain correlation and compared between pSS and HCs. Spearman correlation analysis was performed between the z-value of hippocampal FC in brain regions with significant difference between the two groups and neuropsychological tests/clinical data in pSS. Compared with the controls, the patients with pSS showed decreased hippocampal FC between the left hippocampus and the right inferior occipital gray (IOG)/inferior temporal gray (ITG), as well as between the right hippocampus and right IOG/middle occipital gray (MOG), left MOG, and left middle temporal gray. In addition, increased hippocampal FCs were detected between the left hippocampus and left putamen, as well as between the right hippocampus and right cerebellum posterior lobe. Moreover, the visual reproduction score positively correlated with the FC between right hippocampus and right IOG/MOG. The white matter hyperintensity score negatively correlated with the FC between left hippocampus and right IOG/ITG. In conclusion, patients with pSS suffered decreased hippocampal FC mainly sited in the occipital and temporal cortex with right hippocampal laterality. Altered hippocampal FC might be a potential biomarker in detecting brain function changes and guiding neuroprotection in pSS.
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Halász, Péter. "The relationship of medial temporal lobe epilepsy with the declarative memory system." Journal of Epileptology 24, no. 2 (December 1, 2016): 157–65. http://dx.doi.org/10.1515/joepi-2016-0011.
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SummaryIntroduction.Medial temporal lobe of epilepsy (MTLE) is considered as local/regional epilepsy. However, as was discussed in Part I of this review (Halász, 2016a) there is more evidence regarding the involvement of both temporal lobes so as to consider MTLE as one of the typical bilateral system epilepsies.Aim.To provide contemporary review of MTLE in relation to the declarative memory system and the newly recognized hippocampo-frontal memory consolidation during slow wave sleep.Methods.A review of the available literature on experimental and clinical data and also the authors own studies in MTLE patients.Review, discussion and results.New experimental and clinical neurophysiological data have shown that MTLE is closely linked to the hippocampal memory system. It is likely that hippocampal spiking is the epileptic variations of the normal sharp wave ripple events mediating the encoding and consolidation of memory engrams by a hippocampo-frontal dialogue during slow wave sleep.Conclusions.The source of memory impairment in MTLE patients is not merely the cell loss and synaptic transformation of the hippocampal structure, but the every night interference with memory consolidation due to interictal spiking.
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Tanaka, Nobuhiro, Masami Fujii, Hirochika Imoto, Joji Uchiyama, Kimihiko Nakano, Sadahiro Nomura, Hirosuke Fujisawa, Ichiro Kunitsugu, Takashi Saito, and Michiyasu Suzuki. "Effective suppression of hippocampal seizures in rats by direct hippocampal cooling with a Peltier chip." Journal of Neurosurgery 108, no. 4 (April 2008): 791–97. http://dx.doi.org/10.3171/jns/2008/108/4/0791.
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Object The use of focal brain cooling to eliminate epileptic discharges (EDs) has attracted increasing attention in the scientific community. In this study, the inhibitory effect of selective hippocampal cooling on experimental hippocampal seizures was investigated using a newly devised cooling system with a thermoelectric (Peltier) chip. Methods A copper needle coated with silicone and attached to the Peltier chip was used for the cooling device. The experiments were performed first in a phantom model with thermography and second in adult male Sprague–Dawley rats in a state of halothane anesthesia. The cooling needle, a thermocouple, and a needle electrode for electroencephalography recording were inserted into the right hippocampus. Kainic acid (KA) was injected into the right hippocampus to provoke the EDs. The animals were divided into hippocampal cooling (10 rats) and noncooling (control, 10 rats) groups. Results In the phantom study, the cooling effects (9°C) occurred in the spherical areas around the needle tip. In the rats the temperature of the cooled hippocampus decreased below 20°C within a 1.6-mm radius and below 25°C within a 2.4-mm radius from the cooling center. The temperature at the needle tip decreased below 20°C within 1 minute and was maintained at the same level until the end of the cooling process. The amplitude of the EDs was suppressed to 68.1 ± 4.8% of the precooling value and remained low thereafter. No histological damage due to cooling was observed in the rat hippocampus. Conclusions Selective hippocampal cooling effectively suppresses the KA-induced hippocampal EDs. Direct hippocampal cooling with a permanently implantable system is potentially useful as a minimally invasive therapy for temporal lobe epilepsy and therefore could be an alternative to the temporal lobectomy.
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Sugiyama, Atsuhiko, Hajime Yokota, Shigeki Hirano, Jiaqi Wang, Shoichi Ito, and Satoshi Kuwabara. "Association between Cognitive Impairment and Hippocampal Subfield Volumes in Multiple System Atrophy." Parkinson's Disease 2023 (March 6, 2023): 1–8. http://dx.doi.org/10.1155/2023/8888255.
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This study aimed to explore morphological changes of hippocampal subfields in patients with multiple system atrophy (MSA) with and without cognitive impairment using FreeSurfer-automated segmentation of hippocampal subfield techniques and their relationship with cognitive function. We enrolled 75 patients with MSA classified as cognitively impaired MSA (MSA-CI, n = 40) and cognitively preserved MSA (MSA-CP, n = 35), as well as 68 healthy controls. All participants underwent three-dimensional volume T1-weighted magnetic resonance imaging. The hippocampal subfield volume was measured using FreeSurfer version 7.2 and compared among groups. Regression analyses were performed between the hippocampal subfield volumes and cognitive variables. Compared with healthy controls, the volume of the right cornu ammonis (CA) 2/3 was significantly lower in the MSA-CI group ( P = 0.029 ) and that of the left fimbria was significantly higher in the MSA-CP group ( P = 0.046 ). Results of linear regression analysis showed that the right CA2/3 volume was significantly correlated with the Frontal Assessment Battery score in patients with MSA (adjusted R2 = 0.282, β = 0.227, and P = 0.041 ). The hippocampal subfield volume decreased in patients with MSA-CI, even at the early disease stages. Specific structural changes in the hippocampus might be associated with cognitive deficits in MSA.
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Lathe, R. "Hormones and the hippocampus." Journal of Endocrinology 169, no. 2 (May 1, 2001): 205–31. http://dx.doi.org/10.1677/joe.0.1690205.
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Hippocampal lesions produce memory deficits, but the exact function of the hippocampus remains obscure. Evidence is presented that its role in memory may be ancillary to physiological regulation. Molecular studies demonstrate that the hippocampus is a primary target for ligands that reflect body physiology, including ion balance and blood pressure, immunity, pain, reproductive status, satiety and stress. Hippocampal receptors are functional, probably accessible to their ligands, and mediate physiological and cognitive changes. This argues that an early role of the hippocampus may have been in sensing soluble molecules (termed here 'enteroception') in blood and cerebrospinal fluid, perhaps reflecting a common evolutionary origin with the olfactory system ('exteroception'). Functionally, hippocampal enteroception may reflect feedback control; evidence is reviewed that the hippocampus modulates body physiology, including the activity of the hypothalamus-pituitary-adrenal axis, blood pressure, immunity, and reproductive function. It is suggested that the hippocampus operates, in parallel with the amygdala, to modulate body physiology in response to cognitive stimuli. Hippocampal outputs are predominantly inhibitory on downstream neuroendocrine activity; increased synaptic efficacy in the hippocampus (e.g. long-term potentiation) could facilitate throughput inhibition. This may have implications for the role of the hippocampus and long-term potentiation in memory.
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Ajaz, R., SM Mirsattari, R. Mousavi, and S. Leung. "P.029 Limbic system involvement in absence seizures." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 44, S2 (June 2017): S21. http://dx.doi.org/10.1017/cjn.2017.114.
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Background: Absence epilepsy (AE) is believed to be generated by a thalamocortical network. Our laboratory showed that hippocampal neuronal firings were synchronous with the SWDs in the gamma butyrolactone (GBL) model of AE in rats. Here, we hypothesize that high frequency oscillations (HFOs) in the hippocampus and other parts of the limbic system were phase modulated by SWDs Methods: GBL (200 mg/kg i.p) was injected to induce SWDs in 6 male Long-Evans rats. Spontaneous local field potentials (LFPs) were recorded from electrodes implanted in the hippocampus and ventrolateral thalamus bilaterally and the right frontal cortex. For each LFP, modulation index (MI) gives the cross-frequency amplitude modulation of the HFOs (;90-250 Hz) by the phase of the SWD frequency at 2-8 Hz Results: Phase modulation of the HFOs by 2-8 Hz frequency increased for >45 min after GBL injection. MI increase was higher for hippocampal than thalamic LFPs, and not significant for frontal cortical LFP. MI for the nucleus accumbens LFP (N= 1 rat) also increased after GBL Conclusions: The modulation of HFOs (presumed local neural activity) by SWD frequency provides further support that the hippocampus and connected limbic system may become synchronous with the SWDs in AE
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Nitz, Douglas A., and Bruce L. McNaughton. "Hippocampal EEG and Unit Activity Responses to Modulation of Serotonergic Median Raphe Neurons in the Freely Behaving Rat." Learning & Memory 6, no. 2 (March 1, 1999): 153–67. http://dx.doi.org/10.1101/lm.6.2.153.
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Hippocampal EEG, GABAergic interneurons, and principal cells were recorded simultaneously as rats foraged within one of three environments both before and after modulation of serotonergic inputs to the hippocampus. Median raphe microinjections of the 5-HT1a receptor agonist 8-OH-DPAT were made to produce inhibition of serotonergic neurons in this region. Such microinjections produced behavioral arousal and increases in the amplitude of hippocampal EEG theta. Consistent with the pattern of serotonergic innervation of the hippocampus, the GABAergic interneuron population was affected differentially by the microinjections. Principal cells were generally unaffected by the manipulation and maintained robust spatial firing correlates within the foraging environment. The results provide basic data on the relationship between serotonergic median raphe neurons and hippocampal activity in a behaving animal. The data suggest that behavioral responses to manipulation of the serotonergic system are mediated by brain regions other than the hippocampus or are mediated through changes in the activity of hippocampal interneurons.
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Martin, Claire, Jennifer Beshel, and Leslie M. Kay. "An Olfacto-Hippocampal Network Is Dynamically Involved in Odor-Discrimination Learning." Journal of Neurophysiology 98, no. 4 (October 2007): 2196–205. http://dx.doi.org/10.1152/jn.00524.2007.
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Several studies have shown that memory consolidation relies partly on interactions between sensory and limbic areas. The functional loop formed by the olfactory system and the hippocampus represents an experimentally tractable model that can provide insight into this question. It had been shown previously that odor-learning associated beta band oscillations (15–30 Hz) of the local field potential in the rat olfactory system are enhanced with criterion performance, but it was unknown if these involve networks beyond the olfactory system. We recorded local field potentials from the olfactory bulb (OB) and dorsal and ventral hippocampus during acquisition of odor discriminations in a go/no-go task. These regions showed increased beta oscillation power during odor sampling, accompanied by a coherence increase in this frequency band between the OB and both hippocampal subfields. This coherence between the OB and the hippocampus increased with the onset of the first rule transfer to a new odor set and remained high for all learning phases and subsequent odor sets. However, coherence between the two hippocampal fields reset to baseline levels with each new odor set and increased again with criterion performance. These data support hippocampal involvement in the network underlying odor-discrimination learning and also suggest that cooperation between the dorsal and ventral hippocampus varies with learning progress. Oscillatory activity in the beta range may thus provide a mechanism by which these areas are linked during memory consolidation, similar to proposed roles of beta oscillations in other systems with long-range connections.
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Sun, Haijian, Lin Liu, Chunhua Feng, and Aike Guo. "Modeling Research on Spatiotemporal Dynamics of the Hippocampus." International Journal of Bifurcation and Chaos 07, no. 01 (January 1997): 187–98. http://dx.doi.org/10.1142/s0218127497000121.
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The spatiotemporal dynamics of the hippocampus is studied. We first propose a fractal algorithm to model the growth of hippocampal CA1 pyramidal cells, together with an avalanche model for information transmission. Then the optical records of an epileptic focus in the hippocampus are analyzed and simulated. These processes indicate that the hippocampus normally stays in self-organized criticality with a harmonious spatiotemporal behavioral pattern, that is, showing 1/f fluctuation and power law distribution. In case of a neurological insult, the hippocampal system may step into supercriticality and initiate epilepsy.
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Sepehri, Hamid, Farzaneh Ganji, Zahra Nazari, and Marzieh Vahid. "Effects of Goldblatt hypertension on rats’ hippocampal cholinergic system." Translational Neuroscience 13, no. 1 (January 1, 2022): 72–79. http://dx.doi.org/10.1515/tnsci-2022-0215.
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Abstract Background The classical renin-angiotensin system (RAS) has an important role in the cardiovascular system and water homeostasis in the body. Recently, the existence of RAS with all of its components has been shown in the mammalian brain. RAS participates in many brain activities, including memory acquisition and consolidation. Since the cholinergic neurotransmission in the hippocampus is crucial for these functions, this study aims to evaluate the hippocampal angiotensin receptors (ATs) and choline acetyltransferase (ChAT) mRNA in the renovascular hypertensive rats in captopril- and losartan-treated hypertensive rats. Methods The rats were randomly divided into four groups of eight animals; sham, Goldblatt two kidney one clip (2K1C) hypertensive rats and Goldblatt 2K1C hypertensive rats received 5 mg/kg captopril and Goldblatt 2K1C hypertensive rats received 10 mg/kg losartan. After 8 days of treatment, the rats were sacrificed and angiotensin-converting enzyme (ACE), ChAT, AT1, and AT2 receptor mRNAs in the hippocampus of rats were assessed by real-time PCR. The Morris water maze test was applied to measure the cognitive functioning of the rats. Results Hypertensive rats showed impaired acquisition and memory function in the Morris water maze test. Treatment with ACE inhibitor (captopril) and AT1 receptor antagonist (losartan) reversed the observed acquisition and memory deficit in hypertensive rats. Overexpression of AChE, AT1, and AT2 and low expression of ChAT were noted in the hippocampus of rats with Goldblatt hypertension compared with that of the sham group. Treatment with captopril significantly reversed these changes, while treatment with losartan slightly reduced the mentioned effects. Conclusion The memory-enhancing effect of captopril in renovascular hypertensive rats might lead to increased hippocampal ChAT expression.
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Ismael, Saifudeen, Golnoush Mirzahosseini, Heba A. Ahmed, Arum Yoo, Modar Kassan, Kafait U. Malik, and Tauheed Ishrat. "Renin-Angiotensin System Alterations in the Human Alzheimer’s Disease Brain." Journal of Alzheimer's Disease 84, no. 4 (December 7, 2021): 1473–84. http://dx.doi.org/10.3233/jad-215051.
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Background: Understanding Alzheimer’s disease (AD) in terms of its various pathophysiological pathways is essential to unravel the complex nature of the disease process and identify potential therapeutic targets. The renin-angiotensin system (RAS) has been implicated in several brain diseases, including traumatic brain injury, ischemic stroke, and AD. Objective: This study was designed to evaluate the protein expression levels of RAS components in postmortem cortical and hippocampal brain samples obtained from AD versus non-AD individuals. Methods: We analyzed RAS components in the cortex and hippocampus of postmortem human brain samples by western blotting and immunohistochemical techniques in comparison with age-matched non-demented controls. Results: The expression of AT1R increased in the hippocampus, whereas AT2R expression remained almost unchanged in the cortical and hippocampal regions of AD compared to non-AD brains. The Mas receptor was downregulated in the hippocampus. We also detected slight reductions in ACE-1 protein levels in both the cortex and hippocampus of AD brains, with minor elevations in ACE-2 in the cortex. We did not find remarkable differences in the protein levels of angiotensinogen and Ang II in either the cortex or hippocampus of AD brains, whereas we observed a considerable increase in the expression of brain-derived neurotrophic factor in the hippocampus. Conclusion: The current findings support the significant contribution of RAS components in AD pathogenesis, further suggesting that strategies focusing on the AT1R and AT2R pathways may lead to novel therapies for the management of AD.
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Venturini, Carina Duarte, Suélen Merlo, André Arigony Souto, Marilda da Cruz Fernandes, Rosane Gomez, and Claudia Ramos Rhoden. "Resveratrol and Red Wine Function as Antioxidants in the Nervous System without Cellular Proliferative Effects during Experimental Diabetes." Oxidative Medicine and Cellular Longevity 3, no. 6 (2010): 434–41. http://dx.doi.org/10.4161/oxim.3.6.14741.
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Chronic hyperglycemia increases oxidative stress status and has been associated with neurological complications in diabetic individuals. This study compared the antioxidant properties of red wine or resveratrol in different brain areas of diabetic and non-diabetic rats, and investigated the effect of them on hippocampal cell proliferation in hippocampal dentate gyrus of diabetic rats. Streptozotocin-induced diabetic and control rats were treated with red wine (4 mL/kg), resveratrol (20 mg/kg) or saline, by oral gavage, for 21 days. Lipid peroxidation (TBARS), catalase and superoxide dismutase were measured to evaluate the oxidative stress and the BrdU-positive cells were assessed to measure changes in cellular proliferation. In diabetic animals, resveratrol showed antioxidant property in the hippocampus and in the striatum, while red wine had an antioxidant effect only in the hippocampus. Neither red wine nor resveratrol reversed the lower hippocampal cell proliferation in diabetic rats. Daily doses of red wine or resveratrol have an antioxidant effect in rats depending on the brain area and the glycemic status.
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Eichenbaum, Howard. "The role of the hippocampus in navigation is memory." Journal of Neurophysiology 117, no. 4 (April 1, 2017): 1785–96. http://dx.doi.org/10.1152/jn.00005.2017.
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There is considerable research on the neurobiological mechanisms within the hippocampal system that support spatial navigation. In this article I review the literature on navigational strategies in humans and animals, observations on hippocampal function in navigation, and studies of hippocampal neural activity in animals and humans performing different navigational tasks and tests of memory. Whereas the hippocampus is essential to spatial navigation via a cognitive map, its role derives from the relational organization and flexibility of cognitive maps and not from a selective role in the spatial domain. Correspondingly, hippocampal networks map multiple navigational strategies, as well as other spatial and nonspatial memories and knowledge domains that share an emphasis on relational organization. These observations suggest that the hippocampal system is not dedicated to spatial cognition and navigation, but organizes experiences in memory, for which spatial mapping and navigation are both a metaphor for and a prominent application of relational memory organization.
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Kubota, Don, Laura Lee Colgin, Malcolm Casale, Fernando A. Brucher, and Gary Lynch. "Endogenous Waves in Hippocampal Slices." Journal of Neurophysiology 89, no. 1 (January 1, 2003): 81–89. http://dx.doi.org/10.1152/jn.00542.2002.
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Sharp waves (SPWs) are thought to play a major role in intrinsic hippocampal operations during states in which subcortical and cortical inputs to hippocampus are reduced. This study describes evidence that such activity occurs spontaneously in appropriately prepared rat hippocampal slices. Irregular waves, with an average frequency of approximately 4 Hz, were recorded from field CA3 in slices prepared from the temporal region of hippocampus. The waves persisted for hours and were not accompanied by aberrant discharges. Multi-electrode analyses established that they were locally generated within each of the subfields of CA3 and yet were coherent between subfields. The sharp waves were reversibly blocked by either cholinergic or serotonergic stimulation. Various lines of evidence indicate that they are propagated by the CA3 associational system.
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Grigoryan, Gayane, Niklas Lonnemann, and Martin Korte. "Immune Challenge Alters Reactivity of Hippocampal Noradrenergic System in Prenatally Stressed Aged Mice." Neural Plasticity 2019 (January 21, 2019): 1–13. http://dx.doi.org/10.1155/2019/3152129.
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Prenatal stress (PS) has long-term sequelae for the morphological and functional status of the central nervous system of the progeny. A PS-induced proinflammatory status of the organism may result in an impairment of both hippocampal synaptic plasticity and hippocampus-dependent memory formation in adults. We addressed here the question of how PS-induced alterations in the immune response in young and old mice may contribute to changes in hippocampal function in aging. Immune stimulation (via LPS injection) significantly affected the ability of the hippocampal CA3-CA1 synapse of PS mice to undergo long-term potentiation (LTP). Elevated corticosterone level in the blood of aged PS mice that is known to influence LTP magnitude indicates a chronic activation of the HPA axis due to the in utero stress exposure. We investigated the contribution of adrenergic receptors to the modulation of hippocampal synaptic plasticity of aged mice and found that impaired LTP in the PS-LPS group was indeed rescued by application of isoproterenol (a nonspecific noradrenergic agonist). Further exploration of the mechanisms of the observed phenomena will add to our understanding of the interaction between PS and proinflammatory immune activation and its contribution to the functional and structural integrity of the aging brain.
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Shen, Kelly, Gleb Bezgin, Rajajee Selvam, Anthony R. McIntosh, and Jennifer D. Ryan. "An Anatomical Interface between Memory and Oculomotor Systems." Journal of Cognitive Neuroscience 28, no. 11 (November 2016): 1772–83. http://dx.doi.org/10.1162/jocn_a_01007.
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Visual behavior is guided by memories from prior experience and knowledge of the visual scene. The hippocampal system (HC), in particular, has been implicated in the guidance of saccades: Amnesic patients, following damage to the HC, exhibit selective deficits in their gaze patterns. However, the neural circuitry by which mnemonic representations influence the oculomotor system remains unknown. We used a data-driven, network-based approach on directed anatomical connectivity from the macaque brain to reveal an extensive set of polysnaptic pathways spanning the extrastriate, posterior parietal and prefrontal cortices that potentially mediate the exchange of information between the memory and visuo-oculomotor systems. We additionally show how the potential for directed information flow from the hippocampus to oculomotor control areas is exceptionally high. In particular, the dorsolateral pFC and FEF—regions known to be responsible for the cognitive control of saccades—are topologically well positioned to receive information from the hippocampus. Together with neuropsychological evidence of altered gaze patterns following damage to the hippocampus, our findings suggest that a reconsideration of hippocampal involvement in oculomotor guidance is needed.
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Kouhnavardi, Shima, Maureen Cabatic, M. Carmen Mañas-Padilla, Marife-Astrid Malabanan, Tarik Smani, Ana Cicvaric, Edison Alejandro Muñoz Aranzalez, et al. "miRNA-132/212 Deficiency Disrupts Selective Corticosterone Modulation of Dorsal vs. Ventral Hippocampal Metaplasticity." International Journal of Molecular Sciences 24, no. 11 (May 31, 2023): 9565. http://dx.doi.org/10.3390/ijms24119565.
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Cortisol is a potent human steroid hormone that plays key roles in the central nervous system, influencing processes such as brain neuronal synaptic plasticity and regulating the expression of emotional and behavioral responses. The relevance of cortisol stands out in the disease, as its dysregulation is associated with debilitating conditions such as Alzheimer’s Disease, chronic stress, anxiety and depression. Among other brain regions, cortisol importantly influences the function of the hippocampus, a structure central for memory and emotional information processing. The mechanisms fine-tuning the different synaptic responses of the hippocampus to steroid hormone signaling remain, however, poorly understood. Using ex vivo electrophysiology and wild type (WT) and miR-132/miR-212 microRNAs knockout (miRNA-132/212−/−) mice, we examined the effects of corticosterone (the rodent’s equivalent to cortisol in humans) on the synaptic properties of the dorsal and ventral hippocampus. In WT mice, corticosterone predominantly inhibited metaplasticity in the dorsal WT hippocampi, whereas it significantly dysregulated both synaptic transmission and metaplasticity at dorsal and ventral regions of miR–132/212−/− hippocampi. Western blotting further revealed significantly augmented levels of endogenous CREB and a significant CREB reduction in response to corticosterone only in miR–132/212−/− hippocampi. Sirt1 levels were also endogenously enhanced in the miR–132/212−/− hippocampi but unaltered by corticosterone, whereas the levels of phospo-MSK1 were only reduced by corticosterone in WT, not in miR–132/212−/− hippocampi. In behavioral studies using the elevated plus maze, miRNA-132/212−/− mice further showed reduced anxiety-like behavior. These observations propose miRNA-132/212 as potential region-selective regulators of the effects of steroid hormones on hippocampal functions, thus likely fine-tuning hippocampus-dependent memory and emotional processing.
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Mullins, D., M. Lamar, E. Daly, A. Simmons, K. Murphy, S. Lovestone, and D. Murphy. "Dementia in Alzheimer’s Disease: A Comparison of MRI and 1H-MRS Findings Between Alzheimer’s Disease and Mild Cognitive Impairment." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70929-0.
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Aim:To compare Magnetic Resonance Imaging (MRI) and Magnetic Resonance Spectroscopy (1H-MRS) between people with Alzheimer's disease (AD) and mild cognitive impairment (MCI).Background review:AD is characterised by cognitive impairment. 10-15% of people with MCI progress to dementia each year. The hippocampus is involved in memory functioning and is one of the brain regions first affected by AD. MRI based hippocampal volumetric measurement enables accurate quantification of atrophy. In addition, 1H-MRS can be used to measure concentrations of brain metabolites including myoinositol (mI) and N-acetylaspartate (NAA). NAA is a proxy measure of neuronal density.Method:Subjects with AD (n=46), MCI (n=28) and controls (n=39) were scanned using a 1.5 Tesla MR system. Manual tracing of hippocampal volumes was undertaken using Measure software. 1H-MRS voxels of interest were defined in the left and right hippocampi. A point-resolved spectroscopy pulse sequence produced spectra from each voxel and clearly resolved NAA and mI peaks. Statistical analysis was undertaken using SPSS15.Results:Hippocampal volumes were significantly reduced between AD and controls (p=0.003) and between AD and MCI (p=0.001). Compared to controls, individuals with AD and MCI had a significant reduction in [NAA]. MCI showed a non-significant increase in [mI]. A positive relationship was found between hippocampal volume and [NAA] and between hippocampal volume and [mI] for MCI.Conclusions:AD is associated with decreased viable neuronal density/function (as measured by NAA) and a reduction in hippocampal volume associated with impaired cognitive functioning. The elevated [mI] in MCI may be a “tipping point” into dementia.
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Zhong, Haiquan, Jing Rong, Chunting Zhu, Min Liang, Yingchun Li, and Rong Zhou. "Epigenetic Modifications of GABAergic Interneurons Contribute to Deficits in Adult Hippocampus Neurogenesis and Depression-Like Behavior in Prenatally Stressed Mice." International Journal of Neuropsychopharmacology 23, no. 4 (March 25, 2020): 274–85. http://dx.doi.org/10.1093/ijnp/pyaa020.
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Abstract Background Prenatal stress (PRS) is considered a risk factor for depressive disorder. Adult hippocampal neurogenesis is believed to play a role in the regulation of affective behaviors. GABAergic interneuron is a key modulator in adult hippocampal neurogenesis. Growing evidence indicates that PRS has adverse effects on adult hippocampal neurogenesis and DNA epigenetic modifications of the GABAergic system. The aim of this study was to investigate whether epigenetic GABAergic dysfunction participates in the negative impact of PRS on adult hippocampal neurogenesis and related emotional behaviors. Methods Behavioral tests were used to explore PRS-induced depression-like behaviors of adult female mice. Immunohistochemistry staining, real-time reverse transcription-polymerase chain reaction, western blot, and chromatin immunoprecipitation were employed to detect adult neurogenesis and epigenetic changes of the GABAergic system in the hippocampus of PRS mice. Results PRS mice developed a depression phenotype accompanied by the inhibited maturation of hippocampal newborn neurons. Compared with control mice, PRS mice showed decreased expression of glutamic acid decarboxylase 67 at the mRNA and protein levels. GABAA receptor agonist phenobarbital could rectify the decrease of 5-bromo-2-deoxyuridine/neuronal nuclei double-positive (BrdU+/NeuN+) cells in PRS mice. PRS mice also showed increased expression of DNA methyltransferase 1 and increased binding of DNA methyltransferase 1 to glutamic acid decarboxylase 67 promoter region. The treatment with DNA methyltransferase 1 inhibitor 5-aza-deoxycytidine restored the decrease of BrdU+/NeuN+ cells and depression-like behaviors in PRS mice via improving GABAergic system. Conclusions The present results indicate that epigenetic changes of the GABAergic system are responsible for adult hippocampus neurogenesis and depression-like behaviors in PRS mice.
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Lau, JC, J. DeKraker, KW MacDougall, H. Joswig, AG Parrent, JG Burneo, DA Steven, TM Peters, and AR Khan. "P.063 Stereotactic targeting of hippocampal substructures using ultra-high field magnetic resonance imaging: Feasibility study in patients with epilepsy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, s2 (June 2018): S32—S33. http://dx.doi.org/10.1017/cjn.2018.165.
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Background: The hippocampus can be divided longitudinally into the head, body, and tail; and unfolded medial-to-laterally into the subiculum, cornu ammonis (CA) sectors, and the dentate gyrus. Ultra-high field (≥ 7 Tesla; 7T) magnetic resonance imaging (MRI) enables submillimetric visualization of these hippocampal substructures which could be valuable for surgical targeting. Here, we assess the feasibility of using 7T MRI in conjunction with a novel computational unfolding method for image-based stereotactic targeting of hippocampal substructures. Methods: 53 patients with drug-resistant epilepsy were identified undergoing first-time implantation of the hippocampus. An image processing pipeline was created for computationally transforming post-operative electrode contact locations into our hippocampal coordinate system. Results: Of 178 implanted hippocampal electrodes (88 left; 49.4%), 25 (14.0%) were predominantly in the subiculum, 85 (47.8%) were in CA1, 23 (12.9%) were in CA2, 18 (10.1%) were in CA3/CA4, and 27 (15.2%) were in dentate gyrus. Along the longitudinal axis, hippocampal electrodes were most commonly implanted in the body (92; 51.7%) followed by the head (86; 48.3%). Conclusions: 7T MRI enables high-resolution anatomical imaging on the submillimeter scale in in vivo subjects. Here, we demonstrate the utility of 7T imaging for identifying the relative location of SEEG electrode implantations within hippocampal substructures for the invasive investigation of epilepsy.
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Tidmore, Alyssa, Sucharita M. Dutta, Arriyam S. Fesshaye, William K. Russell, Vania D. Duncan, and Richard A. Britten. "Space Radiation-Induced Alterations in the Hippocampal Ubiquitin-Proteome System." International Journal of Molecular Sciences 22, no. 14 (July 19, 2021): 7713. http://dx.doi.org/10.3390/ijms22147713.
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Exposure of rodents to <20 cGy Space Radiation (SR) impairs performance in several hippocampus-dependent cognitive tasks, including spatial memory. However, there is considerable inter-individual susceptibility to develop SR-induced spatial memory impairment. In this study, a robust label-free mass spectrometry (MS)-based unbiased proteomic profiling approach was used to characterize the composition of the hippocampal proteome in adult male Wistar rats exposed to 15 cGy of 1 GeV/n 48Ti and their sham counterparts. Unique protein signatures were identified in the hippocampal proteome of: (1) sham rats, (2) Ti-exposed rats, (3) Ti-exposed rats that had sham-like spatial memory performance, and (4) Ti-exposed rats that impaired spatial memory performance. Approximately 14% (159) of the proteins detected in hippocampal proteome of sham rats were not detected in the Ti-exposed rats. We explored the possibility that the loss of the Sham-only proteins may arise as a result of SR-induced changes in protein homeostasis. SR-exposure was associated with a switch towards increased pro-ubiquitination proteins from that seen in Sham. These data suggest that the role of the ubiquitin-proteome system as a determinant of SR-induced neurocognitive deficits needs to be more thoroughly investigated.
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Shinoda, Yo, Tetsushi Sadakata, Kazuhito Nakao, Ritsuko Katoh-Semba, Emi Kinameri, Asako Furuya, Yuchio Yanagawa, Hajime Hirase, and Teiichi Furuichi. "Calcium-dependent activator protein for secretion 2 (CAPS2) promotes BDNF secretion and is critical for the development of GABAergic interneuron network." Proceedings of the National Academy of Sciences 108, no. 1 (December 20, 2010): 373–78. http://dx.doi.org/10.1073/pnas.1012220108.
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Calcium-dependent activator protein for secretion 2 (CAPS2) is a dense-core vesicle-associated protein that is involved in the secretion of BDNF. BDNF has a pivotal role in neuronal survival and development, including the development of inhibitory neurons and their circuits. However, how CAPS2 affects BDNF secretion and its biological significance in inhibitory neurons are largely unknown. Here we reveal the role of CAPS2 in the regulated secretion of BDNF and show the effect of CAPS2 on the development of hippocampal GABAergic systems. We show that CAPS2 is colocalized with BDNF, both synaptically and extrasynaptically in axons of hippocampal neurons. Overexpression of exogenous CAPS2 in hippocampal neurons of CAPS2-KO mice enhanced depolarization-induced BDNF exocytosis events in terms of kinetics, frequency, and amplitude. We also show that in the CAPS2-KO hippocampus, BDNF secretion is reduced, and GABAergic systems are impaired, including a decreased number of GABAergic neurons and their synapses, a decreased number of synaptic vesicles in inhibitory synapses, and a reduced frequency and amplitude of miniature inhibitory postsynaptic currents. Conversely, excitatory neurons in the CAPS2-KO hippocampus were largely unaffected with respect to field excitatory postsynaptic potentials, miniature excitatory postsynaptic currents, and synapse number and morphology. Moreover, CAPS2-KO mice exhibited several GABA system-associated deficits, including reduced late-phase long-term potentiation at CA3–CA1 synapses, decreased hippocampal theta oscillation frequency, and increased anxiety-like behavior. Collectively, these results suggest that CAPS2 promotes activity-dependent BDNF secretion during the postnatal period that is critical for the development of hippocampal GABAergic networks.
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Batmunkh, Munkhbaatar, Lkhagvaa Bayarchimeg, Aleksandr N. Bugay, and Oidov Lkhagva. "Monte Carlo track structure simulation in studies of biological effects induced by accelerated charged particles in the central nervous system." EPJ Web of Conferences 204 (2019): 04008. http://dx.doi.org/10.1051/epjconf/201920404008.
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Simulating the biological damage induced by charged particles trajectories (tracks) in the central nervous system (CNS) at different levels of its organization (molecular, cellular, and tissue) is a challenge of modern radiobiology studies. According to the recent experimental studies at particle accelerators, the most radiation-sensitive area of the CNS is the hippocampus. In this regards, the development of measurement-based Monte Carlo simulation of radiation-induced alterations in the hippocampus is of great interest to understand the radiobiological effects on the CNS. The present work investigates the influence of charged particles on the hippocampal cells of the rat brain using the Geant4 Monte Carlo radiation transport code. The applied computer simulation provides a method to simulate physics processes and chemical reactions in the developed model of the rat hippocampus, which contains different types of neural cells - pyramidal cells, mature and immature granular cells, mossy cells, and neural stem cells. The distribution of stochastic energy depositions has been obtained and analyzed in critical structures of the hippocampal neurons after irradiation with 600 MeV/u iron particles. The computed energy deposition in irradiated hippocampal neurons following a track of iron ion suggests that most of the energy is accumulated by granular cells. The obtained quantities at the level of molecular targets also assume that NMDA and GABA receptors belong to the most probable targets in the irradiated neural cells.
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Del Rio-Bermudez, Carlos, Jangjin Kim, Greta Sokoloff, and Mark S. Blumberg. "Active Sleep Promotes Coherent Oscillatory Activity in the Cortico-Hippocampal System of Infant Rats." Cerebral Cortex 30, no. 4 (January 10, 2020): 2070–82. http://dx.doi.org/10.1093/cercor/bhz223.
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Abstract Active sleep (AS) provides a unique developmental context for synchronizing neural activity within and between cortical and subcortical structures. In week-old rats, sensory feedback from myoclonic twitches, the phasic motor activity that characterizes AS, promotes coherent theta oscillations (4–8 Hz) in the hippocampus and red nucleus, a midbrain motor structure. Sensory feedback from twitches also triggers rhythmic activity in sensorimotor cortex in the form of spindle bursts, which are brief oscillatory events composed of rhythmic components in the theta, alpha/beta (8–20 Hz), and beta2 (20–30 Hz) bands. Here we ask whether one or more of these spindle-burst components are communicated from sensorimotor cortex to hippocampus. By recording simultaneously from whisker barrel cortex and dorsal hippocampus in 8-day-old rats, we show that AS, but not other behavioral states, promotes cortico-hippocampal coherence specifically in the beta2 band. By cutting the infraorbital nerve to prevent the conveyance of sensory feedback from whisker twitches, cortical-hippocampal beta2 coherence during AS was substantially reduced. These results demonstrate the necessity of sensory input, particularly during AS, for coordinating rhythmic activity between these two developing forebrain structures.
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Dahmen, Brigitte, Vanessa B. Puetz, Wolfgang Scharke, Georg G. von Polier, Beate Herpertz-Dahlmann, and Kerstin Konrad. "Effects of Early-Life Adversity on Hippocampal Structures and Associated HPA Axis Functions." Developmental Neuroscience 40, no. 1 (December 14, 2017): 13–22. http://dx.doi.org/10.1159/000484238.
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Early-life adversity (ELA) is one of the major risk factors for serious mental and physical health risks later in life. ELA has been associated with dysfunctional neurodevelopment, especially in brain structures such as the hippocampus, and with dysfunction of the stress system, including the hypothalamic-pituitary-adrenal (HPA) axis. Children who have experienced ELA are also more likely to suffer from mental health disorders such as depression later in life. The exact interplay of aberrant neurodevelopment and HPA axis dysfunction as risks for psychopathology is not yet clear. We investigated volume differences in the bilateral hippocampus and in stress-sensitive hippocampal subfields, behavior problems, and diurnal cortisol activity in 24 children who had experienced documented ELA (including out-of-home placement) in a circumscribed duration of adversity only in their first 3 years of life in comparison to data on 25 control children raised by their biological parents. Hippocampal volumes and stress-sensitive hippocampal subfields (Cornu ammonis [CA]1, CA3, and the granule-cell layer of the dentate gyrus [GCL-DG]) were significantly smaller in children who had experienced ELA, taking psychiatric diagnoses and dimensional psychopathological symptoms into account. ELA moderated the relationship between left hippocampal volume and cortisol: in the control group, hippocampal volumes were not related to diurnal cortisol, while in ELA children, a positive linear relationship between left hippocampal volume and diurnal cortisol was present. Our findings show that ELA is associated with altered development of the hippocampus, and an altered relationship between hippocampal volume and HPA axis activity in youth in care, even after they have lived in stable and caring foster family environments for years. Altered hippocampal development after ELA could thus be associated with a risk phenotype for the development of psychiatric disorders later in life.
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Astakhova, E. A., S. E. Cherenkova, E. V. Marchenko, K. I. Sebelev, and M. V. Aleksandrov. "The relationship of bioelectric activity and structural changes in the hippocampus at pharmacoresistant temporal lobe epilepsy." Translational Medicine 8, no. 2 (June 10, 2021): 5–13. http://dx.doi.org/10.18705/2311-4495-2021-8-2-5-13.
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Background. Epilepsy is one of the most common neurological diseases globally. The unified concept about the role of hippocampus in the development of pharmacoresistant temporal lobe epilepsy is currently missing. Patients with pharmacoresistant temporal lobe epilepsy is often carried out by invasive electrocorticography to identify an epileptic focus. Registration of bioelectric activity of the hippocampus and comparison of data from the MRI pattern of the patient will determine the neurophysiological correlates of structural changes in hippocampus.Objective. The aim of the work was to determine the neurophysiological correlates of structural changes in the hippocampus in patients with focally caused temporal lobe epilepsy.Design and methods. The study was based on the analysis of the results of extraoperative invasive monitoring of the bioelectrical activity of the cortex and hippocampal complex, performed in 19 patients with focally caused drug-resistant epilepsy. The quantitative analysis included 34 tracks of hippocampal activity.Results. A distinctive feature of the bioelectrical activity of the hippocampal complex with its structural damage is the stable dominance of delta activity, which makes up 40–45 % of the total spectrum power. When the hippocampal complex is included in the epileptic system, high-index epileptiform activity is recorded. In the absence of structural damage to the hippocampal complex, the pattern is predominantly formed by the activity of theta and alpha frequency ranges. However, in the group of patients with the absence of a neuroimaging picture of sclerotic changes in the hippocampus, in 63 % of cases, a neurophysiological pattern of “prolapse” was recorded on the electrocorticogram. The spontaneous activity of the hippocampus had a low coherent relationship with the parameters of activity in the cortex of the ipsilateral and contralateral temporal lobes.Conclusions. The electrophysiological correlate of MR-positive structural changes in the hippocampal complex in drug-resistant epilepsy is the pattern of “loss of bioelectric activity”. Spontaneous hippocampal activity is generated independently of activity in the cortex of the ipsilateral and contralateral temporal lobes.
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Perez, Stephanie M., Amiksha Shah, Amber Asher, and Daniel J. Lodge. "Hippocampal deep brain stimulation reverses physiological and behavioural deficits in a rodent model of schizophrenia." International Journal of Neuropsychopharmacology 16, no. 6 (July 1, 2013): 1331–39. http://dx.doi.org/10.1017/s1461145712001344.
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Abstract Subcortical dopamine system dysregulation has been suggested to underlie the positive symptoms of schizophrenia. Recent preclinical investigations and human imaging studies have proposed that the augmented dopamine system function observed in schizophrenia patients may be secondary to aberrant hippocampal activity. Thus, we posit that the hippocampus represents a novel therapeutic target for the treatment of schizophrenia. Here we provide evidence of the effectiveness of a unique approach aimed at decreasing hippocampal function in a rodent model of schizophrenia. Specifically, in a rodent model of schizophrenia, we demonstrate that ventral hippocampal (vHipp) deep brain stimulation (DBS) can normalize aberrant dopamine neuron activity and behaviours associated with positive symptoms. In addition, we provide evidence that this approach may also be effective in restoring deficits in cognitive function, often left unaltered by conventional antipsychotic medications. Therefore, we have provided initial preclinical evidence demonstrating the feasibility of hippocampal DBS as a potential novel approach for the treatment of schizophrenia.
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Eichenbaum, Howard, Tim Otto, and Neal J. Cohen. "Two functional components of the hippocampal memory system." Behavioral and Brain Sciences 17, no. 3 (September 1994): 449–72. http://dx.doi.org/10.1017/s0140525x00035391.
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AbstractThere is considerable evidence that the hippocampal system contributes both to (1) the temporary maintenance of memories and to (2) the processing of a particular type of memory representation. The findings on amnesia suggest that these two distinguishing features of hippocampal memory processing are orthogonal. Together with anatomical and physiological data, the neuropsychological findings support a model of cortico-hippocampal interactions in which the temporal and representational properties of hippocampal memory processing are mediated separately. We propose that neocortical association areas maintain shortterm memories for specific items and events prior to hippocampal processing as well as providing the final repositories of long-term memory. The parahippocampal region supports intermediate-term storage of individual items, and the hippocampal formation itself mediates an organization of memories according to relevant relationships among items. Hippocampal-cortical interactions produce (i) strong and persistent memories for events, including their constituent elements and the relationships among them, and (ii) a capacity to express memories flexibly across a wide range of circumstances.
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Nyberg, Lars, Nina Karalija, Alireza Salami, Micael Andersson, Anders Wåhlin, Neda Kaboovand, Ylva Köhncke, et al. "Dopamine D2 receptor availability is linked to hippocampal–caudate functional connectivity and episodic memory." Proceedings of the National Academy of Sciences 113, no. 28 (June 23, 2016): 7918–23. http://dx.doi.org/10.1073/pnas.1606309113.
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D1 and D2 dopamine receptors (D1DRs and D2DRs) may contribute differently to various aspects of memory and cognition. The D1DR system has been linked to functions supported by the prefrontal cortex. By contrast, the role of the D2DR system is less clear, although it has been hypothesized that D2DRs make a specific contribution to hippocampus-based cognitive functions. Here we present results from 181 healthy adults between 64 and 68 y of age who underwent comprehensive assessment of episodic memory, working memory, and processing speed, along with MRI and D2DR assessment with [11C]raclopride and PET. Caudate D2DR availability was positively associated with episodic memory but not with working memory or speed. Whole-brain analyses further revealed a relation between hippocampal D2DR availability and episodic memory. Hippocampal and caudate D2DR availability were interrelated, and functional MRI-based resting-state functional connectivity between the ventral caudate and medial temporal cortex increased as a function of caudate D2DR availability. Collectively, these findings indicate that D2DRs make a specific contribution to hippocampus-based cognition by influencing striatal and hippocampal regions, and their interactions.
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ASHTARI, M., B. S. GREENWALD, E. KRAMER-GINSBERG, J. HU, H. WU, M. PATEL, P. AUPPERLE, and S. POLLACK. "Hippocampal/amygdala volumes in geriatric depression." Psychological Medicine 29, no. 3 (May 1999): 629–38. http://dx.doi.org/10.1017/s0033291799008405.
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Background. The hippocampus, amygdala and related functional circuits have been implicated in the regulation of emotional expression and memory processes, which are affected in major depression. Several recent investigations have reported abnormalities in these structures in adult and elderly depressives.Methods. Elderly DSM-III-R unipolar depressives (N=40) and normal controls (N=46) participated in a magnetic resonance imaging study (1.0T). Brain images were obtained in the coronal plane. Using established anatomical guidelines for structure delineation, volumetric measurements of left and right hippocampus and anterior hippocampus/amygdala complex were completed under blinded conditions using a semi-automated computer mensuration system, with patients and controls in random order.Results. Medial temporal volumes did not significantly distinguish either elderly depressed and age-similar normal control subjects, or late onset and early onset depressed patients (ANCOVA). Major overlap of measured volumes existed between patient and control groups. In depressives, hippocampal volumes significantly correlated with age, and cognitive and depression ratings, but not with number of prior depressive episodes or age-at-onset of first depression.Conclusions. Hippocampal volumes do not discriminate a typical clinical population of elderly depressed patients from age-similar normal control subjects. If hippocampal dysfunction contributes to a diagnosis of syndromal depression in the elderly, such dysfunction does not appear to be regularly reflected in structural abnormalities captured by volumetric measurement as conducted. On the other hand, relationships between hippocampal volumes and clinical phenomena in depressives, but not controls, suggest potentially meaningful interactions between hippocampal structure and the expression of major depression in the elderly.
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Ye, Jing, Menno P. Witter, May-Britt Moser, and Edvard I. Moser. "Entorhinal fast-spiking speed cells project to the hippocampus." Proceedings of the National Academy of Sciences 115, no. 7 (January 31, 2018): E1627—E1636. http://dx.doi.org/10.1073/pnas.1720855115.
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The mammalian positioning system contains a variety of functionally specialized cells in the medial entorhinal cortex (MEC) and the hippocampus. In order for cells in these systems to dynamically update representations in a way that reflects ongoing movement in the environment, they must be able to read out the current speed of the animal. Speed is encoded by speed-responsive cells in both MEC and hippocampus, but the relationship between the two populations has not been determined. We show here that many entorhinal speed cells are fast-spiking putative GABAergic neurons. Using retrograde viral labeling from the hippocampus, we find that a subset of these fast-spiking MEC speed cells project directly to hippocampal areas. This projection contains parvalbumin (PV) but not somatostatin (SOM)-immunopositive cells. The data point to PV-expressing GABAergic projection neurons in MEC as a source for widespread speed modulation and temporal synchronization in entorhinal–hippocampal circuits for place representation.
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Aggleton, John P. "Looking beyond the hippocampus: old and new neurological targets for understanding memory disorders." Proceedings of the Royal Society B: Biological Sciences 281, no. 1786 (July 7, 2014): 20140565. http://dx.doi.org/10.1098/rspb.2014.0565.
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Although anterograde amnesia can occur after damage in various brain sites, hippocampal dysfunction is usually seen as the ultimate cause of the failure to learn new episodic information. This assumption is supported by anatomical evidence showing direct hippocampal connections with all other sites implicated in causing anterograde amnesia. Likewise, behavioural and clinical evidence would seem to strengthen the established notion of an episodic memory system emanating from the hippocampus. There is, however, growing evidence that key, interconnected sites may also regulate the hippocampus, reflecting a more balanced, integrated network that enables learning. Recent behavioural evidence strongly suggests that medial diencephalic structures have some mnemonic functions independent of the hippocampus, which can then act upon the hippocampus. Anatomical findings now reveal that nucleus reuniens and the retrosplenial cortex provide parallel, disynaptic routes for prefrontal control of hippocampal activity. There is also growing clinical evidence that retrosplenial cortex dysfunctions contribute to both anterograde amnesia and the earliest stages of Alzheimer's disease, revealing the potential significance of this area for clinical studies. This array of findings underlines the importance of redressing the balance and the value of looking beyond the hippocampus when seeking to explain failures in learning new episodic information.
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Kitchigina, Valentina F. "Theta Oscillations and Reactivity of Hippocampal Stratum Oriens Neurons." Scientific World JOURNAL 10 (2010): 930–43. http://dx.doi.org/10.1100/tsw.2010.90.
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The supposition was advanced that the neuronal theta rhythmicity is the key mode of signal selection at the hippocampal level. To address this hypothesis, the experimental data on the responses of putative hippocampal interneurons of the stratum oriens CA1-CA3 to stimulation during enhanced theta rhythm and after its blockade are reviewed. Both a strong increase and a decrease of the natural theta rhythm disturbed the reactions of hippocampal neurons; during theta augmentation, the responses were masked or disappeared, and after theta blockade, they lost the ability to habituate. In both cases, two important events were broken: the resetting of the background activity and the phase-locking of theta cycles to stimulus. These data allow one to suppose that only important stimuli are normally capable to evoke these events and these stimuli are selected for recording. When the response to a significant stimulus occurs, the following theta prevents the responses to other stimuli. This probably protects the hippocampal activity from interference from irrelevant signals. Presumably, the absence of the theta deprives the hippocampus of this protection. During enhanced and persistent theta oscillations, the reset disappeared and theta bursts were generated without stimulus locking. In this state, the system is probably closed and the information cannot be recorded. During the theta blockade, the reset was too long and did not habituate. In this case, the system is open for any signals and the hippocampus loses the ability to select signal. This analysis suggests that information selection in the hippocampus may be performed with the participation of nonpyramidal neurons.
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McCoy, Alexandra M., Thomas D. Prevot, Dishary Sharmin, James M. Cook, Etienne L. Sibille, and Daniel J. Lodge. "GL-II-73, a Positive Allosteric Modulator of α5GABAA Receptors, Reverses Dopamine System Dysfunction Associated with Pilocarpine-Induced Temporal Lobe Epilepsy." International Journal of Molecular Sciences 24, no. 14 (July 18, 2023): 11588. http://dx.doi.org/10.3390/ijms241411588.
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Although seizures are a hallmark feature of temporal lobe epilepsy (TLE), psychiatric comorbidities, including psychosis, are frequently associated with TLE and contribute to decreased quality of life. Currently, there are no defined therapeutic protocols to manage psychosis in TLE patients, as antipsychotic agents may induce epileptic seizures and are associated with severe side effects and pharmacokinetic and pharmacodynamic interactions with antiepileptic drugs. Thus, novel treatment strategies are necessary. Several lines of evidence suggest that hippocampal hyperactivity is central to the pathology of both TLE and psychosis; therefore, restoring hippocampal activity back to normal levels may be a novel therapeutic approach for treating psychosis in TLE. In rodent models, increased activity in the ventral hippocampus (vHipp) results in aberrant dopamine system function, which is thought to underlie symptoms of psychosis. Indeed, we have previously demonstrated that targeting α5-containing γ-aminobutyric acid receptors (α5GABAARs), an inhibitory receptor abundant in the hippocampus, with positive allosteric modulators (PAMs), can restore dopamine system function in rodent models displaying hippocampal hyperactivity. Thus, we posited that α5-PAMs may be beneficial in a model used to study TLE. Here, we demonstrate that pilocarpine-induced TLE is associated with increased VTA dopamine neuron activity, an effect that was completely reversed by intra-vHipp administration of GL-II-73, a selective α5-PAM. Further, pilocarpine did not alter the hippocampal α5GABAAR expression or synaptic localization that may affect the efficacy of α5-PAMs. Taken together, these results suggest augmenting α5GABAAR function as a novel therapeutic modality for the treatment of psychosis in TLE.
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Eichenbaum, Howard. "The Hippocampal System and Declarative Memory in Animals." Journal of Cognitive Neuroscience 4, no. 3 (July 1992): 217–31. http://dx.doi.org/10.1162/jocn.1992.4.3.217.
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Theoretical arguments and empirical data are presented in favor of the hypothesis that the hippocampal system supports a declarative memory capacity in animals as well as humans. This view is advanced by identifying two prominent characteristics of human declarative memory and by operationalizing and evaluating them using both experimental lesion and single unit recording studies on animals. First, hippocampal processing is not selective to any particular category of learning materials; instead, it supports comparisons among all kinds of information in memory, resulting in a representation of critical relations between items. Conversely, individual representations are supported outside the hippocampal system. Second, hippocampal-dependent, relational memory representations involve a flexible organization that permits inferences from memory in novel situations. Conversely, hippocampal-independent individual representations can support only repetition of procedures acquired during original learning. Correspondences between the neuropsychological and neurophysiological findings presented serve to indicate how these properties of hippocampal representation support declarative memory across behavioral paradigms and across species.
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Huang, Chu-Chung, Edmund T. Rolls, Chih-Chin Heather Hsu, Jianfeng Feng, and Ching-Po Lin. "Extensive Cortical Connectivity of the Human Hippocampal Memory System: Beyond the “What” and “Where” Dual Stream Model." Cerebral Cortex 31, no. 10 (May 19, 2021): 4652–69. http://dx.doi.org/10.1093/cercor/bhab113.
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Abstract The human hippocampus is involved in forming new memories: damage impairs memory. The dual stream model suggests that object “what” representations from ventral stream temporal cortex project to the hippocampus via the perirhinal and then lateral entorhinal cortex, and spatial “where” representations from the dorsal parietal stream via the parahippocampal gyrus and then medial entorhinal cortex. The hippocampus can then associate these inputs to form episodic memories of what happened where. Diffusion tractography was used to reveal the direct connections of hippocampal system areas in humans. This provides evidence that the human hippocampus has extensive direct cortical connections, with connections that bypass the entorhinal cortex to connect with the perirhinal and parahippocampal cortex, with the temporal pole, with the posterior and retrosplenial cingulate cortex, and even with early sensory cortical areas. The connections are less hierarchical and segregated than in the dual stream model. This provides a foundation for a conceptualization for how the hippocampal memory system connects with the cerebral cortex and operates in humans. One implication is that prehippocampal cortical areas such as the parahippocampal TF and TH subregions and perirhinal cortices may implement specialized computations that can benefit from inputs from the dorsal and ventral streams.
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Ananyeva, N. I., E. V. Andreev, T. A. Salomatina, L. R. Akhmerova, R. V. Ezhova, N. G. Neznanov, and N. N. Zalutskaya. "MR MORPHOMERY OF THE HIPPOCAMPUS IN NORMAL VOLUNTEERS AND PATIENTS WITH PSYHOTIC DISORDERS DISEASE." Diagnostic radiology and radiotherapy, no. 2 (August 4, 2019): 50–58. http://dx.doi.org/10.22328/2079-5343-2019-10-2-50-58.
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Role of limbic system, first of all, hippocampal formation, is carefully analyzed in literature because of its involvement in different psychiatric diseases. Results are contradictory, may be because of insufficient data of normal volumes of structures involving in cognitive and affective functioning of the brain. Hippocampus is very complex organized structure consisting of different subfields and subregions which probably differently changes in different psychiatric diseases. Aim of our study was to analyzed changes in volumes of the whole hippocampus, its subregions and subfields in different psychiatric diseases. In our study we have analyzed MRI morphometry of hippocampal formation in healthy volunteers, patients with Alzheimerdisease (AD) in early stage, vascular dementia (VD), depression based on medical literatureandourexperience. Patients were divided on 4 groups: 10 patients with early Alzheimer disease, 10 normal volunteers, 10 patients with vascular dementia and 10 patients with depression. We have determined method of definition and volume evaluation of different hippocampal subfields. We find difference in the volumes of CA3, molecular stratum and fascia dentatain early stage of AD; in the volume of hippocampal tail, molecular stratum of fascia dentataand CA3 in patients with VD; in molecular stratum of fasciadentata, fimbria and CA3 in patients with depression because of role of these fields in coordination of hippocampal activity.
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Behroozi, Mehdi, Felix Ströckens, Martin Stacho, and Onur Güntürkün. "Functional Connectivity Pattern of the Internal Hippocampal Network in Awake Pigeons: A Resting-State fMRI Study." Brain, Behavior and Evolution 90, no. 1 (2017): 62–72. http://dx.doi.org/10.1159/000475591.
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In the last two decades, the avian hippocampus has been repeatedly studied with respect to its architecture, neurochemistry, and connectivity pattern. We review these insights and conclude that we unfortunately still lack proper knowledge on the interaction between the different hippocampal subregions. To fill this gap, we need information on the functional connectivity pattern of the hippocampal network. These data could complement our structural connectivity knowledge. To this end, we conducted a resting-state fMRI experiment in awake pigeons in a 7-T MR scanner. A voxel-wise regression analysis of blood oxygenation level-dependent (BOLD) fluctuations was performed in 6 distinct areas, dorsomedial (DM), dorsolateral (DL), triangular shaped (Tr), dorsolateral corticoid (CDL), temporo-parieto-occipital (TPO), and lateral septum regions (SL), to establish a functional connectivity map of the avian hippocampal network. Our study reveals that the system of connectivities between CDL, DL, DM, and Tr is the functional backbone of the pigeon hippocampal system. Within this network, DM is the central hub and is strongly associated with DL and CDL BOLD signal fluctuations. DM is also the only hippocampal region to which large Tr areas are functionally connected. In contrast to published tracing data, TPO and SL are only weakly integrated in this network. In summary, our findings uncovered a structurally otherwise invisible architecture of the avian hippocampal formation by revealing the dynamic blueprints of this network.
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Xu, Wenbo, Xiaoxiao Yao, Fangyi Zhao, Haisheng Zhao, Ziqian Cheng, Wei Yang, Ranji Cui, Songbai Xu, and Bingjin Li. "Changes in Hippocampal Plasticity in Depression and Therapeutic Approaches Influencing These Changes." Neural Plasticity 2020 (November 26, 2020): 1–16. http://dx.doi.org/10.1155/2020/8861903.
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Depression is a common neurological disease that seriously affects human health. There are many hypotheses about the pathogenesis of depression, and the most widely recognized and applied is the monoamine hypothesis. However, no hypothesis can fully explain the pathogenesis of depression. At present, the brain-derived neurotrophic factor (BDNF) and neurogenesis hypotheses have highlighted the important role of plasticity in depression. The plasticity of neurons and glial cells plays a vital role in the transmission and integration of signals in the central nervous system. Plasticity is the adaptive change in the nervous system in response to changes in external signals. The hippocampus is an important anatomical area associated with depression. Studies have shown that some antidepressants can treat depression by changing the plasticity of the hippocampus. Furthermore, caloric restriction has also been shown to affect antidepressant and hippocampal plasticity changes. In this review, we summarize the latest research, focusing on changes in the plasticity of hippocampal neurons and glial cells in depression and the role of BDNF in the changes in hippocampal plasticity in depression, as well as caloric restriction and mitochondrial plasticity. This review may contribute to the development of antidepressant drugs and elucidating the mechanism of depression.
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McNaughton, B. L., C. A. Barnes, J. L. Gerrard, K. Gothard, M. W. Jung, J. J. Knierim, H. Kudrimoti, et al. "Deciphering the hippocampal polyglot: the hippocampus as a path integration system." Journal of Experimental Biology 199, no. 1 (January 1, 1996): 173–85. http://dx.doi.org/10.1242/jeb.199.1.173.
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Hippocampal 'place' cells and the head-direction cells of the dorsal presubiculum and related neocortical and thalamic areas appear to be part of a preconfigured network that generates an abstract internal representation of two-dimensional space whose metric is self-motion. It appears that viewpoint-specific visual information (e.g. landmarks) becomes secondarily bound to this structure by associative learning. These associations between landmarks and the preconfigured path integrator serve to set the origin for path integration and to correct for cumulative error. In the absence of familiar landmarks, or in darkness without a prior spatial reference, the system appears to adopt an initial reference for path integration independently of external cues. A hypothesis of how the path integration system may operate at the neuronal level is proposed.
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Campos, Alline C., Zaira Ortega, Javier Palazuelos, Manoela V. Fogaça, Daniele C. Aguiar, Javier Díaz-Alonso, Silvia Ortega-Gutiérrez, et al. "The anxiolytic effect of cannabidiol on chronically stressed mice depends on hippocampal neurogenesis: involvement of the endocannabinoid system." International Journal of Neuropsychopharmacology 16, no. 6 (July 1, 2013): 1407–19. http://dx.doi.org/10.1017/s1461145712001502.
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Abstract Cannabidiol (CBD), the main non-psychotomimetic component of the plant Cannabis sativa, exerts therapeutically promising effects on human mental health such as inhibition of psychosis, anxiety and depression. However, the mechanistic bases of CBD action are unclear. Here we investigate the potential involvement of hippocampal neurogenesis in the anxiolytic effect of CBD in mice subjected to 14 d chronic unpredictable stress (CUS). Repeated administration of CBD (30 mg/kg i.p., 2 h after each daily stressor) increased hippocampal progenitor proliferation and neurogenesis in wild-type mice. Ganciclovir administration to GFAP-thymidine kinase (GFAP-TK) transgenic mice, which express thymidine kinase in adult neural progenitor cells, abrogated CBD-induced hippocampal neurogenesis. CBD administration prevented the anxiogenic effect of CUS in wild type but not in GFAP-TK mice as evidenced in the novelty suppressed feeding test and the elevated plus maze. This anxiolytic effect of CBD involved the participation of the CB1 cannabinoid receptor, as CBD administration increased hippocampal anandamide levels and administration of the CB1–selective antagonist AM251 prevented CBD actions. Studies conducted with hippocampal progenitor cells in culture showed that CBD promotes progenitor proliferation and cell cycle progression and mimics the proliferative effect of CB1 and CB2 cannabinoid receptor activation. Moreover, antagonists of these two receptors or endocannabinoid depletion by fatty acid amide hydrolase overexpression prevented CBD-induced cell proliferation. These findings support that the anxiolytic effect of chronic CBD administration in stressed mice depends on its proneurogenic action in the adult hippocampus by facilitating endocannabinoid-mediated signalling.
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Zimatkin, S. M., T. V. Klimuts, and A. V. Zaerko. "Structural organization of the rat hyppocampal formation." Сибирский научный медицинский журнал 43, no. 3 (June 22, 2023): 4–14. http://dx.doi.org/10.18699/ssmj20230301.
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The review examines the historical aspects of the hippocampus nomenclature. Its anatomical study began by the ancient Greeks, who called the unusual–looking structure a “ram’s horn” – cornu ammonis. The term “hippocampus” (ancient Greek: ἱππόκαμπος, from ἵππος, “horse” and κάμπος, “sea monster”, or “sea-horse”) was first introduced in the sixteenth century by anatomist J.C. Arantius. The term “hippocampal formation” is currently applied to a group of cytoarchitectonically different adjacent areas, including, along with the hippocampus itself, the dentate gyrus, subiculum, presubiculum, parasubiculum and entorhinal cortex. The reason for including these six regions in the “hippocampal formation” group is that they are connected to each other by unique and largely unidirectional pathways. The review is devoted to the spatial, morphological and cyto- and myeloarchitectonic organization of all departments of the rat hippocampus formation and the distinctive neuroanatomic characteristics of its departments. Comparative features of the structure of the hippocampus formation of a rat, monkey and human are described. Although the volume of the hippocampus is about 10 times larger in monkeys and 100 times larger in humans compared to rats, the basic architecture of the hippocampus formation is common, although there are some species differences. The relatively simple organization of the main cellular layers in combination with the highly organized laminar distribution of hippocampal neuron processes contributes to its use as a model system in modern neuroscience.
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Tesche, C. D., and J. Karhu. "Interactive Processing of Sensory Input and Motor Output in the Human Hippocampus." Journal of Cognitive Neuroscience 11, no. 4 (July 1999): 424–36. http://dx.doi.org/10.1162/089892999563517.
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Recent studies of visuomotor integration suggest that the motor system may be intimately involved in the detection of salient features of the sensory scene. The final stages of sensory processing occur in hippocampal structures. We measured human neuromagnetic responses during motor reaction to an auditory cue embedded in high-speed multimodal stimulation. Our results demonstrate that large-scale cognitive networks may recruit additional resources from the hippocampus during sensorimotor integration. Hippocampal activity from 300 msec before to 200 msec after cued movements was enhanced significantly over that observed during self-paced movements. The dominant hippocampal activity appeared equally synchronized to both sensory input and motor output, consistent with timing by an intrinsic mechanism, possibly provided by ongoing theta oscillations.
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Lukito, Elizabeth Feloni, Kevin Tandarto, Maureen Miracle Stella, Ignatius Ivan, Harvey Sudharta, Gilbert Golahi, Kenny Wijaya Sutanto, et al. "The Association between PM2.5 Exposure and Hippocampal Volume: A Systematic Review." Asian Pacific Journal of Environment and Cancer 5, no. 1 (June 28, 2022): 11–16. http://dx.doi.org/10.31557/apjec.2022.5.1.11-16.
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Background: Existing air quality is decreasing, as evidenced by the increase in air pollution. Air pollution does not only affect the respiratory system, but also affecting the nervous system, and furthermore causing impaired cognitive function that can be predicted through the image of the hippocampus. Objective: This study wanted to determine the significance of the relationship between PM2.5 (Particulate Matter) pollutant exposure and hippocampal volume in adults. Method: This research is a PRISMA 2020 based systematic study using Google Scholar, PubMed, and Proquest as databases. Research inclusion criteria were studies with subjects over 19 years old, using MRI techniques, published in English, having sufficient data for extraction. Result: There are 5 studies from 2015 to 2020 which stated that there was no statistically significant relationship between PM2.5 pollutant exposure and hippocampal volume (n = 5) (P-value > 0.05, 0.71, 0.8, 0.32), and the study obtained significant results (n = 1) (P-value < 0.005). Discussion: Although the results of the study did not prove a significant difference in hippocampal volume, several recent theories regarding hippocampal neurogenesis in adults are able to support these results. Conclusion: From this study, it was not proven that there was a significant relationship between PM2.5 pollutant exposure and hippocampal volume.