• Title/Summary/Keyword: Hippocampal function

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Hippocampal Volume and Memory Function in Patients with Posttraumatic Stress Disorder (외상후 스트레스 장애 환자에서 해마용적과 기억기능)

  • Chung, Moon-Yong;Chung, Hwa-Yong;Ryu, Hyun;Chung, Hae-Gyung;Choi, Jin-Hee
    • Korean Journal of Biological Psychiatry
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    • v.8 no.1
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    • pp.131-139
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    • 2001
  • This study was conducted to evaluate the effect of PTSD on memory function and hippocampal volume, and to identify major variables correlated to hippocampal volume and memory function. Thirty four Vietnam veterans were collected for this study, among whom eighteen were PTSD patients and sixteen were combat control subjects. The author used Impact of Event Scale(IES), Combat Exposure Scale(CES), Hamilton Depression Rating Scale(HDRS) and Beck Depression Inventory (BDI). Korea Memory Assessment Scale(K-MAS) was assessed for memory function. Magnetic resonance imaging(MRI) was used to measure hippocampal volume. There were significant differences between PTSD and Non-PTSD veterans in IES, HDRS and BDI. Significant difference was found in verbal memory and total memory of K-MAS between PTSD and Non-PTSD veterans. There was significant difference in hippocampal volume between PTSD and Non-PTSD veterans. Short term memory, verbal memory and total memory were positively correlated to hippocampal volume. Hippocampal volume was negatively correlated to IES, HDRS, and BDI. These results suggest that PTSD severity be associated with hippocampal atrophy and memory dysfunction. Reduced or smaller hippocampal volume may be preexisting risk factor for stress exposure or the development of PTSD on combat exposure.

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Influence of Molarless Condition on the Hippocampal Formation in Mouse: a Histological Study (구치부 치관삭제가 생쥐 해마복합체에 미치는 영향에 관한 조직학적 연구)

  • Kim, Yong-Chul;Kang, Dong-Wan
    • Journal of Dental Rehabilitation and Applied Science
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    • v.23 no.2
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    • pp.179-186
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    • 2007
  • The decrease of masticatory function caused by tooth loss leads to a decrease of cerebral blood flow volume resulting in impairment of cognitive function and learning memory disorder. However, the reduced mastication-mediated morphological alteration in the central nervous system (CNS) responsible for senile deficit of cognition, learning and memory has not been well documented. In this study, the effect of the loss of the molar teeth (molarless condition) on the hippocampal expression of glial fibrillary acidic protein (GFAP) protein was studied by immunohistochemical techniques. The results were as follows : 1. The molarless mice showed a lower density of pyramidal cells in the cornu ammonis 1 (CA1) and dentate gyrus (DG) region of the hippocampus than control mice. 2. Immunohistochemical analysis showed that the molarless condition enhanced the time-dependent increase in the cell density and hypertrophy of GFAP immunoreactivity in the CA1 region of the hippocampus. The molarless condition enhanced an time-dependent decrease in the number of neurons in the hippocampal formation and the time-dependent increase in the number and hypertrophy of GFAP-labeled cells in the same region. The data suggest a possible link between reduced mastication and histological changes in hippocampal formation that may be one risk factor for senile impairment of cognitive function and spatial learning memory.

Adult hippocampal neurogenesis and related neurotrophic factors

  • Lee, Eu-Gene;Son, Hyeon
    • BMB Reports
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    • v.42 no.5
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    • pp.239-244
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    • 2009
  • New neurons are continually generated in the subgranular zone of the dentate gyrus and in the subventricular zone of the lateral ventricles of the adult brain. These neurons proliferate, differentiate, and become integrated into neuronal circuits, but how they are involved in brain function remains unknown. A deficit of adult hippocampal neurogenesis leads to defective spatial learning and memory, and the hippocampi in neuropsychiatric diseases show altered neurogenic patterns. Adult hippocampal neurogenesis is not only affected by external stimuli but also regulated by internal growth factors including BDNF, VEGF and IGF-1. These factors are implicated in a broad spectrum of pathophysiological changes in the human brain. Elucidation of the roles of such neurotropic factors should provide insight into how adult hippocampal neurogenesis is related to psychiatric disease and synaptic plasticity.

Cognitive Dysfunction and Hippocampal Damage Induced by Hypoxic-Ischemic Brain Injury and Prolonged Febrile Convulsions in Immature Rats

  • Byeon, Jung Hye;Kim, Gun-Ha;Kim, Joo Yeon;Sun, Woong;Kim, Hyun;Eun, Baik-Lin
    • Journal of Korean Neurosurgical Society
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    • v.58 no.1
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    • pp.22-29
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    • 2015
  • Objective : Perinatal hypoxic-ischemic encephalopathy (HIE) and prolonged febrile seizures (pFS) are common neurologic problems that occur during childhood. However, there is insufficient evidence from experimental studies to conclude that pFS directly induces hippocampal injury. We studied cognitive function and histological changes in a rat model and investigated which among pFS, HIE, or a dual pathologic effect is most detrimental to the health of children. Methods : A rat model of HIE at postnatal day (PD) 7 and a pFS model at PD10 were used. Behavioral and cognitive functions were investigated by means of weekly open field tests from postnatal week (PW) 3 to PW7, and by daily testing with the Morris water maze test at PW8. Pathological changes in the hippocampus were observed in the control, pFS, HIE, and HIE+pFS groups at PW9. Results : The HIE priming group showed a seizure-prone state. The Morris water maze test revealed a decline in cognitive function in the HIE and HIE+pFS groups compared with the pFS and control groups. Additionally, the HIE and HIE+pFS groups showed significant hippocampal neuronal damage, astrogliosis, and volume loss, after maturation. The pFS alone induced minimal hippocampal neuronal damage without astrogliosis or volume loss. Conclusion : Our findings suggest that pFS alone causes no considerable memory or behavioral impairment, or cellular change. In contrast, HIE results in lasting memory impairment and neuronal damage, gliosis, and tissue loss. These findings may contribute to the understanding of the developing brain concerning conditions caused by HIE or pFS.

Effect of Hoelen Cum Radix on learning and memory enhancement via stimulation of neuronal differentiation in the hippocampus of the mouse brain (복신(茯神)의 인지기능 향상 및 해마 신경세포분화 촉진에 대한 효능 연구)

  • Choi, Jin Gyu;Sim, Yeomoon;Kim, Wonnam;Kim, Sun Yeou;Oh, Myung Sook
    • The Korea Journal of Herbology
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    • v.30 no.2
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    • pp.43-48
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    • 2015
  • Objectives : The aim of this study was to investigate the memory enhancing properties of extract of Hoelen Cum Radix (HCR) and its possible mechanism in mice of normal condition. Methods : We evaluated the effects of HCR on cognitive function and memory enhancement in normal mice. Male ICR mice were orally administrated with HCR 100 mg/kg for 7 days and equal volume of saline was administrated to the control group in the same condition. We conducted two behavioral tests which measure the spatial working memory (Y-maze test) and cognitive fear memory (passive avoidance test). We also investigated whether HCR affects the hippocampal neurogenesis in the brain. To assess the effects of HCR on neural progenitor cell differentiation and neurite outgrowth in the early stage of hippocampal neurogenesis, we performed doublecortin (DCX), a direct neurogenesis marker, immunohistochemical analysis in the dentate gyrus (DG) of the mouse hippocampus. Results : HCR significantly enhanced memory and cognitive function as determined by the Y-maze test (p<0.05) and passive avoidance test (p<0.001). Moreover, HCR increased DCX positive cells (p<0.01) and neurite length (p<0.01) compared to the control group. These results indicated that HCR stimulates differentiation of neural progenitor cells and promotes neurite outgrowth in hippocampal DG of the mice. Conclusion : We concluded that HCR shows memory enhancing effects through the stimulation of hippocampal neurogenesis as a consequence of accelerated neuronal differentiation and neurite outgrowth in the DG of the hippocampus after HCR treatment.

Effect of Yanggyuksanhwa-tang on Ischemic Damage in Organotypic Hippocampal Slice Culture (양격산화탕(凉膈散火湯)이 뇌해마 조직배양의 허혈손상에 따른 신경세포손상에 미치는 영향)

  • Lee, Hwan-Sung;Park, Sung-Joon;Jung, Kwang-Sik;Sohn, Young-Joo;Jung, Hyuk-Sang;Park, Dong-Il;Sohn, Nak-Won
    • The Journal of Internal Korean Medicine
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    • v.29 no.1
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    • pp.231-242
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    • 2008
  • Objectives : We can find out the experimental reports of Yanggyuksanhwa-tang, which has the function of regulating blood pressure related with cerebral disease, and increasing local cerebral blood stream volume, also has the recoveries for the damage of vessel endothelium, and endothelium hypertrophy caused by angiospasm after subarachnoid hemorrhage, and reduces the contraction of smooth muscle, so simultaneously improves necrosis. The aim of this study is to investigate effect of Yanggyuksanhwa-tang protecting neuronal cells from being damaged by brain ischemia through using organotypic hippocampal slice cultures. Methods : We caused ischemic damage to organotypic hippocampal slice cultures by oxygen and glucose deprivation, and Yanggyuksanhwa-tang extract was added to cultures. Thereafter we measured area percentage of propidium iodide (PI)-stained neuronal cell, lactate dehydrogenase (LDH) levels in culture media and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells. Results : Area percentage of PI-stained neuronal cells and count of TUNEL-positive cells in CA1 and DG area of organotypic hippocampal slice culture were significantly decreased in pertinent density level of Yanggyuksanhwa-tang extract. LDH levels in culture media of organotypic hippocampal slice culture were significantly decreased in pertinent density level of Yanggyuksanhwa-tang extract. Conclusions : Within pertinent density level, Yanggyuksanhwa-tang has cell protection effect that prevents brain ischemia damaging neuronal cells and apoptosis increasing.

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Effects of Repetitive Transcranial Magnetic Stimulation on Enhancement of Cognitive Function in Focal Ischemic Stroke Rat Model (국소 허혈성 뇌졸중 모델 흰쥐의 인지기능에 반복경두개자기자극이 미치는 효과)

  • Lee, Jung-In;Kim, Gye-Yeop;Nam, Ki-Won;Lee, Dong-Woo;Kim, Ki-Do;Kim, Kyung-Yoon
    • Journal of the Korean Society of Physical Medicine
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    • v.7 no.1
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    • pp.11-20
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    • 2012
  • Purpose : This study is intended to examine the repetitive transcranial magnetic stimulation on cognitive function in the focal ischemic stroke rat model. Methods : This study selected 30 Sprague-Dawley rats of 8 weeks. The groups were divided into two groups and assigned 15 rats to each group. Control group: Non-treatment after injured by focal ischemic stroke; Experimental group: application of repetitive transcranial magnetic stimulation(0.1 Tesla, 25 Hz, 20 min/time, 2 times/day, 5 days/2 week) after injured by focal ischemic stroke. To assess the effect of rTMS, the passive avoidance test, spatial learning and memory ability test were analyzed at the pre, 1 day, $7^{th}$ day, $14^{th}$ day and immunohistochemistric response of BDNF were analyzed in the hippocampal dentate gyrus at $7^{th}$ day, $14^{th}$ day. Results : In passive avoidance test, the outcome of experimental group was different significantly than the control group at the $7^{th}$ day, $14^{th}$ day. In spatial learning and memory ability test, the outcome of experimental group was different significantly than the control group at the $7^{th}$ day, $14^{th}$ day. In immunohistochemistric response of BDNF in the hippocampal dentate gyrus, experimental groups was more increased than control group. Conclusion : These result suggest that improved cognitive function by repetitive transcranial magnetic stimulation after focal ischemic stroke is associated with dynamically altered expression of BDNF in hippocampal dentate gyrus and that is related with synaptic plasticity.

Impaired Hippocampal Synaptic Plasticity and Enhanced Excitatory Transmission in a Novel Animal Model of Autism Spectrum Disorders with Telomerase Reverse Transcriptase Overexpression

  • Rhee, Jeehae;Park, Kwanghoon;Kim, Ki Chan;Shin, Chan Young;Chung, ChiHye
    • Molecules and Cells
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    • v.41 no.5
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    • pp.486-494
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    • 2018
  • Recently, we have reported that animals with telomerase reverse transcriptase (TERT) overexpression exhibit reduced social interaction, decreased preference for novel social interaction and poor nest-building behaviors-symptoms that mirror those observed in human autism spectrum disorders (ASD). Overexpression of TERT also alters the excitatory/inhibitory (E/I) ratio in the medial prefrontal cortex. However, the effects of TERT overexpression on hippocampal-dependent learning and synaptic efficacy have not been investigated. In the present study, we employed electrophysiological approaches in combination with behavioral analysis to examine hippocampal function of TERT transgenic (TERT-tg) mice and FVB controls. We found that TERT overexpression results in enhanced hippocampal excitation with no changes in inhibition and significantly impairs long-term synaptic plasticity. Interestingly, the expression levels of phosphorylated CREB and phosphorylated $CaMKII{\alpha}$ were significantly decreased while the expression level of $CaMKII{\alpha}$ was slightly increased in the hippocampus of TERT-overexpressing mice. Our observations highlight the importance of TERT in normal synaptic function and behavior and provide additional information on a novel animal model of ASD associated with TERT overexpression.

New Four-herb Formula Ameliorates Memory Impairments via Neuroprotective Effects on Hippocampal Cells (한약재 4종 복합추출물의 해마신경세포 보호를 통한 기억력 개선)

  • Ahn, Sung Min;Choi, Young Whan;Shin, Hwa Kyoung;Choi, Byung Tae
    • Journal of Life Science
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    • v.26 no.4
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    • pp.475-483
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    • 2016
  • The current study was conducted to evaluate beneficial effects of a new formula (CWC-9) using four traditional Oriental medicinal herbs, Cynanchum wilfordii, Rehmannia glutinosa, Polygala tenuifolia, and Acorus gramineus, on hippocampal cells and memory function. To examine the neuroprotective effects of a new four-herb extract, cell viability, cytotoxicity, and reactive oxygen species (ROS) assays were performed in HT22 cells and behavioral tests (Morris water maze and passive avoidance retention), Western blot, and immunohistochemistry were performed in a mouse model of focal cerebral ischemia. In HT22 hippocampal cells, pretreatment with CWC-9 resulted in significantly reduced glutamate-induced cell death with suppression of ROS accumulation caused by glutamate. In a mouse model of focal cerebral ischemia, we observed significant improvement of spatial and short-term memory function by treatment with CWC-9. Phosphorylated p38 mitogen-activated protein kinases (MAPK) in hippocampus of ischemic mice were decreased by treatment with CWC-9, but phosphorylated phosphatidylinositol-3 kinase (PI3K) and cAMP response element binding protein (CREB) were significantly enhanced. By immunohistochemical analysis, we confirmed higher expression of phosphorylation of CREB in the hippocampal neurons of CWC-9 treated mice. These results suggest that new multi-herb formula CWC-9 mainly exerted beneficial effects on cognitive function through regulation of neuro-protective signaling pathways associated with CREB.

Hippocampus and Schizophrenia (해마와 정신분열병)

  • Chung, Young Chul
    • Korean Journal of Biological Psychiatry
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    • v.10 no.1
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    • pp.20-44
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    • 2003
  • Schizophrenics suffer not only psychotic symptoms but also cognitive deficits such as an attentional difficulty, memory impairment, poor abstraction, etc. These cognitive abnormalities have been reported to be significantly related to the social and occupational outcome in schizophrenia. Thus, it is important to explore the cause and pathophysiology for the cognitive abnormalities in patients with schizophrenia. In this regard, hippocampus is one of the most promising brain areas to search for the clue because it is closely involved in memory related function. In fact, during the past several decades, there have been extensive studies supporting hippocampal abnormalities as a cause of schizophrenia in both clinical and preclinical field. In this review, basic anatomical knowledge about hippocampus and major findings of preclinical and clinical studies which investigated the correlation between schizophrenia and hippocampus were highlighted. The contents are 1) anatomical structure of hippocampus, 2) neuronal pathway and receptor distribution in hippocampus, 3) function of hippocampus, 4) hippocampal animal model for schizophrenia, 5) hippocampus-related studies on antipsychotic drugs, and 6) clinical studies in hippocampus in patients with schizophrenia.

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