• Journal of the Institute of Electronics Engineers of Korea SP
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• v.42 no.5 s.305
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• pp.55-62
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• 2005

In this paper, we propose the face recognition system using HNMA(Hippocampal Neuron Modeling Algorithm) which can remodel the cerebral cortex and hippocampal neuron as a principle of a man's brain in engineering, then it can learn the feature-vector of the face images very fast and construct the optimized feature each image. The system is composed of two parts. One is feature-extraction and the other is teaming and recognition. In the feature extraction part, it can construct good-classified features applying PCA(Principal Component Analysis) and LDA(Linear Discriminants Analysis) in order. In the learning part, it cm table the features of the image data which are inputted according to the order of hippocampal neuron structure to reaction-pattern according to the adjustment of a good impression in the dentate gyrus region and remove the noise through the associate memory in the CA3 region. In the CA1 region receiving the information of the CA3, it can make long-term memory learned by neuron. Experiments confirm the each recognition rate, that are face changes, pose changes and low quality image. The experimental results show that we can compare a feature extraction and learning method proposed in this paper of any other methods, and we can confirm that the proposed method is superior to existing methods.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1850-1855
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• 2004

The purpose of this report is to investigate the electroacupuncture effect on the cholinergic neuronal activation in the hippocampal CA1 section. The electroacupuncture was performed on S36 of white rats and its consequencies were investigated by immunohistochemical method. Hippocampal CA1 sections of Sprague Dawley white male rats electroacupunctured on S36 at 20㎐ and 100㎐ are stained by cresyl violet to show that the values of 100㎐ and 20㎐ group increased significantly compared to sham group's one. Especially, 100㎐ group shows stronger neuronal activation compared to 20㎐ group. Induction of AChE, a neurotransmitter, in hippocampal CA1 is increased significantly in 100㎐ and 20㎐ group compared to sham group. Especially 20㎐ group shows higher AChE immunoreaction than 100㎐ does, although it wasn't significant enough. Induction of NGF(Nerve Growth Factor) in hippocampal CA1 sections was observed higher in 20㎐ and 100㎐ group than in sham group. Especially, 20㎐ group shows higher NGF immunoreaction compared to 100㎐. The facts above indicate that the eletroacupucture is effect to the cholinergic neuronal activation of hippocampus induced by focal ischemia.

• Animal cells and systems
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• v.13 no.4
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• pp.357-362
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• 2009

Hesperidin, the most abundant polyphenolic compound found in citrus fruits, has been known to possess neuroprotective, sedative, and anticonvulsive effects on the nervous system. In a recent electrophysiological study, it was reported that hesperidin induced biphasic change in population spike amplitude in hippocampal CA1 neurons in response to both single spike stimuli and theta-burst stimulation depending on its concentration. However, the precise mechanism by which hesperidin acts on neuronal functions has not been fully elucidated. Here, using whole-cell patch-clamp recording, we revealed that hesperidin did not affect excitatory synaptic activities such as basal synaptic transmission and theta-burst LTP. Moreover, in a current injection experiment, spike number, resting membrane potential and action potential threshold also remained unchanged. Taken together, these results indicate that the effects of hesperidin on the neuronal functions such as spiking activity might not be attributable to either modification of excitatory synaptic transmissions or changes in membrane excitability in hippocampal CA1 neuron.

• BMB Reports
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• v.54 no.6
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• pp.317-322
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• 2021

CCCTC-binding factor (CTCF), a zinc finger protein, is a transcription factor and regulator of chromatin structure. Forebrain excitatory neuron-specific CTCF deficiency contributes to inflammation via enhanced transcription of inflammation-related genes in the cortex and hippocampus. However, little is known about the long-term effect of CTCF deficiency on postnatal neurons, astrocytes, or microglia in the hippocampus of adult mice. To address this, we knocked out the Ctcf gene in forebrain glutamatergic neurons (Ctcf cKO) by crossing Ctcf-floxed mice with Camk2a-Cre mice and examined the hippocampi of 7.5-10-month-old male mice using immunofluorescence microscopy. We found obvious neuronal cell death and reactive gliosis in the hippocampal cornu ammonis (CA)1 in 7.5-10-month-old cKO mice. Prominent rod-shaped microglia that participate in immune surveillance were observed in the stratum pyramidale and radiatum layer, indicating a potential increase in inflammatory mediators released by hippocampal neurons. Although neuronal loss was not observed in CA3, and dentate gyrus (DG) CTCF depletion induced a significant increase in the number of microglia in the stratum oriens of CA3 and reactive microgliosis and astrogliosis in the molecular layer and hilus of the DG in 7.5-10-month-old cKO mice. These results suggest that long-term Ctcf deletion from forebrain excitatory neurons may contribute to reactive gliosis induced by neuronal damage and consequent neuronal loss in the hippocampal CA1, DG, and CA3 in sequence over 7 months of age.

• 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.

• The Journal of Korean Medicine
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• v.29 no.5
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• pp.29-40
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• 2008

Objectives : It has been reported that Sophorae Subprostratae Radix (SSR) has a neuroprotective effect on cerebral ischemia in animals. In the present study, the authors investigated the neuroprotective effect of SSR on glutamate excitotoxicity. Glutamate excitotoxicity was induced by using NMDA, AMPA, and KA in PC12 cells and in organotypic hippocampal slice cultures. Methods :Methanolic extract of SSR was added at 0.5, 5, and 50 ${\mu}$g/ml to culture media for 24 hours. The effects of SSR were evaluated by measuring of cell viability, PI-stained neuronal cell death, TUNEL-positive cells, and MAP-2 immunoreactivity. Results : SSR increased PC12 cell viabilities significantly against AMPA-induced excitotoxicity, but not against NMDA-induced or KA-induced excitotoxicity. In organotypic hippocampal slice cultures damaged by NMDA-induced excitotoxicity, SSR attenuated neuronal cell death significantly in the CA1, CA3, and DG hippocampal regions and reduced TUNEL-positive cells significantly in CA1 and DG regions. In organotypic hippocampal slice cultures damaged by AMPA-induced excitotoxicity, SSR attenuated neuronal cell death and reduced TUNEL-positive cell numbers significantly in the CA1 and DG regions. In organotypic hippocampal slice cultures damaged by KA-induced excitotoxicity, SSR attenuated neuronal cell death significantly in CA3, but did not reduce TUNEL-positive cell numbers in CA1, CA3 or DG. In organotypic hippocampal slice cultures damaged by NMDA-induced excitotoxicity, SSR attenuated pyramidal neuron neurite retraction and degeneration in CA1. Conclusions : These results suggest that the neuroprotective effects of SSR are related to antagonistic effects on the NMDA and AMPA receptors of neuronal cells damaged by excitotoxicity and ischemia.

• BMB Reports
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• v.31 no.2
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• pp.117-122
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• 1998

Changes of lipocortin 1 (LC1) in the brain induced by immobilization stress were investigated in rats. Rats were immobilized for 0,1,2,3,4, and 5 h, and the brain slices were immunostained with anti-human LC1 antibodl (anti-LC1). Immunoreactivity of LCI (iLC1) was most prominent in neuronal cell bodies and processes of hippocampal CA regions and dentate gyrus. At rest without stress, most of the LC1 in the neuron located in the cytoplasm with the nuclei exhibiting relatively scarce immunoreactivity. Immobilization stress changed this intracellular distribution of LC1 by increasing nuclear LC1. The change was apparent in 1 h and reached the peak by 3 h. However, by 5 h of immobilization, the distribution pattern returned to that of the resting state. This transient nuclear translocation of LC1 was most prominent in $CA_1$ pyramidal neurons, and was not observed in areas other than the hippocampus. Adrenalectomy abolished this transient translocation of LC1. The roles of hippocampal LC1 as a mediator of glucocorticoid feedback signal and/or as an intracellar stress signaling protein could be suggested.

• Journal of Korea Multimedia Society
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• v.13 no.4
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• pp.504-511
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• 2010

In this paper, we propose the face region recognition system for City-Security CCTV(Closed Circuit Television) using hippocampal neural network which is modelling of human brain's hippocampus. This system is composed of feature extraction, learning and recognition part. The feature extraction part is constructed using PCA(Principal Component Analysis) and LDA(Linear Discriminants Analysis). In the learning part, it can label the features of the image-data which are inputted according to the order of hippocampal neuron structure to reaction-pattern according to the adjustment of a good impression in a dentate gyrus and remove the noise through the auto-associative memory in the CA3 region. In the CA1 region receiving the information of the CA3, it can make long-term memory learned by neuron. Experiments confirm the each recognition rate, that are shape change and light change. The experimental results show that we can compare a feature extraction and learning method proposed in this paper of any other methods, and we can confirm that the proposed method is superior to existing methods.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.2
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• pp.43-49
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• 2008

Flavonoids have been shown to affect calcium signaling in neurons. However, there are no reports on the effect of apigenin on glutamate-induced calcium signaling in neurons. We investigated whether apigenin affects glutamate-induced increase of free intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in cultured rat hippocampal neurons, using fura-2-based digital calcium imaging and microfluorimetry. The hippocampal neurons were used between 10 and 13 days in culture from embryonic day 18 rats. Pretreatment of the cells with apigenin ($1{\mu}M$ to $100{\mu}M$) for 5 min inhibited glutamate ($100{\mu}M$, 1 min) induced $[Ca^{2+}]_i$ increase, concentration-dependently. Pretreatment with apigenin ($30{\mu}M$) for 5 min significantly decreased the $[Ca^{2+}]_i$ responses induced by two ionotropic glutamate receptor agonists, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA, $10{\mu}M$, 1 min) and N-methyl-D-aspartate (NMDA, $100{\mu}M$, 1 min), and significantly inhibited the AMPA-induced peak currents. Treatment with apigenin also significantly inhibited the $[Ca^{2+}]_i$ response induced by 50 mM KCl solution, decreased the $[Ca^{2+}]_i$ responses induced by the metabotropic glutamate receptor agonist, (S)-3,5-dihydroxy-phenylglycine (DHPG, 100 $[Ca^{2+}]_i$, 90 s), and inhibited the caffeine (10 mM, 2 min)-induced $[Ca^{2+}]_i$ responses. Furthermore, treatment with apigenin ($30{\mu}M$) significantly inhibited the amplitude and frequency of 0.1 mM $[Mg^{2+}]_o$-induced $[Ca^{2+}]_i$ spikes. These data together suggest that apigenin inhibits glutamate-induced calcium signaling in cultured rat hippocampal neurons.

• Molecular & Cellular Toxicology
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• v.4 no.3
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• pp.218-223
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• 2008

Oxidative stress is believed to contribute to the neuronal damage induced by cerebral ischemia/reperfusion injury. The present study was undertaken to evaluate the possible antioxidant neuroprotective effect of hydroxyfullerene (a radical absorbing cage molecule) against neuronal death in hippocampal CA1 neurons following transient global cerebral ischemia in the rat. Transient global cerebral ischemia was induced in male Wistar rats by four vessel- occlusion (4VO) for 10 min. Lipid peroxidation in brain tissues was determined by measuring the concentrations of thiobarbituric acid-reactive substances (TBARS). Furthermore, the apoptotic effects of ${H_2}{O_2}$ on PC12 cells were also investigated. Cell viabilities were measured using MTT [3-(4,5-dimethylthiazolyl-2)-2,-5-diphenyltetrazolium bromide] assays. Hydroxyfullerene, when administered to rats at 0.3-3 mg/kg i.p. at 0 and 90 minutes after 4-VO was found to significantly reduce CA1 neuron death by 72.4% on hippocampal CA1 neurons. Our findings suggest that hydroxyfullerene protects neurons from transient global cerebral injury in the rat hippocampus by reducing oxidative stress and lipid peroxidation levels, which contribute to apoptotic cell death.