• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.63.2-63.2
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• 2008

• 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.

• Molecules and Cells
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• v.37 no.3
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• pp.248-256
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• 2014

N-acetylglucosamine kinase (GlcNAc kinase or NAGK; EC 2.7.1.59) is a N-acetylhexosamine kinase that belong to the sugar kinase/heat shock protein 70/actin superfamily. In this study, we investigated both the expression and function of NAGK in neurons. Immunohistochemistry of rat brain sections showed that NAGK was expressed at high levels in neurons but at low levels in astrocytes. Immunocytochemistry of rat hippocampal dissociate cultures confirmed these findings and showed that NAGK was also expressed at low levels in oligodendrocytes. Furthermore, several NAGK clusters were observed in the nucleoplasm of both neuron and glia. The overexpression of EGFP- or RFP (DsRed2)-tagged NAGK in rat hippocampal neurons (DIV 5-9) increased the complexity of dendritic architecture by increasing the numbers of primary dendrites and dendritic branches. In contrast, knockdown of NAGK by shRNA resulted in dendrite degeneration, and this was prevented by the co-expression of RFP-tagged NAGK. These results suggest that the upregulation of dendritic complexity is a non-canonical function of NAGK.

• Journal of the Institute of Electronics Engineers of Korea SP
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• v.43 no.4 s.310
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• pp.46-54
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• 2006

Recently, the important of a personal identification is increasing according to expansion using each on-line commercial transaction and personal ID-card. Although a personal ID-card embedded RFID(Radio Frequency Identification) tag is gradually increased, the way for a person's identification is deficiency. So we need automatic methods. Because RFID tag is vary small storage capacity of memory, it needs effective feature extraction method to store personal biometrics information. We need new recognition method to compare each feature. In this paper, we studied the face verification system using Hippocampal neuron modeling algorithm which can remodel the 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 mainly. One is feature extraction using NMF(Non-negative Matrix Factorization) and LDA(Linear Discriminants Analysis) mixture algorithm and the other is hippocampal neuron modeling and recognition simulation experiments confirm the each recognition rate, that are face changes, pose changes and low-level quality image. The results of experiments, 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 the existing method.

• 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 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.

• Archives of Pharmacal Research
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• v.27 no.5
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• pp.524-530
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• 2004

Epilepsy or the occurrence of spontaneous recurrent epileptiform discharges (SREDs, seizures) is one of the most common neurological disorders. Shift in the balance of brain between excitatory and inhibitory functions due to different types of structural or functional alterations may cause epileptiform discharges. N-Methyl-D-aspartate (NMDA) receptor dysfunctions have been implicated in modulating seizure activities. Seizures and epilepsy are clearly dependent on elevated intracellular calcium concentration ([C $a^{2+}$]$_{i}$ ) by NMDA receptor activation and can be prevented by NMDA antagonists. This perturbed [C $a^{2+}$]$_{i}$ levels is forerunner of neuronal death. However, therapeutic tools of elevated [C $a^{2+}$]$_{i}$ level during status epilepticus (SE) and SREDs have not been discovered yet. Our previous study showed fast inhibition of ginseng total saponins and ginsenoside R $g_3$ on NMDA receptor-mediated [C $a^{2+}$]$_{i}$ in cultured hippocampal neurons. We, therefore, examined the direct modulation of ginseng on hippocampal neuronal culture model of epilepsy using fura-2-based digital $Ca^{2+}$ imaging and neuronal viability assays. We found that ginseng total saponins and ginsenoside R $g_3$ inhibited $Mg^{2+}$ free-induced increase of [C $a^{2+}$]$_{i}$ and spontaneous [C $a^{2+}$]$_{i}$ oscillations in cultured rat hippocampal neurons. These results suggest that ginseng may playa neuroprotective role in perturbed homeostasis of [C $a^{2+}$]$_{i}$ and neuronal cell death via the inhibition of NMDA receptor-induced SE or SREDs.d SE or SREDs..

• 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 Life Science
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• v.16 no.6
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• pp.955-959
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• 2006

A dynamic cycle of addition and removal of O-linked N-acetylglucosamine (O-GlcNAc) at serine and threonine residues is emerging as a key regulator of nuclear and cytoplasmic protein activity. In this work, immunocytochemistry was carried out to investigate the subcellular expression of GlcNAc kinase (NAGK, EC 2.7.1.59) that catalyzes the phosphorylation of GlcNAc to GlcNAc 6-phosphate. Immunostainings of cultured rat hippocampal neurons revealed patchy or punctate distribution of NAGK. When NAGK is doublestained with caveolin-1 or flotillin, markers for caveolae and lipid rafts, respectively, NAGK was co-localized with these markers. These results indicate that most, if not all, of the NAGK immunopunctae represent caveolae and lipid rafts, and suggest NAGK's role in these membrane microdomains.

• Journal of Medicine and Life Science
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• v.15 no.2
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• pp.62-66
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• 2018

A-type $K^+$ ($I_A$) channels are transiently activated in the suprathreshold membrane potential and then rapidly inactivated. These channels play roles to control the neuronal excitability in pyramidal neurons in hippocampi. We here electrophysiologically tested if regulatory functions of $I_A$ channels might be targeted by acute activation of glutamatergic synaptic transmission in cultured hippocampal neurons(DIV 6~8). The application of high KCl in recording solutions(10 mM, 2 min) to increase presynaptic glutamate release, significantly reduced the peak of somatic $I_A$ without changes of gating kinetics. This indicates that neuronal excitation induced by the enhancement of synaptic transmission may process with distinctive signaling cascades to affect voltage-dependent ion channels in hippocampal neurons. Therefore, it is possible that short-lasting enhancement of synaptic transmission is functionally restricted in local synapses without effects on intracellular signaling cascades affecting a whole neuron, efficiently and rapidly enhancing synaptic functions in hippocampal network.