• Toxicological Research
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• v.14 no.3
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• pp.349-356
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• 1998

We identified S9940, a novel microbial metabolite from Streptomyces spp., to inhibit the release of neurotransmitter from PC12 cells. S9940 is an inhibitor of trifiated norepinephrine ([$^{3}H$]-NE) release in high $K^+$ buffer solution containing ionomycin, indicating that S9940 inhibits neurotransmitter release after the influx of $Ca^{2+}$ ions. We also examined the effect of S9940 on $\beta-glucuronidase$ release from guinea pig neurophils and the effect on the neurite extension of PC12 cells and rat hippocampal neurons. As a result, S9940 inhibited $\beta-glucuronidase$ release: when treated with $5{\mu}g/ml$ of S9940, which prevented [$^{3}H$]-NE release, the inhibition of neurite extension for both PC12 cells and rat hippocampal neurons was observed.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.89-89
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• 2002

It is well known that oxygen radicals induce neuronal cell damage by initiation of lipid peroxidation chain reaction. Recent work has been also demonstrated that enzymatically generated free radicals cause the release of glutamate and aspartate from cultured rat hippocampal slices.(omitted)

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.5
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• pp.1019-1024
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• 2009

Diabetic neuropathy is characterized by the decrease of cell viability in neuron, which is induced by the hyperglycemia. HT22 cell is the neuron cell line originated from hippocampus. Ginsenosides have been reported to retain anti-diabetic effect. However, the preventive effect of ginsenosides in the condition of diabetic neuropathy was not elucidated. Thus, this study was conducted to examine the protective effect of ginsenoside total saponin (GTS), panoxadiol (PD), and panoxatriol (PT) in the high glucose-induced cell death of HT22 cells, an in vitro cellular model for diabetic neuropathy. In present study, high glucose increased lactate dehydrogenase(LDH) activity, the lipid peroxide(LPO) formation and induced the decrease of cell viability. These effects were completely prevented by the treatment of GTS, but partially prevented by the treatment of PD and PT. High glucose also increased the expression of Bax and cleaved form of caspase-3 but decreased that of Bcl-2. These effects of high glucose on Bax, Bcl-2 and cleaved form of caspase-3 were completely prevented by the treatment of GTS, but partially prevented by the treatment of PD and PT in HT22 cells. In conclusion, ginsenosides prevented high glucose-induced cell death of hippocampal neuron through the inhibition of oxidative stress and apoptosis in HT 22 cells.

• 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.

• Molecules and Cells
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• v.43 no.6
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• pp.581-589
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• 2020

Neurons have multiple dendrites and single axon. This neuronal polarity is gradually established during early processes of neuronal differentiation: generation of multiple neurites (stages 1-2); differentiation (stage 3) and maturation (stages 4-5) of an axon and dendrites. In this study, we demonstrated that the neuron-specific n-glycosylated protein NELL2 is important for neuronal polarization and axon growth using cultured rat embryonic hippocampal neurons. Endogenous NELL2 expression was gradually increased in parallel with the progression of developmental stages of hippocampal neurons, and overexpression of NELL2 stimulated neuronal polarization and axon growth. In line with these results, knockdown of NELL2 expression resulted in deterioration of neuronal development, including inhibition of neuronal development progression, decreased axon growth and increased axon branching. Inhibitor against extracellular signal-regulated kinase (ERK) dramatically inhibited NELL2-induced progression of neuronal development and axon growth. These results suggest that NELL2 is an important regulator for the morphological development for neuronal polarization and axon growth.

• 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.

• Molecules and Cells
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• v.22 no.1
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• pp.8-12
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• 2006

Neuron-derived orphan receptor (NOR-1) is a member of the thyroid/steroid receptor superfamily that was originally identified in forebrain neuronal cells undergoing apoptosis. In addition to apoptotic stimuli, activation of several signal transduction pathways including direct neuronal depolarization regulates the expression of NOR-1. In this study we tested whether the expression of NOR-1 is changed following transient ischemic injury in the adult rat brain. NOR-1 mRNA increased rapidly in the dentate gyrus of the hippocampal formation and piriform cortex 3 h after transient global ischemia and returned to basal level at 6 h. On the other hand, oxygen-glucose deprivation of cultured cerebral cortical neurons did not alter the expression of NOR-1. These results suggest that expression of NOR-1 is differentially regulated in different brain regions in response to globally applied brain ischemia, but that hypoxia is not sufficient to induce its expression.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.85-95
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• 2001

This study was designed to examine the effects of two antidepressant drugs on the expression of c-fos mRNA in cultured embryonic rat hippocampal neurons. The drugs used were imipramine and amitriptyline. On the fourth day of culture, hippocampal neurons were treated with variable concentrations of each drug. Competitive RT-PCR(Reverse Transcriptase-PCR) analysis was used to quantify the c-fos mRNA expression induced by each drug. Experimental results showed that acute and direct treatment with imipramine and amitriptyline with relatively low concentrations(imipramine ${\leq}10{\mu}M$, amitriptylne ${\leq}10{\mu}M$) had no inductive effect on the expression of c-fos mRNA in the rat hippocampal neurons. However, after treatment with relatively high concentrations(imipramine ${\geq}100{\mu}M$, amitriptyline ${\geq}100{\mu}M$) c-fos mRNA was not detected. These findings suggest the followings. Firstly, the action mechanisms of these drugs on the hippocampal neurons might not be mediated by c-fos but by other immediate-early genes(IEGs). Secondly, their actions may be mediated indirectly via other areas of the brain. Thirdly, the expression of c-fos might be inhibited by high concentrations of these drugs, or the high concentrations could induce cell death. Finally, though cell death remains to be confirmed, the inhibition of c-fos induction or cell death could play a role in the cognitive impairments known to be adverse effects of some antidepressants. This study is believed to be a first step toward understanding the mechanisms of learning and memory. Further studies are needed to investigate the expression of various IEGs and changes in the hippocampal neurons of rat resulting from chronic treatment with antidepressant drugs.

• Journal of Life Science
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• v.16 no.2 s.75
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• pp.315-322
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• 2006

FS11052, a novel microbial metabolite from Streptomyces spp. was identified as a small molecular substance and shown inhibition activities for the release of neurotransmitter from rat hippocampal neuron and PC12 cells. FS11052 is an inhibitor of tritiated norepinephrine ($[^3H]-NE$) release in high $K^+$ buffer solution containing ionomycin, indicating that FS11052 inhibits neurotransmitter release after the influx of $Ca^{2+}$ ions. When examined the effect of FS11052 on glucuronidase release from guinea pig neutrophils, FS11052 inhibited glucuronidase release: when treated with $5{\mu}g/ml$ of FS11052, which was not induced cellular cytotoxicity. The fact that the glucuronidase release in neutrophil and norepinephrine release in neuron was inhibited suggests the similarity in the locations and the mechanisms of FS11052 action targets. When treated with $5{\mu}g/ml$ of FS11052, $[^3H]-NE$ release and neurite extension for both rat hippocampal neurons and PC12 cells were prevented. These observations of FS11052 functioning as an inhibitor of neurotransmitter release suggest that FS11052 has an important role in synaptic transmission in neuron.

• 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.