• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.169.2-170
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• 2003

Erythropietin (EPO), a hematopoietic factor is also required for normal brain development, and its receptor is localized in brain. Therefore, it is possible that EPO could act as a neurotropic factor inducing differentiation of neurons. The present study, we therefore investigated whether EPO can increase differentiation of undifferentiated cortical neuron isolated from postneonatal (Day 1) rat brains and PC12 cell, undifferentiated dopaminagic cell line. EPO dose (1-100 U/ml) dependently increased cell differentiation and expression of differentiation marker gene (neurofilament and tyrosine hydroxylase) in both cells. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.94.3-95
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• 2003

Familial form of Alzheimer's disease (FAD) is caused by mutations in presenilin-l (PS-1) and presenilin-2 (PS-2). PS1 and PS2 mutation are known to similar effects on the production of amyloid peptide (A ) and cause of neuronal cell dath in the brain of patient of Alzheimer's disease. The importance of the alternation of cellular calcium homeostasis in the neuronal cell death by PS1 mutation in a variety of experimental systems has been demonstrated. However, no studies on the effect of PS2 of mutant PS2 on cellular calcium homeostasis, and relevance of its change to neuronal cell vulnerability against neurotoxins have been reported. (omitted)

• BMB Reports
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• 제57권4호
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• pp.182-187
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• 2024

Neural stem cells (NSCs) in the adult hippocampus divide infrequently; the endogenous molecules modulating adult hippocampal neurogenesis (AHN) remain largely unknown. Here, we show that ErbB3 binding protein 1 (Ebp1), which plays important roles in embryonic neurodevelopment, acts as an essential modulator of adult neurogenic factors. In vivo analysis of Ebp1 neuron depletion mice showed impaired AHN with a low number of hippocampal NSCs and neuroblasts. Ebp1 leads to transcriptional repression of Bmp4 and suppression of Ascl1 promoter methylation in the dentate gyrus of the adult hippocampus reflecting an unusually high level of Bmp4 and low Ascl1 level in neurons of Ebp1-deficient mice. Therefore, our findings suggests that Ebp1 could act as an endogenous modulator of the interplay between Bmp4 and Ascl1/Notch signaling, contributing to AHN.

• 대한한의학회지
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• 제21권2호
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• pp.25-36
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• 2000

Objectives : This study demonstrates the effects of Daejo-hwan on learning and memory impairment induced by L-NAME (75 mg/kg) treatment and on cerebral ischemic damage induced by middle cerebral artery (MCA) occlusion in rats. Methods : Daejo-hwan emulsion (73.3 mg/100 g/l ml) was administered to rats along a timed study schedule. The Moms water maze was used for learning and memory test of the rats. The MCA was occluded by using the intraluminal thread method. The brain slices were stained by 2 % triphenyl tetrazolium chloride (TTC) and 1 % cresyl violet solution. Infarct size, neuron cell number and size in penumbra was measured by using computer image analysis system. Results : 1. The escape latency of the Daejo-hwan treated group decreased significantly with respect to the control group. 2.The memory score of the Daejo-hwan treated group showed increase tendency, And the swimming distance was not different between the normal, the control, and the Daejo-hwan treated group. 3. The infarct size of the Daejo-hwan treated group decreased significantly with respect to the control group. 4. The total infarct volume of the Daejo-hwan treated group showed decrease tendency. And the brain edema index of the Daejo-hwan treated group decreased significantly with respect to the control group. 5. The neuron cell number and cell size in penumbra of the Daejo-hwan treated group increased significantly with respect to the control group. Conclusions : According to the above results, it is supposed that Daejo-hwan is clinically applicable to the vascular dementia.

• 대한임상검사과학회지
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• 제47권1호
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• pp.51-58
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• 2015

Ethanol has long been implicated in triggering apoptotic neurodegeneration. Alcohol also may indirectly harm the fetus by imparing the mother's physiology. We examined the effects of ethanol on immature brain of mice. Three-weeks-old female ICR strain mice daily intraperitoneally injected with ethanol at the concentration of 4 and 20% in saline for 0, 6, and 24 hours and 1 and 4 weeks. The mice were weighted and sacrificed, and the brains were ectomized for the present histological, immunohistochemical and TUNEL assays. Based on the histologic hematoxylin and eosin stain, immunohistochemical expression of glutamate receptor protein and neuronal cell adhesion molecule (NCAM) were evaluated. The cerebral cortex of the ethanol-treated group showed few typical symptoms of apoptosis such as chromosome condensation and disintegration of the cell bodies. TUNEL staining revealed DNA fragmentation in the 6 and 24 hours. This results demonstrated that acute ethanol administration causes neuronal cell death. I found that either glutamate receptor inhibition or activation could induce cerebellar degeneration as ethanol effect. Neuronal death also can be induced by excess activity of certain neurotransmitter, including glutamate. Neurons must establish cell-to-cell contact during growth and development in order to survive, migrate to their final destination, and develop appropriate connections with neighboring cell. Purkinje cell in cerebellar are especially vulnerable to the cell death and degeneration. After ethanol treatment in cerebellar, NCAM had decreased by 4 weeks. This result suggest that apoptosis seems to be involved in the slow elimination of neuron and cerebellar degeneration.

• Applied Microscopy
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• 제24권3호
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• pp.1-9
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• 1994

별늑대거미의 전측안은 전중안과 함께 전방을 향하여 앞이마 제 1 열에 위치하고 있었으며, 조직학적 조성은 각막, 렌즈, 초자체, 그리고 망막으로 이루어져 있었다. 큐티클성 각막층은 표피의 외큐티클(exocuticle)과 연결되어 있었고, 렌즈는 두개의 볼록렌즈가 내외 양방향으로 연결된 biconvex type이었고, 초자체는 단층의 원주세포로 오목렌즈 모양으로 관찰되었다. 망막을 구성하는 시세포는 단극성 신경세포 (unipolar neuron)로 확인되었으며, 크기가 시세포의 길이에 비하여 큰 세포체가 매우 불규칙 한 크기로 분포하고 있었다. 미세융모로 이루어진 감간체는 세포체 아래에 분포하고 있었으며, 이 부위의 시세포 사이에서는 전자밀도가 높은 색소과립이 관찰되었다. 교질세포는 시세포의 세포체 사이에 분포하였고, 반사층(tapetum)은 감간과 시세포 미부(intermediate segment) 부위 사이에 4-5 정도의 층을 이루어 존재하였다.

• Applied Microscopy
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• 제28권3호
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• pp.363-377
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• 1998

After the investigation on the eye of Incilaria fruhstorieri with light and electron microscopes, the following results were obtained. The eye of Incilaria fruhstorferi comprises cornea, lens, vitreous body, retina, and optic nerve inward from the outside. Cornea is composed of squamous, cuboid, columnar and irregular cells, which appear to be light due to their low electron density. In their cytoplasms, glycogen granules, multivesicular body, and nucleus were observed. Vitreous body, located behind non-cellular transparent lens, is filled with long and short microvilli protruding from the retinal epithelia. Retinal epithelium, the organ to perceive objects, is divided into four parts; microvillar layer pigment layer, nuclear layer, and neutrophils layer, from the apical portion. Microvillar layer consists of the type-I photoreceptor cells and pigmented granule cells. In the apical portion of their cytoplasms, long microvilli (length, $19{\mu}m$) , short microvilli (length, $8{\mu}m$), and rolled microvilli grow thick in the irregular and mixed forms. Photoreceptor cells are classified into type-I and type-II, according to their structures. The type-I cell has the apical portion rising roundly like a fan and the lower part which looks like the helve of a fan. In the cytoplasm of the apical portion, there are clear vesicles, cored vesicles, ovoid mitochondria, and microfilaments, and in the cytoplasm of the lower part, photic vesicles with their diameters about 60nm aggregate densely. The type-II photoreceptor cell, located at the lower end of the type-I cells, has a very large ovoid nucleus 3nd no microvilli. In the cytoplasm of the type-II cell, the photic vesicles with sizes 60nm aggregate more densely than in the cytoplasm of the type-I cell. Pigmented cells are classified into type-A and type-B, according to their structures. The type-A is identified to be a large cell containing round granules (diameter, $0.5{\mu}m$) of very high electron density, while the type-B is identified as a small cell where the irregular granules (diameter, $0.6{\mu}m$) of a little lower electron density amalgamate. Nuclear layer ranges from the bottom of pigment layer to the top of the capsule, and contains three kinds of nuclei (nuclei of the type-II photoreceptor cell, pigmented granule cell, and accessory neuron). The capsules covering the outmost part of the eyeball are composed of collagenous fiber and three longitudinal muscle layers (the thickness of each longitudinal muscle layer, $0.4{\mu}m$) and thick circular muscle layer (thickness, $0.3{\mu}m$). Around the capsules, there is a neurophile layer consisting of neurons and nerve fibers. Each neuron has a relatively large ovoid nucleus for its cytoplasm, and in the karyosome, large lumps of keterochromatin form a wheel nucleus.

• Clinical and Experimental Pediatrics
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• 제49권10호
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• pp.1100-1105
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• 2006

목 적 : 신경세포 분화에 있어 NELL2가 세포 주기와 세포자 멸사에 어떤 영향을 미치는지를 규명하고자 하였다. 방 법 : HiB5 세포에 NELL2를 전달감염시켜 배양하여 세포수를 측정하였다. 세포자멸사를 분석하기 위해 DNA 분절검사를 시행하였으며 PI염색으로 DNA양을 측정하였다. 세포주기의 조절에 관여하는 단백질에 대한 NELL2의 효과를 측정하기 위하여 Western blot과 면역염색을 시행하였다. 결 과 : NELL2를 전달감염시킨 군에서 세포수가 의미가 있게 적었고 DNA 분절검사에서 세포자멸사를 확인하였으며 $G_1$ 정지가 증가하였다. Western blot과 면역염색결과 Rb단백, p53, E2F1(KH-95)이 NELL2를 전달감염시킨 군에서 증가하고 cyclin D가 NELL2를 전달감염시킨 군에서 감소하였다. 결 론 : HiB5 세포에서 NELL2에 의하여 일정 수준에서의 세포자멸사가 동반되고 세포 주기에 있어 $G_1$기의 정지가 일어나며 세포주기를 조절하는 단백질의 변화가 발생함을 확인하였다. 따라서 NELL2가 뇌에서 신경세포 분화에 중요한 역할을 할 걸로 생각된다.

• Biomolecules & Therapeutics
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• 제32권1호
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• pp.154-161
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• 2024

Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder that causes progressive paralysis. L-Citrulline is a nonessential neutral amino acid produced by L-arginine via nitric oxide synthase (NOS). According to previous studies, the pathogenesis of ALS entails glutamate toxicity, oxidative stress, protein misfolding, and neurofilament disruption. In addition, L-citrulline prevents neuronal cell death in brain ischemia; therefore, we investigated the change in the transport of L-citrulline under various pathological conditions in a cell line model of ALS. We examined the uptake of [¹⁴C]L-citrulline in wild-type (hSOD1wt/WT) and mutant NSC-34/ SOD1^G93A (MT) cell lines. The cell viability was determined via MTT assay. A transport study was performed to determine the uptake of [¹⁴C]L-citrulline. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was performed to determine the expression levels of rat large neutral amino acid transported 1 (rLAT1) in ALS cell lines. Nitric oxide (NO) assay was performed using Griess reagent. L-Citrulline had a restorative effect on glutamate induced cell death, and increased [¹⁴C]L-citrulline uptake and mRNA levels of the large neutral amino acid transporter (LAT1) in the glutamate-treated ALS disease model (MT). NO levels increased significantly when MT cells were pretreated with glutamate for 24 h and restored by co-treatment with L-citrulline. Co-treatment of MT cells with L-arginine, an NO donor, increased NO levels. NSC-34 cells exposed to high glucose conditions showed a significant increase in [¹⁴C]L-citrulline uptake and LAT1 mRNA expression levels, which were restored to normal levels upon co-treatment with unlabeled L-citrulline. In contrast, exposure of the MT cell line to tumor necrosis factor alpha, lipopolysaccharides, and hypertonic condition decreased the uptake significantly which was restored to the normal level by co-treating with unlabeled L-citrulline. L-Citrulline can restore NO levels and cellular uptake in ALS-affected cells with glutamate cytotoxicity, pro-inflammatory cytokines, or other pathological states, suggesting that L-citrulline supplementation in ALS may play a key role in providing neuroprotection.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.153.2-154
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• 2003

Pathophysiological elevation of intracellular calcium concentration ([$Ca^{2+}$]$_i$) in the neuron has been considered as an important responsible factor in the neuronal cell damages. However, the mechanism of increase of [$Ca^{2+}$]$_i$ through ryanodine receptor (RyR), the relationship between [$Ca^{2+}$]$_i$ level and cell damages have not been fully demonstrated. (omitted)