• Molecules and Cells
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• 제45권4호
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• pp.169-176
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• 2022

A primary cilium, a hair-like protrusion of the plasma membrane, is a pivotal organelle for sensing external environmental signals and transducing intracellular signaling. An interesting linkage between cilia and obesity has been revealed by studies of the human genetic ciliopathies Bardet-Biedl syndrome and Alström syndrome, in which obesity is a principal manifestation. Mouse models of cell type-specific cilia dysgenesis have subsequently demonstrated that ciliary defects restricted to specific hypothalamic neurons are sufficient to induce obesity and hyperphagia. A potential mechanism underlying hypothalamic neuron cilia-related obesity is impaired ciliary localization of G protein-coupled receptors involved in the regulation of appetite and energy metabolism. A well-studied example of this is melanocortin 4 receptor (MC4R), mutations in which are the most common cause of human monogenic obesity. In the paraventricular hypothalamus neurons, a blockade of ciliary trafficking of MC4R as well as its downstream ciliary signaling leads to hyperphagia and weight gain. Another potential mechanism is reduced leptin signaling in hypothalamic neurons with defective cilia. Leptin receptors traffic to the periciliary area upon leptin stimulation. Moreover, defects in cilia formation hamper leptin signaling and actions in both developing and differentiated hypothalamic neurons. The list of obesity-linked ciliary proteins is expending and this supports a tight association between cilia and obesity. This article provides a brief review on the mechanism of how ciliary defects in hypothalamic neurons facilitate obesity.

• 동의생리병리학회지
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• 제19권6호
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• pp.1640-1646
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• 2005

An oriental medicinal drugs Jahageo (JHG, Hominis placenta) were examined to determine its effects on the responsiveness of central nervous system neurons after injury. We found that JHG was involved in neurite outgrowth of DRG sensory axons. JHG treatment also increased expression of axonal growth-associated protein GAP-43 in DRG sensory neurons after sciatic nerve injury and in the injured spinal cord. JHG treatment during the spinal cord injury increased induction levels of cell division cycle 2 (Cdc2) protein in DRG as well as in the spinal cord. Histochemical investigation showed that induced Cdc2 in the injured spinal cord was found in non-neuronal cells. These results suggest that JHG regulates activities of non-neuronal cells such as oligodendrocyte and astrocyte in responses to spinal cord injury and protects neuronal responsiveness after axonal damage.

• The Korean Journal of Physiology and Pharmacology
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• 제2권4호
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• pp.427-433
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• 1998

In brain hypoxic-ischemia, an excess release of glutamate and a marked production of reactive oxygen species (ROS) occur in neuronal and non-neuronal cells. The present study investigated the effect of the biological antioxidants dihydrolipoic acid (DHLA) and lipoic acid (LA) on N-methyl-D-aspartate (NMDA)- and ROS-induced neurotoxicity in cultured rat cortical neurons. DHLA enhanced NMDA-evoked rises in intracellular calcium concentration ($[Ca^{2+}]_i$). In contrast, LA did not alter the NMDA-evoked calcium responses but decreased after a brief treatment of dithiothreitol (DTT), which possesses a strong reducing potential. Despite the modulation of NMDA receptor-mediated rises in $[Ca^{2+}]_i$, neither DHLA nor LA altered the NMDA receptor-mediated neurotoxicity, as assessed by measuring the amount of lactate dehydrogenase released from dead or injured cells. DHLA, but not LA, prevented the neurotoxicity induced by xanthine/xanthine oxidase-generated superoxide radicals. Both DHLA and LA decreased the glutathione depletion-induced neurotoxicity. The present data may indicate that biological antioxidants DHLA and LA protect neurons from ischemic injuries via scavenging oxygen free radicals rather than modulating the redox modulatory site(s) of NMDA receptor.

• 대한의생명과학회지
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• 제15권3호
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• pp.261-263
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• 2009

Methylprednisolone is a synthetic glucocorticoid which is usually taken intravenously for many neurosurgical diseases which cause edema including brain tumor, and trauma including spinal cord injury. Methylprednisolone reduces swelling and decreases the body's immune response. It is also used to treat many immune and allergic disorders, such as arthritis, lupus, psoriasis, asthma, ulcerative colitis, and Crohn's disease. To identify genes expressed during methylprednisolone treatment against neurons of rats (PC12 cells), DNA microarray method was used. We have isolated 2 gene groups (up- or down-regulated genes) which are methylprednisolone differentially expressed in neurons. Lipocalin 3 is the gene most significantly increased among 772 up-regulated genes (more than 2 fold over-expression) and Aristaless 3 is the gene most dramatically decreased among 959 down-regulated genes (more than 2 fold down-expression). The gene increased expression of Fgb, Thbd, Cfi, F3, Kngl, Serpinel, C3, Tnfrsf4 and Il8rb are involved stress-response gene, and Nfkbia, Casp7, Pik3rl, I11b, Unc5a, Tgfb2, Kitl and Fgf15 are strongly associated with development. Cell cycle associated genes (Mcm6, Ccnb2, Plk1, Ccnd1, E2f1, Cdc2a, Tgfa, Dusp6, Id3) and cell proliferation associated genes (Ccl2, Tnfsf13, Csf2, Kit, Pim1, Nr3c1, Chrm4, Fosl1, Spp1) are down-regulated more than 2 times by methylprednisolone treatment. Among the genes described above, 4 up-regulated genes are confirmed those expression by RT-PCR. We found that methylprednisolone is related to expression of many genes associated with stress response, development, cell cycle, and cell proliferation by DNA microarray analysis. However, We think further experimental molecular studies will be needed to figure out the exact biological function of various genes described above and the physiological change of neuronal cells by methylprednisolone. The resulting data will give the one of the good clues for understanding of methylprednisolone under molecular level in the neurons.

• 대한한방내과학회지
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• 제24권2호
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• pp.181-189
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• 2003

The goal of this study is to investigate whether Uncariae Ramulus et Uncus can protect nerve cells against ischemic neuronal damage is caused by middle cerebral artery occlusion (MCAO) in rats' brains and to investigate whether the neuroprotective effect of Uncariae Ramulus et Uncus is concerned with IEGs(immediate early genes) expression. Uncariae Ramulus et Uncus(l00mg/kg) was administered immediately after 2 hours of MCAO and maintained for 7 days. On 7th days after 2 hours of MCAO, the brains of rats were sliced through the hippocampus. c-Fos immunohistochemistry stain and Cresyl violet stain were done for microscopic examination. Each number of viable neurons and c-Fos immunoreactive cells in CA1 was counted. The density of neurons and c-Fos immunoreactive cells were significantly decreased in MCAO-operated ischemic rats compared to that sham-operated rats. Administration of Uncariae Ramulus et Uncus group significantly elevated MCAO-induced decrease in density of neurons, and elevated MCAO-induced decrease in c-Fos immunoreactive cells. These results suggest that the neuroprotective effect of Uncariae Ramulus et Uncus against focal cerebral ischemia. Also, we hypothesized that neuroprotective mechanism of Uncariae Ramulus et Uncus is related to IEGs expression.

• The Korean Journal of Physiology
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• 제30권1호
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• pp.105-116
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• 1996

Rendering the brain ischemic would evoke the cerebral ischemic reflex which is characterized by an arterial pressor response, apnea and bradycardia. Since the rostral ventrolateral medulla (RVLM) is known to play a key role in the maintenance of normal cardiopulmonary activity, during the cerebral ischemic reflex some cardiac related cells should be excited and respiration related cells inhibited. In this context, the responses of RVLM neurons to systemie and focal hypoxia were analyzed in the present study. Twenty-five adult cats of either sex were anesthetized with ${\alpha}-chloralose$ and the single neuronal activities were identified from RVLM area. For the induction of focal hypoxia in the recording site, sodium cyanide was applied iontophoretically and for systemic hypoxia the animal was ventilated with nitrogen gas for a twenty-second period. Cellular activities were analyzed in terms of their discharge pattern and responses to the hypoxia by using post-stimulus time and single-pass time histograms. Of eighteen cardiac related cells recorded from the RVLM area, twelve cells were excited by iontophoresed sodium cyanide and of twenty-five respiration related cells, fourteen cells were excited by iontophoresed sodium cyanide. Remaining cells were either inhibited or unaffected. Eight of fifteen cells tested with iontophoresed sodium lactate were excited and remaining seven cells were inhibited. Systemic hypoxia induced by nitrogen gas inhalation elevated the arterial blood pressure, but excited, inhibited or unaffected the single neuronal activities. Some cells showed initial excitation followed by inhibition during the systemic hypoxia. Bilateral vagotomy resulted in a decrease of arterial pressor response to the systemic hypoxia, and a slight decrease in the rhythmicity related to cardiac and/or respiratory rhythms. The single neuronal responses to either systemic or focal hypoxia were not affected qualitatively by vagotomy. From the above results, it was concluded that the majority of the cardiac- and respiration- related neurons in the rostral ventrolateral medulla be excited by hypoxia, not through the mediation of peripheral chemoreceptors, and along with the remaining inhibited cells, all these cells be involved in the mediation of cerebral ischemic reflex.

• 대한생식의학회:학술대회논문집
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• 대한불임학회 2005년도 제48차 춘계 학술대회
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• pp.116.2-117
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• 2005

• 대한생식의학회:학술대회논문집
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• 대한불임학회 2002년도 제42차 춘계학술대회
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• pp.91.2-92
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• 2002

• Applied Microscopy
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• 제18권1호
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• pp.1-20
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• 1988

There's been arguments on the different morphological status between the nucleus accumbens septi and nucleus fundus striati of ventral striatum. Authors carried out the comparative study on the neuronal cell types of these nuclei, in the chick and the rat. Results are summarized as follows: In the nucleus accumbens septi of the chick, there found 3 main cell types. Type I cells are oval or spindle-shaped. They are the most abundant cell types, comprising more than 80% of neurons. The pale nucleus is usually indented. The cytoplasm is also pale and contains small amount of mitochondria, rough r-ER and Golgi complexes. This cell has a few symmetric synapses on the cell membrane. Type II cells are pale large cells. They are polygonal or irregularly-shaped. They contain pale spherical nucleus, and the pale cytoplasm with relatively large amount of mitochondria, free ribosomes and well-developed Golgi complexes. Some axo-somatic synapes are found on the cell. Type III cells are oval or spherical-shaped. The nucleus is relatively pale and large, In the dense cytoplasm, well developed. r-ER formed typical Nissl's body, and there found many mitochondria, ribosomes and lysosomes. In the chick fundus striati nucleus, there also found 3 main cell types. Type I cells are small and spindle-shaped. This type is the most abundant one and constitutes more the 80% of the neurons. Morphological features other than it's shape, is generally similar with that of Type I cell in the nucleus accumbens. Type II cells are irregularly shaped large cells. Dense cytoplasm contains large amount of cell organelles. Some axo-somatic synapses are found. Type III cells are small dense cells. This oval cell contains the oval nucleus, and the plentiful cytoplasm with well developed r-ER, ribosomes and mitochondria. In the nucleus accumbens septi of the rat, there found 4 main cell types. Type I cells are small, oval or spherical cells, comprising more than 90% of all the neurons. Spherical nucleus shows typical chromatin rim along the nuclear membrane. Dense cytoplasm contains many ribosomes and mitochondria. Type II cells are large oval cells. The eccentric nucleus is deeply invaginated. Pale cytoplasm contains large amount of ribosomes, Golgi complexes, mitochondria, and dense bodies. Type III cells are pale, large, oval cells. They contain moderate amount of ribosomes and mitochondria, and some scattered stacks of r-ER. Type IV cells are small pale cells. Small oval nucleus is indented and shows chromatin rim. Only small amount of ribosomes and mitochondria can be found. In the nucleus fundus striati of the rat, there also found 4 main cell types. Type I cells are spherical or oval cells, comprising more than 90% of the neurons. The chromatin rim of the spherical nucleus is not so prominent as compared to the rim of type I cell in the nucleus accumbens septi. The cytoplasm contains moderate amount of mitochondria, ribosomes and some scattered r-ER. A few axo-somatic synapses were found. Type II cells are small round or polygonal cells. Golgi complexes are especially well-developed in this cell type. The cytoplasm also contains moderate amount of mitochondria, ribosomes, and dense bodies. Type III cells are small cells. The large nucleus shows prominent chromatin rim. The cytoplasm contains many ribosomes and mitochondria. Type IV cells are large, spheircal or oval cells. The nucleus is deeply indented. The plentiful cytoplasm contains large amount of ribosomes, mitochondria, Golgi complexes, neurotubules, but not r-ER. In the present study, it is clear that the nucleus accumbens septi and the nucleus fundus striati are independant cell groups, according to their cytoarchitectonics and the ultrastructural features of their cell types.

• Molecules and Cells
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• 제24권3호
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• pp.416-423
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• 2007

Alterations in the glycan chains of cell surface glycoconjugates are frequently involved biological processes such as cell-cell interaction, cell migration, differentiation and development. Cultured embryonic (E18) rat cortical neurons underwent apoptosis in response to camptothecin, and lectin histochemistry showed that binding to apoptotic neurons of FITC-conjugated Maackia amurensis agglutinin (MAA), which is specific for terminal ${\alpha}2,3$-sialic acid residues, increased progressively with increasing concentrations of camptothecin. Analysis of the total proteins of apoptotic neurons by SDS-PAGE, and lectin blotting using HRP-labeled MAA, revealed that the expression of terminal ${\alpha}2,3$-sialic acid residues on an unknown protein with an apparent molecular mass of 25.6 kDa also increased in apoptotic neurons. NP-HPLC analysis of the total cellular N-glycans of normal and apoptotic neurons demonstrated that the expression of structurally simpler biantennary types of N-glycans fell by 49% during apoptosis whereas the more branched triantennary types of N-glycans with terminal sialic acid residues increased by up to 59%. These results suggest that increased surface expression of ${\alpha}2,3$-sialic acid residues and hyperglycosylation of N-glycans is a common feature of cellular responses to changes in cell physiology such as tumorigenesis and apoptosis.