• Molecules and Cells
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• 제37권3호
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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.

• 대한수의학회지
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• 제60권4호
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• pp.203-207
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• 2020

This study presents neuronal migration pattern of dopamine (DA) neurons generated in separate regions occupying the ventral mesencephalic territory. A single pulse 5-bromodeoxyuridine (BrdU) was administered at embryonic day (E)10-E15. Distribution of tyrosine hydroxylase (TH) positive cells was determined at E13-postnatal day 0 (P0) by immunohistochemistry. BrdU positive cells labeled at E10 were spread out uniformly in the mesencephalon from E13 to E15, migrating through dorsal and ventral routes at E17 and P0. TH expression labeled at E10 was observed at E13 in the ventromedial region and clearly formed in the ventral tegmental area (VTA) at E15. At E17, TH expression in the substantia nigra (SN) was observed in the ventrolateral region, spreading more outward of the mesencephalon at P0. Generation of TH-positive cells labeled at E13 was also observed in VTA and SN of the mesencephalon at E17 and P0. The expression of these cells labeled after E15 was markedly decreased. These results demonstrated that an almost complete primary structure of DA neuron was formed at the early embryonic stage in the ventral mesencephalon, showing the most active neuronal migration was occurred at E13-E17.

• 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.

• Journal of Chest Surgery
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• 제25권8호
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• pp.806-811
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• 1992

The primary neuroendocrine carcinomas[NEC] of the lung are relatively rare. There are classified histologically into the following groups. 1] bronchial carcinoid, 2] well differentiated neuroendocrine carcinoma[WDNC], 3] intermediate cell neuroendocrine carci-noma[ICNC], 4] small cell neuroendocrie carcinoma[SCNC]. The NE cells can be found throughout the mucosa of the bronchial tree by the electron microscopy. By the immunocytochemistry, Neuron-specific enolase[NSE], serotonin, born-csin, and calcitonin are found in normal solitary NE cells and neuroepithelial bodies. The immunohistochemistry has the advantage that it can be applied on routine pathology specimens. The NSE was localized in all of the NE granule bearing tumors but also present in 57 per cent of the non NE carcinomas. Together the combination of chromogranin A, bombesin and NSE should provide an exellent signature for tumor cells expressing NE features, such as carcinoids and other NE carcinomas. We have experienced two cases of primary pulmonary NEC in 59 and 29 years old men. The former was admitted due to exertional dyspnea and left chest pain, the latter, newly developed mass on chest X-ray. They were treated by Lt pneumonectomy with LN dissection and RLL resection with LN dissection The postoperative diagnoses were could be confirmed by NSE study as NEC which were SCNEC and INEC in subgroups. The postoperative courses were uneventful.

• 한국한의학연구원논문집
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• 제4권1호통권4호
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• pp.99-114
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• 1998

The effect of herbal medicine on glutamate mediated neurotoxicity was studied in mouse neurons in primary culture. Immature cerebral cortex neurons (ED14) were maintained for up to 2 weeks in vitro, and we investigated the expression pattern of neuron differentiation and cytotoxicity of cell death, including LDH activity. Neuronal maturation initiated on day 7 and the susceptibility to glutamate-induced cell death was highly sensitive on Day 11 (Fig. 1). Thus, the exposure of the neurons to glutamate caused a dose$(0.1mM{\sim}1mM)$ and time$(4h{\sim}24h)$-dependent neurotoxicity(Fig. 4). Glutamate-induced neurodegeneration was prevented by Shipchondaebotang(SD), Yollyounggobondan(YG), Yugmijihwangwon(YJ) and the death of neurons exposed to glutamate was blocked by the NMDA receptor antagonist MK-801 (Fig. 5).

• 대한본초학회지
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• 제23권3호
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• pp.53-60
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• 2008

Objectives : Oxidative stress has a critical role in neurodegenerative diseases. In this study, we investigated the antioxidant and neuroprotective effects of the ethanolic extract of Banryong-hwan (BRHE) in SH-SY5Y cells and primary rat mesencephalic dopaminergic neurons. Methods : To assess the antioxidant effects, we carried out 1,1-diphenyl-2-picrylhydrazyl(DPPH) free radical scavenging assay, 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid)(ABTS) radical cation decolorization assay, and determination of total polyphenolic content. We evaluated the effect of BRHE treatment on neuroprotection against 6-hydroxydopamine(6-OHDA) toxicity using thiazolyl blue tetrazolium bromide(MTT) assay, nitric oxide(NO) assay, reactive oxygen species(ROS) assay in SH-SY5Y cells and tyrosine hydroxylase(TH) immunocytochemistry in primary rat mesencephalic dopaminergic neurons. Results : BRHE showed IC50 values of 328.10 ${\mu}g/mL$ and 43.12 ${\mu}g/mL$ in DPPH assay and in ABTS assay, respectively. Total polyphenolic content was 180.76 ${\mu}g/mL$. In SH-SY5Y cells, BRHE significantly attenuated the toxicity induced by 6-OHDA at the concentrations of 25-100 ${\mu}g/mL$ pre- and post- treatment in MTT assay. While 6-OHDA increased the NO and ROS contents, BRHE decreased them in a dose dependent manner. Moreover, in primary dopaminergic neuron culture, BRHE significantly protect-ed the dopaminergic cell loss against 6-OHDA toxicity up to 136% at the concentration of 75 ${\mu}g/mL$. Conclusions : These results demonstrate that BRHE has neuroprotective effect against 6-OHDA induced neurotoxicity through decreasing NO and ROS generation.

• Annals of Clinical Neurophysiology
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• 제4권2호
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• pp.98-107
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• 2002

Multifocal motor neuropathy (MMN) is a chronic immune-mediated peripheral myelinopathy. The major clinical features include slowly progressive, painless, and asymmetric weakness, usually of distal limb muscle. Early in the course of the disease, weakness is not necessarily associated with muscle atrophy, owing to the initial primary involvement of peripheral myelin. Chronic progressive weakness is often associated with some degree of concurrent axonal loss and subsequent muscle atrophy. Sensory symptoms are usually mild or absent, and involvement of cranial and respiratory muscles is rare. The findings of multifocal motor conduction block, abnormal temporal dispersion, and focal conduction slowing at segments not at risk for common entrapment or compression injury, associated with normal sensory conduction studies along the same segments, are the hallmark electrophysiologic features of MMN. The slow progression and absence of upper motor neuron signs are the major clinical points that separate MMN from amyotrophic lateral sclerosis. The role of GM1 antibodies, found in high titers in 22~84% of MMN patients, remains uncertain. The contention that MMN is an autoimmune disorder is largely based on the often dramatic improvement in symptoms following the administration of intravenuos immunoglobulin or cyclophosphamide.

• 대한후두음성언어의학회지
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• 제23권2호
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• pp.104-110
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• 2012

The usages of botulinum toxin were most commonly for the treatment of spasmodic dysphonia in the otolaryngology field. It has been not only widely used in otolaryngology-Head Neck surgery but also plastic surgery, ophthalmology, rehabilitation medicine, and orthopedics. Now botulinum toxin is used such as blepharospasm (excessive blinking), strabismus, cosmetic, muscle spasms, upper motor neuron syndrome, severe primary axillary hyperhidrosis (excessive sweating), cervical dystonia (spasmodic torticollis), chronic migraine, bruxism, and achalasia. The indication of this drug still gradually expanding with the times. In this articles, the author will demontrate how to use the botulinum toxin for treating cricopharyngeal spasm, arytenoid dislocation, sialocele, Frey syndrome, contact granuloma, bilateral vocal fold paralysis, and mutaional falsetto instead of conventional surgical treatment.

• 대한치과보존학회:학술대회논문집
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• 대한치과보존학회 2001년도 추계학술대회(제116회) 및 13회 Workshop 제3회 한ㆍ일 치과보존학회 공동학술대회 초록집
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• pp.581.1-581
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• 2001

Trigeminal nerve functions movement and sensation on orofacial region. Therefore, it is very important in dental clinic. Neurons with their cell bodies in trigeminal ganglion of trigeminal nerve root are primary sensory neurons and playa role of tactile sense, pressure, vibration and pain of orofacial area. Transmission of these senses depends on ion channels, we know that trigeminal ganglion neuron exists many kind of ion channels. Methods of definition on ion channel are several, but in this study we use immunostaining for detection of ion channels.(omitted)

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.123-123
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• 2003

Primary cultures of rat fetus brain exhibit phenotypes of neuron, oligodendrocyte, and astrocyte from "neurospheres". To understand the role of mitogen-activated protein kinase (MAPK) cascade and gap junctional intercellular communication (GJIC) in the differentiation of neurosphere-derived astrocyte, we investigated the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the cultured astrocyte morphology.(omitted)