• PNF and Movement
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• 제4권1호
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• pp.51-62
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• 2006

Purpose : The purposes of this study were to test the effect of proprioceptive and vestibular sensory input on expression of BDNF after traumatic brain injury in the rat. Subject : The control group was sacrificed at 24 hours after traumatic brain injury. The experimental group I was housed in standard cage for 7 days. The experimental group II was housed in standard cage after intervention to proprioceptive and vestibular sensory(balance training) for 7 days. Method : Traumatic brain injury was induced by weight drop model and after operation they were housed in individual standard cages for 24 hours. After 7th day, rats were sacrificed and cryostat coronal sections were processed individual1y in goat polyclonal anti-BDNF antibody. The morphologic characteristics and the BDNF expression were investigated in injured hemisphere section and contralateral brain section from immunohistochemistry using light microscope. Result : The results of this experiment were as follows: 1. In control group, cell bodies in lateral nucleus of cerebellum, superior vestibular nucleus, purkinje cell layer of cerebellum and pontine nucleus changed morphologically. 2. The expression of BDNF in contralateral hemisphere of group II were revealed. 3. On 7th day after operation, immunohistochemical response of BDNF in lateral nucleus, superior vestibular nucleus, purkinje cell layer and pontine nucleus appeared in group II. Conclusion : The present results revealed that intervention to proprioceptive and vestibular sensory input is enhance expression of BDNF and it is useful in neuronal reorganization improvement after traumatic brain injury.

• 대한기계학회:학술대회논문집
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• 대한기계학회 2007년도 춘계학술대회A
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• pp.405-408
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• 2007

Vestibular hair cells, the sensory receptors of vestibular organs, selectively amplify miniscule stimuli to attain high sensitivity. Such selective amplification results in compressive nonlinear sensitivity, which plays an important role in expanding dynamic range while ensuring robustness of the system. In this study, negative stiffness mechanism, a mechanism responsible for the selective amplification by vestibular hair cells, is applied to a simple mechanical system consisting of an array of inverted pendulums. The structure and working principle of the system have been inspired by gating spring hypothesis proposing that opening and closing of transduction channels contributes to the global stiffness of vestibular hair bundle. Parameter study was carried out to analyze the effect of each parameter on the compressive nonlinearity of suggested model.

• 전자공학회논문지
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• 제51권9호
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• pp.190-199
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• 2014

본 논문에서는 섬모 번들 특성 모델과 통합 전정 유모세포 모델을 제안한다. 기존 전정기관 모델에 관한 연구는 외력이 없는 상태에서 전정 유모세포의 섬모 번들이 가지는 특성이나 시냅스에서 발생하는 활동전위만을 대상으로 진행되었으며 섬모번들의 고유 특성을 고려한 전정신경의 활동전위에 대한 연구는 이루어지지 않았다. 제안된 통합 전정 유모세포 모델은 외력을 반영하였고 서로 다른 규칙성을 가진 유모세포에 대해 각각의 섬모번들의 반강성 특성을 고려하였고 이를 기존의 외력없는 모델과 비교하였다. 그 결과 외부 자극의 변화에 따른 주파수 변화가 큰 불규칙적 신경섬유와 중간규칙적 신경섬유에서는 반강성 구간의 감소를 보였으나 그렇지 않은 규칙적 신경섬유에서는 기존의 반강성 특성과 유사한 특성을 보여주었다. 또한 제안된 전정 유모세포 모델을 통해 11개의 주파수 대역에서의 모델링 데이터와 기존의 동물 실험 데이터가 거의 일치함을 보여 주었다. 제안된 섬모 번들 특성 모델이 적절히 모델링되었음이 확인된다.

• 대한의용생체공학회:의공학회지
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• 제34권4호
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• pp.218-225
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• 2013

In this paper hair bundle feature model and integration method for hair cell models were proposed. The proposed hair bundle feature model was based on spring-damper-mass model. Input of integrated vestibular hair cell model was frequency and output was interspike interval of hair cell that was reflected the feature of hair bundles. Irregular afferents that had a great gain variation showed reduction of negative stiffness section. Regular afferents that had a small gain variation, however, showed same feature with base negative stiffness feature. As a result, integrated vestibular hair cell model showed almost the same modeling data with experimental data in the modeled eleven frequency bands. It is verified that the proposed model is a good model for hair bundle feature modeling.

• The Korean Journal of Physiology and Pharmacology
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• 제7권2호
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• pp.73-77
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• 2003

The effects of nitric oxide on the vestibular function recovery following unilateral labyrinthectomy (UL) were studied. Sprague-Dawley male rats, treated with nitric oxide liberating agent sodium nitroprusside (SNP) and NOS inhibitor $N^G$-nitro-L-arginine methyl ester (L-NAME), were subjected to destruction of the unilateral vestibular apparatus, and then spontaneous nystagmus was observed in the rat. To explore the effects of nitric oxide on the neuronal excitability, whole cell patch clamp technique was applied on isolated medial vestibular nuclear neurons. The frequency of spontaneous nystagmus in SNP treated rats was lesser than that of spontaneous nystagmus in control animals. In contrast, pre-UL treatment with L-NAME resulted in a significant increase in spontaneous nystagmus frequency. In addition, SNP increased the frequency of spontaneous action potential in isolated medial vestibular nuclear neurons. Potassium currents of the vestibular nuclear neurons were inhibited by SNP. After blockade of calcium dependent potassium currents by high EGTA (11 mM) in a pipette solution, SNP did not inhibit outward potassium currents. 1H-[1,2,4] oxadiazolo [4,3-a] quinozalin-1-one (ODQ), a specific inhibitor of soluble guanylyl cyclase, inhibited the effects of SNP on the spontaneous firing and the potassium current. These results suggest that nitric oxide after unilateral labyrinthectomy would help to facilitate vestibular compensation by inhibiting calcium-dependent potassium currents through increasing intracellular cGMP, and consequently would increase excitability in ipsilateral vestibular nuclear neurons.

• Molecular & Cellular Toxicology
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• 제4권3호
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• pp.177-182
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• 2008

Caveolin proteins are mediators of cell death or the survival of injured cells, and they are inhibitors of various signaling pathways. The expression of caveolin-, which is involved in the protein kinase A (PKA) signaling pathway, was examined in the differentiated mouse vestibular cell line UB/UE-1 after gentamicin ototoxicity. Caveolae in the vestibular hair cell of healthy guinea pigs were observed through an electron microscope. UB/UE-1 cells were cultured at 95% $CO_2$ with 5% $O_2$ at $33^{\circ}C$ for 48 hours and at 95% $CO_2$ with 5% $O_2$ at $39^{\circ}C$ for 24 hours for differentiation. Cells were treated with 1 mM gentamicin, 0.02 mM H89 (PKA inhibitor), and then incubated for 24 hours. Caveolin-1 expression was examined by western blotting and PKA activity by a $PepTag^{(R)}$ assay. Caveolae were observed in the vestibular hair cells of healthy guinea pigs by electron microscopy. Caveolin-1 was expressed spontaneously in differentiated UB/UE-1 cells and increased after gentamicin treatment. PKA was also over-activated by gentamicin treatment. Both gentamicin-induced caveolin-1 expression and PKA over-activation were inhibited by H89. These results indicate that gentamicin-induced caveolin-1 expression is mediated by the PKA signaling pathway. We conclude that caveolae/ caveolin activity, induced via a PKA signaling pathway, may be one of the mechanisms of gentamicin-induced ototoxicity.

• The Korean Journal of Physiology and Pharmacology
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• 제10권3호
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• pp.131-135
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• 2006

Coeruleo-vestibular pathway which connects locus coeruleus and vestibular nuclei is noradrenergic. This study was designed to elucidate the effects of phenylephrine on the spontaneous activity of acutely isolated medial vestibular nuclear neurons of rat by whole-cell patch-clamp technique. Sprague-Dawley rats, aged 14 to 16 days, were used. After enzymatic digestion, dissociated medial vestibular neurons were transferred to a recording chamber mounted on an inverted microscope, and spontaneous action potentials were recorded by standard patch-clamp techniques. In current-clamp mode, the frequency of spontaneous action potential of medial vestibular nuclear neurons was decreased by phenylephrine (n=15). Phenylephrine increased the amplitude of afterhyperpolarization without changes in the resting membrane potential and spike width. In voltage-clamp mode, the whole potassium currents of the medial vestibular nuclear neurons were increased by phenylephrine (n=12). These experimental results suggest that ${\alpha}-receptor$ mediates the inhibitory effects on the neuronal activity of the medial vestibular nuclear neuron.

• Journal of Korean Neurosurgical Society
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• 제56권1호
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• pp.51-54
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• 2014

Gastric cancer is one of the most common causes of cancer-related death in Asian countries, including Korea. We experienced a case of leptomeningeal carcinomatosis (LC) from gastric cancer that was originally misdiagnosed as vestibular schwannoma based on the similar radiological characteristics. To our knowledge, LC from gastric cancer is very rare. In conclusion, our experience with this case suggests that clinicians should consider the possibility of delayed leptomeningeal metastasis when treating patients with gastric cancer.

• International Journal of Oral Biology
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• 제34권4호
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• pp.215-222
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• 2009

Medial vestibular nucleus (MVN) neurons are involved in the reflex control of the head and eyes, and in the recovery of vestibular function after the formation of peripheral vestibular lesions. In our present study, whole cell patch clamp recordings were carried out on MVN neurons in brainstem slices from neonatal rats to investigate the actions of a group I metabotropic glutamate receptor (mGluR) agonist upon synaptic transmission and ionic currents. Application of the mGluR I agonist (S)-3,5- dihydroxyphenylglycine (DHPG) increased the frequency of miniature inhibitory postsynaptic currents (mIPSCs) but had no effect upon amplitude distributions. To then identify which of mGluR subtypes is responsible for the actions of DHPG in the MVN, we employed two novel subtype selective antagonists. (S)-(+)-$\alpha$-amino-a-methylbenzeneacetic acid (LY367385) is a potent competitive antagonist that is selective for mGluR1, whereas 2-methyl-6-(phenylethynyl)-pyridine (MPEP) is a potent noncompetitive antagonist of mGluR5. Both LY367385 and MPEP antagonized the DHPG-induced increase of mIPSCs, with the former being more potent. DHPG was also found to induce an inward current, which can be enhanced under depolarized conditions. This DHPG-induced current was reduced by both LY367385 and MPEP. The DHPG-induced inward current was also suppressed by the PLC blocker U-73122, the $IP_3$ receptor antagonist 2-APB, and following the depletion of the intracellular $Ca^{2+}$ pool by thapsigargin. These data suggest that the DHPG-induced inward current may be mainly regulated by the intracellular $Ca^{2+}$ store via the PLC-$IP_3$ pathway. In conclusion, mGluR I, via pre- and postsynaptic actions, may modulate the excitability of the MVN neurons.

• PNF and Movement
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• 제5권1호
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• pp.9-17
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• 2007

Purpose : The purpose of this study was to test the effect of balance training for proprioceptive and vestibular sensory stimulation and therapeutic environment on expression of BDNF after traumatic brain injury in the rat. Subject : Twelve Sprague-Dawley rats were randomly assigned into group I and group II. After traumatic brain injury, group I was housed in standard cage for 7 days. Group II was housed in therapeutic cage after balance training for 7 days. Method : Traumatic brain injury was induced by weight drop model and after operation they were housed in individual standard cages for 24 hours. After 7th day, the rats were sacrificed and cryostat coronal sections were processed individually in goat polyclonal anti-BDNF antibody. The morphologic characteristics and the BDNF expression were investigated in injured hemisphere section from immunohistochemistry using light microscope. Result : Immunohistochemical response of BDNF in lateral nucleus, purkinje cell layer, superior vestibular nucleus and pontine nucleus appeared very higher in group II than in group I Conclusion : The present result revealed that simultaneously application of balance training for proprioceptive and vestibular sensory stimulation input and therapeutic environment in traumatic brain injured rats is enhance expression of BDNF and it is facilitates neural plasticity.