• The Korean Journal of Pain
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• 제22권1호
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• pp.1-15
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• 2009

Neuropathic pain is often refractory to intervention because of the complex etiology and an incomplete understanding of the mechanisms behind this type of pain. Glial cells, specifically microglia and astrocytes, are powerful modulators of pain and new targets of drug development for neuropathic pain. Glial activation could be the driving force behind chronic pain, maintaining the noxious signal transmission even after the original injury has healed. Glia express chemokine, purinergic, toll-like, glutaminergic and other receptors that enable them to respond to neural signals, and they can modulate neuronal synaptic function and neuronal excitability. Nerve injury upregulates multiple receptors in spinal microglia and astrocytes. Microglia influence neuronal communication by producing inflammatory products at the synapse, as do astrocytes because they completely encapsulate synapses and are in close contact with neuronal somas through gap junctions. Glia are the main source of inflammatory mediators in the central nervous system. New therapeutic strategies for neuropathic pain are emerging such as targeting the glial cells, novel pharmacologic approaches and gene therapy. Drugs targeting microglia and astrocytes, cytokine production, and neural structures including dorsal root ganglion are now under study, as is gene therapy. Isoform-specific inhibition will minimize the side effects produced by blocking all glia with a general inhibitor. Enhancing the anti-inflammatory cytokines could prove more beneficial than administering proinflammatory cytokine antagonists that block glial activation systemically. Research on therapeutic gene transfer to the central nervous system is underway, although obstacles prevent immediate clinical application.

• The Journal of Korean Physical Therapy
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• 제23권6호
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• pp.49-53
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• 2011

Purpose: The purpose of this study is to investigate whether dual-hemisphere transcranial direct current stimulation (tDCS) could induce more cortical activity, compared to single-hemisphere, using functional MRI (fMRI). Methods: One right-handed healthy subject was recruited. Three phases of dual-hemisphere tDCS (i.e. anodal tDCS over the left-dominant primary sensoriomotor cortex (SM1) and cathodal tDCS over the right-non dominant SM(1) were consecutively delivered on to a subject, during fMRI scanning. The voxel count and the intensity index in the averaged cortical map were analyzed among the three tDCS phases. Results: Our result showed that cortical activation was observed on all the three phases of the dual-hemisphere tDCS. Voxel count and intensity index were as following; 912 and 4.07 in the first phase, 1102 and 3.90 in the second phase, 1031 and 3.80 in the third phase. Conclusion: This study demonstrated that application of the dual-hemisphere tDCS could induce cortical activity and maintain to recruit cortical neurons. Our findings suggested that application of dual-hemisphere tDCS could produce efficiency of the ongoing tDCS effect to facilitate cortical excitability.

• Biomolecules & Therapeutics
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• 제14권1호
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• pp.19-24
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• 2006

Atrial chambers serve as mechanosensory systems during the haemodynamic or mechanical disturbances, which initiates arrhythmia. Atrial myocytes, lacking t-tubules, have two functionally separate sarcoplasmic reticulums (SRs): those at the periphery close to the surface membrane, and those at the cell interior (center) not associated with the membrane. To explore possible role of fluid pressure (FP) in the regulation of atrial local $Ca^{2+}$ signaling we investigated the effect of FP on subcellular $Ca^{2+}$ signals in isolated rat atrial myocytes using confocal microscopy. FP was applied to whole area of single myocyte with pressurized automatic micro-jet (200-400 $mmH_2O$) positioned close to the cell. Application of FP enhanced spontaneous occurrences of peripheral and central $Ca^{2+}$ sparks with larger effects on the peripheral release sites. Unitary properties of single sparks were not altered by FP. Exposure to higher FP often triggered longitudinal $Ca^{2+}$ wave. These results suggest that fluid pressure may directly alter excitability of atrial myocytes by activating $Ca^{2+}$-dependent ionic conductance in the peripheral membrane and by enhancing spontaneous activation of central myofilaments.

• 대한물리치료과학회지
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• 제10권1호
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• pp.65-73
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• 2003

The purpose of this study was to determine whether neuromuscular electrical stimulation(NMES), applied over the antagonist or the agonist, would alter the H reflex. Attention was focused on the roles of stimulus location. We used normal eight subjects without neuromuscular disease which were divided into 3 groups; the subjects were diveded into group of antagonist, agonist, antagonist-agonist. All groups were meted of eight subjects. Neuromuscular electrical stimulation was administered for 15 minutes. All subjects were subjected to three tests, including a pre-test, post-test and post-20 minute test. The data were analyzed by repeated measures ANOVA and paired t-test. The results were as follows; 1. H latencies were significantly increased in agonist and antagonist-agonist group (p<.01). 2. H/M intervals were significantly increased in agonist and antagonist-agonist group (p<.01). 3. H amplitudes were significantly increased in agonist (p<.001) and antagonist-agonist group (p<.01). 4. H/M ratios were significantly decreased in agonist and antagonist-agonist group (p<.01). In agonist group. H-reflex amplitudes and H/M ratios were more significantly decreased than antagonist group. Future studies will need to determine what influence NMES may have on the excitability of spinal motor neurons in people having UMN syndrome.

• 대한치과마취과학회지
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• 제10권2호
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• pp.203-208
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• 2010

Tremors are trembling movements and are seen in association with alcoholic intoxication, certain drugs, thyrotoxicosis, multiple sclerosis, hysteria, and nervous tension. Dental fears, such as, pain, drill, unknown, dependency, helplessness, mutilation and oral change, induce the neuroendocrine response (release of epinephrine and norepinephrine, etc). The clinical manifestations of epinephrine or other vasopressor overdose include : anxiety, tenseness, restlessness, throbbing headache, tremor, perspiration, weakness, dizziness, pallor, palpitation and respiratory difficulty. Signs of local anesthetic overdose appear clinically whenever the anesthetic level in the blood rises to an appropriate level in an individual. The clinical signs of moderate overdose levels include : talkativeness, apprehension, excitability, slurred speech, tremor and muscular twitching. This is a case report about the severe tremor care after the endodontic treatment under right mandibular block anesthesia in a 56-years old female patient.

• Korean Journal of Acupuncture
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• 제23권2호
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• pp.105-111
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• 2006

Objectives: We investigated the effect of electroacupuncture on epileptic rat model and its underlying mechanisms on suppression of the epilepsy. Methods: It was used pentylenetetrazol $(35{\sim}40\;mg/kg.\;i.p)$ induced epileptic rat model and square wave electrical stimulations (5 mA, 5, 40 or 80 Hz frequency) was applied to acupoints on 'Dazhui' and 'Taichong' for 30min. Results: Electroacupuncture suppressed spikes and slow waves of EEG due to the epileptic condition. Out of electroacupuncture, a high frequency of 80Hz had a better effect for suppress epileptic EEG wave. Conclusions: Electroacupuncture can markedly reduce the excitability of cerebral cortex and strengthen the inhibitory process, checking epilepsy wave. Some intrathalamic nuclei have a promoting or inhibiting effect on epileptic EEG wave. This experimental study we are proposed to Electro-acupuncture can suppression epileptic rat model and it's scientific mechanisms.

• 대한수의학회지
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• 제31권1호
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• pp.33-40
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• 1991

For the observations of both the membrane properties and the excitability on the unfertilized eggs of female mice, changes of the membrane resistance and the membrane potential by hyerpolarizing current stimulation were recorded. As current-voltage relation was linear over the entire range (-180mV~+60mV), membrane resistance($R_m$) was calculated from the amplitude of electrotonic potential to a given stimulus current. Also the presence of anode-break excitation was confirmed. The results were as follows; 1. There was a linear relation between the membrane resistance and resting membrane potential, the expected input resistance was 61. 4M$\Omega$(resting membrane potential was $-18.9{\pm}8.7mV$, mean${\pm}$SD, n=30). 2. Transient depolarization with overshoot was generated just after hyperpolarizing current stimulus and showed the dependency of stimulus duration. 3. Transient depolarization lasted over 30ms, amplitude of these depolarization was increased by high $Ca^{{+}{+}}$(20mM) and inhibited by $Ca^{{+}{+}}$-antagonist, $Mn^{{+}{+}}$. 4. From the above results, it was suggested that the unfertilized mouse egg showed the characteristics of the excitable cell.

• The Korean Journal of Physiology
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• 제20권2호
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• pp.199-208
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• 1986

The effects of $Mg^{++}$ upon the spontaneous contraction activated by 1 IU/l oxytocin were studied in the isolated rat uterine muscle. Longitudinal muscle strips u·ere prepared from the rat uteri at the estrous stage. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% $O_2$ and kept at $35^{\circ}C$. The results obtained were as follows: 1) In the uterine strips contracting spontaneously, as $Mg^{++}$ concentration increased in the Tyrode solution the amplitude of peak tension decreased in all the experimental solutions containing the various concentrations of $Ca^{++}\;(0.5{\sim}4 mM)$. And the amplitude of peak tension increased in inverse proportion to the $[Mg^{++}]/[Ca^{++}]\; ratio$. It is suggested that the tension-lowering effect of $Mg^{++}$ would be developed through decreasing intracellular ionized free calcium ion concentration by uncertain mechanism. 2) The frequency of the uterine contraction activated by oxytocin increased as the $[Mg^{++}]/[Ca^{++}]\;ratio$ ratio increased up to 1/2, but the frequency decreased above this ratio. It is speculated that $Mg^{++}$ would influence the excitability control action of $Ca^{++}$.

• International Journal of Oral Biology
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• 제40권2호
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• pp.103-109
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• 2015

Growing evidence suggests that mitochondrial reactive oxygen species (ROS) are involved in various pain states. This study was performed to investigate whether ROS-induced changes in neuronal excitability in trigeminal subnucleus caudalis are related to ROS generation in mitochondria. Confocal scanning laser microscopy was used to measure ROS-induced fluorescence intensity in live rat trigeminal caudalis slices. The ROS level increased during the perfusion of malate, a mitochondrial substrate, after loading of 2',7'-dichlorofluorescin diacetate ($H_2DCF-DA$), an indicator of the intracellular ROS; the ROS level recovered to the control condition after washout. When pre-treated with phenyl N-tert-butylnitrone (PBN) and 4-hydroxy-2,2,6,6-tetramethylpiperidene-1-oxyl (TEMPOL), malate-induced increase of ROS level was suppressed. To identify the direct relation between elevated ROS levels and mitochondria, we applied the malate after double-loading of $H_2DCF-DA$ and chloromethyl-X-rosamine (CMXRos; MitoTracker Red), which is a mitochondria-specific fluorescent probe. As a result, increase of both intracellular ROS and mitochondrial ROS were observed simultaneously. This study demonstrated that elevated ROS in trigeminal subnucleus caudalis neuron can be induced through mitochondrial-ROS pathway, primarily by the leakage of ROS from the mitochondrial electron transport chain.

• Journal of Ginseng Research
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• 제21권1호
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• pp.1-12
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• 1997

Ginseng, the root of Panax ginseng C.A. Meyer, is well-known oriental herbal medicine. The number of paper reporting the effects on its physiological, pharmacological, and behavioral effects has been increased every year, since ginsenosides isolated from ginseng are known to be biologically active components. This brief review summarizes some of new findings from recently published papers on ginsenosides or ginseng saponins. Therefore, this paper includes the various effects of ginsenosides on neuronal cell growths, on behavior of experimental animals, on enzyme activities, on the release and uptake of neurotransmitters, on neuronal cell excitability, on the motility of intestine, on antitumor activity, on cardiovascular system and metabolism. In spite of various effects of ginsenosides on various cells or organs, it is still to date impossible for one to clearly explain the exact mechanism on the action of ginsenosides. However, in this article I will discuss several papers providing possible explanations on the physiological and pharmacological actions including signal transudation pathway of ginsenosides. The elucidation of the exact mechanism of ginsenosides on cellular or molecular level will not only give us a chance to explain why people have used ginseng as an elixir of life for several thousands of year but also give us a crucial chance to apply ginseng to modern medicine.