• Journal of the Korean Society of Physical Medicine
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• v.5 no.4
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• pp.527-534
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• 2010

Purpose : The application of tape to modulation of pain and muscular excitability has become common clinical practice among musculoskeletal physical therapy. However, the techniques of the tape application has been relied on empirical evidence in preference to the neurophysiological evidence. Thus, the mechanism of taping has to be elucidated further. The aim of this study was to determine whether elastic and non-elastic taping across a muscle does indeed change ${\alpha}$-motor neuron excitability. Methods : The study was performed on 10 neurologically healthy adults. Two different types of tape were applied to skin overlying gastrocnemius. The elastic tape stretched up to 120% of its original length but non-elastic tape didn't stretched up of its original length. The tape applied across the direction on thickest part of the gastrocnemius. The ${\alpha}$-motor neuron excitability of the gastrocnemius was assessed using the gastrocnemius H-reflex. The amplitude of the M-wave and H-reflex were measured across three conditions: before tape application, with tape and with the tape removed. Results : No significant changes of the excitability of the ${\alpha}$-motor neuron were obtained across three condition, either in the elastic and non-elastic tape. Conclusion : From the results, I could come to the conclusion that further clinical work will be required.

• The Journal of Korean Physical Therapy
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• v.19 no.1
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• pp.11-22
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• 2007

Purpose: The purpose of this study were to analysis the effect on change of spinal neuron excitability during gait training of hemiplegia patients by the functional electrical stimulation. Methods: Thirty six hemiplegia patients participated in this study. Stimulation conditions of FES were pulse rate 35pps, pulse width $250{\mu}s$, and on-time 0.3 second, treatment hour was 30 min. and treatment period was once a day for five days a week through six weeks. For functional evaluations before and after treatment, Modified Ashworth Scale (MAS), active range of motion (AROM), Hmax threshold, H/Mmax ratio were measured and the following conclusions were obtained. Results: Functional evaluation showed significant changes in experimental group as MAS(p<0.01), AROM(p<0.001), compared to control group. In spinal neuron excitability evaluation, change of Hmax threshold was significantly reduced in both non weight bearing (p<0.001) and bearing condition (p<0.05), H/Mmax ratio was significantly reduced in non weight bearing (p<0.05) and bearing condition (p<0.05). Conclusion: In conclusion, application of FES to hemiplegia patients in recovery stage during gait training improved mitigation of muscular spasticity, balance adjustment and moving ability and it was interpreted that it was caused by mitigation of muscular spasticity by the spinal neuron excitability.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.2
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• pp.432-437
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• 2007

Reactive oxygen species (ROS) are toxic agents that may be involved in various neurodegenerative diseases. Recent studies indicate that ROS are also involved in persistent pain through a spinal mechanism. In the present study, whole cell patch clamp recordings were carried out on substantia gelatinosa (SG) neurons in spinal cord slice of neonatal rats to investigate the effects of ROS on neuronal excitability and excitatory synaptic transmission. In current clamp condition, tert-buthyl hydroperoxide (t-BuOOH), an ROS donor, induced a electrical hyperexcitability during t-BuOOH wash-out followed by a brief inhibition of excitability in SG neurons. Application of t-BuOOH depolarized membrane potential of SG neurons and increased the neuronal firing frequencies evoked by depolarizing current pulses. Phenyl-N-tert-buthylnitrone (PBN), an ROS scavenger, antagonized t-BuOOH induced hyperexcitability. IN voltage clamp conditions, t-BuOOH increased the frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs). In order to determine the site of action of t-BuOOH, miniature excitatory postsynaptic currents (mEPSCs) were recorded. t-BuOOH increased the frequency and amplitude of mEPSCs, indicating that it may modulate the excitability of the SG neurons via pre- and postsynaptic actions. These data suggest that ROS generated by peripheral nerve injury can induce central sensitization in spinal cord.

• BMB Reports
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• v.51 no.1
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• pp.3-4
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• 2018

Parkinson's disease (PD) is a debilitating disorder resulting from loss of dopamine neurons. In dopamine deficient state, the basal ganglia increases inhibitory synaptic outputs to the thalamus. This increased inhibition by the basal ganglia output is known to reduce firing rate of thalamic neurons that relay motor signals to the motor cortex. This 'rate model' suggests that the reduced excitability of thalamic neurons is the key for inducing motor abnormalities in PD patients. We reveal that in response to inhibition, thalamic neurons generate rebound firing at the end of inhibition. This rebound firing increases motor cortical activity and induces muscular responses that triggers Parkinsonian motor dysfunction. Genetic and optogenetic intervention of the rebound firing prevent motor dysfunction in a mouse model of PD. Our results suggest that inhibitory synaptic mechanism mediates motor dysfunction by generating rebound excitability in the thalamocortical pathway.

• The Journal of the Korea Contents Association
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• v.9 no.9
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• pp.278-286
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• 2009

The aims of this study were to determined whether excitability of the $\alpha$-motor neuron is modulated by stretching and this changes were associated with flexibility of the muscle. In this study, $\alpha$-motor neuron excitability was measured by using the Hmax/Mmax ratio of the gastrocnemius H-reflex, and muscle flexibility was measured with the range of motion of the ankle dorsiflexion. The gastrocnemii of 10 healthy volunteers were stretched for 4 minutes(2 minutes stretching, 1 minute rest, and 2 minutes stretching) in each session by manual force. The Hmax/Mmax ratio of the H-reflex, as well as the range of motion of the ankle dosiflexion was measured through four different conditions: before stretching, as soon as after $1^{st}$ stretching, as soon as after $2^{nd}$ stretching and at 48 hours after $2^{nd}$ stretching. Excitability of the $\alpha$-motor neuron was decreased significantly after $1^{st}$ and $2^{nd}$ stretching(p<0.05). Furthermore, the range of the dorsiflexion was increased significantly after $1^{st}$ and $2^{nd}$ stretching(p<0.05). However, the excitability of the $\alpha$-motor neuron and range of the dorsiflexion at 48 hours after $2^{nd}$ stretching were not different from those of before stretching. These results suggest that reduced $\alpha$-motor neuron excitability of the gastrocnemius and increased flexibility of the ankle dorsiflexion would be followed by activation of the type III mechanoreceptor which around the ankle joint and the Golgi tendon organ in the gastrocnemius.

• International Journal of Oral Biology
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• v.38 no.1
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• pp.5-12
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• 2013

Recent studies indicate that reactive oxygen species (ROS) can act as modulators of neuronal activity, and are critically involved in persistent pain primarily through spinal mechanisms. In this study, we investigated the effects of NaOCl, a ROS donor, on neuronal excitability and the intracellular calcium concentration ($[Ca^{2+}]_i$) in spinal substantia gelatinosa (SG) neurons. In current clamp conditions, the application of NaOCl caused a membrane depolarization, which was inhibited by pretreatment with phenyl-N-tert-buthylnitrone (PBN), a ROS scavenger. The NaOCl-induced depolarization was not blocked however by pretreatment with dithiothreitol, a sulfhydryl-reducing agent. Confocal scanning laser microscopy was used to confirm whether NaOCl increases the intracellular ROS level. ROS-induced fluorescence intensity was found to be increased during perfusion of NaOCl after the loading of 2',7'-dichlorofluorescin diacetate ($H_2DCF$-DA). NaOCl-induced depolarization was not blocked by pretreatment with external $Ca^{2+}$ free solution or by the addition of nifedifine. However, when slices were pretreated with the $Ca^{2+}$ ATPase inhibitor thapsigargin, NaOCl failed to induce membrane depolarization. In a calcium imaging technique using the $Ca^{2+}$-sensitive fluorescence dye fura-2, the $[Ca^{2+}]_i$ was found to be increased by NaOCl. These results indicate that NaOCl activates the excitability of SG neurons via the modulation of the intracellular calcium concentration, and suggest that ROS induces nociception through a central sensitization.

• International Journal of Oral Biology
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• v.39 no.4
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• pp.229-236
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• 2014

Reactive oxygen species (ROS) and nitrogen species (RNS) are implicated in cellular signaling processes and as a cause of oxidative stress. Recent studies indicate that ROS and RNS are important signaling molecules involved in nociceptive transmission. Xanthine oxidase (XO) system is a well-known system for superoxide anions ($O{_2}^{{\cdot}_-}$) generation, and sodium nitroprusside (SNP) is a representative nitric oxide (NO) donor. Patch clamp recording in spinal slices was used to investigate the role of $O{_2}^{{\cdot}_-}$ and NO on substantia gelatinosa (SG) neuronal excitability. Application of xanthine and xanthine oxidase (X/XO) compound induced membrane depolarization. Low concentration SNP ($10{\mu}M$) induced depolarization of the membrane, whereas high concentration SNP (1 mM) evoked membrane hyperpolarization. These responses were significantly decreased by pretreatment with phenyl N-tert-butylnitrone (PBN; nonspecific ROS and RNS scavenger). Addition of thapsigargin to an external calcium free solution for blocking synaptic transmission, led to significantly decreased X/XO-induced responses. Additionally, X/XO and SNP-induced responses were unchanged in the presence of intracellular applied PBN, indicative of the involvement of presynaptic action. Inclusion of GDP-${\beta}$-S or suramin (G protein inhibitors) in the patch pipette decreased SNP-induced responses, whereas it failed to decrease X/XO-induced responses. Pretreatment with n-ethylmaleimide (NEM; thiol-alkylating agent) decreased the effects of SNP, suggesting that these responses were mediated by direct oxidation of channel protein, whereas X/XO-induced responses were unchanged. These data suggested that ROS and RNS play distinct roles in the regulation of the membrane excitability of SG neurons related to the pain transmission.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.2
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• pp.135-141
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• 2014

The downregulation of A-type $K^+$ channels ($I_A$ channels) accompanying enhanced somatic excitability can mediate epileptogenic conditions in mammalian central nervous system. As $I_A$ channels are dominantly targeted by dendritic and postsynaptic processings during synaptic plasticity, it is presumable that they may act as cellular linkers between synaptic responses and somatic processings under various excitable conditions. In the present study, we electrophysiologically tested if the downregulation of somatic $I_A$ channels was sensitive to synaptic activities in young hippocampal neurons. In primarily cultured hippocampal neurons (DIV 6~9), the peak of $I_A$ recorded by a whole-cell patch was significantly reduced by high KCl or exogenous glutamate treatment to enhance synaptic activities. However, the pretreatment of MK801 to block synaptic NMDA receptors abolished the glutamate-induced reduction of the $I_A$ peak, indicating the necessity of synaptic activation for the reduction of somatic $I_A$. This was again confirmed by glycine treatment, showing a significant reduction of the somatic $I_A$ peak. Additionally, the gating property of $I_A$ channels was also sensitive to the activation of synaptic NMDA receptors, showing the hyperpolarizing shift in inactivation kinetics. These results suggest that synaptic LTP possibly potentiates somatic excitability via downregulating $I_A$ channels in expression and gating kinetics. The consequential changes of somatic excitability following the activity-dependent modulation of synaptic responses may be a series of processings for neuronal functions to determine outputs in memory mechanisms or pathogenic conditions.

• Journal of the Korean Society of Physical Medicine
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• v.10 no.1
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• pp.63-69
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• 2015

PURPOSE: Low-intensity exercise with transient restriction of blood flow to muscle could be an alternative rehabilitation method which avoids the problems associated with conventional high-intensity exercise. However, the mechanism of low-intensity exercise with transient restriction of blood flow is not clearly known. Thus, the purpose of this study was to investigate the mechanism of improvement of muscular function after low-intensity exercise with transient restriction of blood flow using H-reflex analysis. METHODS: Twenty one healthy young adults with no medical history of neurological or musculoskeletal disorder voluntarily participated in this study. The ${\alpha}$-motor neuron excitability of the triceps surae was assessed using the H-reflex. The amplitude of the M-wave and H-reflex were measured across three conditions: rest, after low-intensity exercise without restriction of blood flow and after low-intensity exercise with restriction of blood flow. The subjects performed low-intensity ankle plantar flexion exercise at their own pace for one minute without or with transient restriction of blood flow achieved by a sphygmomanometer cuff on popliteal fossa at a pressure of 120mm of mercury(120 mmHg). RESULTS: No significant changes of the excitability of the ${\alpha}$-motor neuron were obtained across three different conditions. CONCLUSION: This study found that low-intensity exercise with transient restriction of blood flow did not influence to ${\alpha}$-motor neuron excitability of the triceps surae. From the results, I could come to the conclusion that further study will be required.

• Journal of Magnetics
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• v.19 no.2
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• pp.192-196
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• 2014

The aim of the present study was to examine the effects of high and low frequency repetitive transcranial magnetic stimulation on motor cortical excitability and the balance function in subacute stroke patients. Twenty-four subjects were randomly assigned to either the high frequency (HF) rTMS group, or the low frequency (LF) rTMS group, with 12 subjects each. All subjects received routine physical therapy. In addition, both groups performed a total of 20 sessions of rTMS for 20 minutes, once a day, 5 times per week, for a 4-week period. In the HF rTMS group, 10 Hz rTMS was applied daily to the hotspot of the lesional hemisphere; and in the LF rTMS group, 1 Hz rTMS was applied daily to the hotspot of the nonlesional hemisphere. Motor cortex excitability was determined by motor evoked potentials, and the balance function was evaluated by use of the Balance Index (BI) and the Berg Balance Scale (BBS), before and after the intervention. The change rate in the value of each variable differed significantly between the two groups (p<0.05). Furthermore, significant differences were observed between all post-test variables of the two groups (p<0.05). In the HF rTMS, significant differences were found in all the pre- and post-test variables (p<0.05). On the other hand, in the LF rTMS, significant difference was observed only between the pre- and post-test results of BI and BBS (p<0.05). The findings demonstrate that HF rTMS can be more helpful in improving the motor cortical excitability and balance function of patients with subacute stroke treatment than LF rTMS, and that it may be used as a practical adjunct to routine rehabilitation.