• The Transactions of The Korean Institute of Electrical Engineers
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• v.59 no.1
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• pp.217-219
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• 2010

Spasticity is a motor disorder characterized by a velocity dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex. The aim of this study is to develop a portable system for quantifying the grade of spasticity which could calculate the biomechanical as well as neurophysiologic parameters, and for determining the relationship between the Tonic Stretch Reflex Threshold (TSRT) and Modified Ashworth Scale (MAS). Eleven patients with stroke participated in the study (6 males and 5 females, the average age of $64.5\pm16.0$ years). As a results, the mean and standard deviation values of the TSRT were $129.8\pm4.2$, $123.4\pm5.2$ and $119.1\pm2.6$ in the MAS 1, MAS 1+ and MAS 2 groups, respectively. Also, there was a negative correlation between the TSRT and MAS (rho=-0.72, p<0.05). This demonstrated that the TSRT could be made clinically available for the more objective and reliable evaluation of the spasticity, instead of using the conventional clinical scales and an isokinetic dynamometer.

• BMB Reports
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• v.45 no.11
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• pp.635-640
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• 2012

To understand the effects of HCN as potential mediators in the pathogenesis of epilepsy that evoke long-term impaired excitability; the present study was designed to elucidate whether the alterations of HCN expression induced by status epilepticus (SE) is responsible for epileptogenesis. Although HCN1 immunoreactivity was observed in the hippocampus, its immunoreactivities were enhanced at 12 hrs following SE. Although, HCN1 immunoreactivities were reduced in all the hippocampi at 2 weeks, a re-increase in the expression at 2-3 months following SE was observed. In contrast to HCN1, HCN 4 expressions were un-changed, although HCN2 immunoreactive neurons exhibited some changes following SE. Taken together, our findings suggest that altered expressions of HCN1 following SE may be mainly involved in the imbalances of neurotransmissions to hippocampal circuits; thus, it is proposed that HCN1 may play an important role in the epileptogenic period as a compensatory response.

• The Korean Journal of Pain
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• v.26 no.3
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• pp.265-269
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• 2013

Background: Transforaminal epidural steroid injections are known to reduce inflammation by inhibiting synthesis of various proinflammatory mediators and have been used increasingly. The anti-inflammatory properties of opioids are not as fully understood but apparently involve antagonism sensory neuron excitability and pro-inflammatory neuropeptide release. To date, no studies have addressed the efficacy of transforaminal epidural morphine in patients with radicular pain, and none have directly compared morphine with a tramadol for this indication. The aim of this study was to compare morphine and tramadol analgesia when administered via epidural injection to patients with lumbar radicular pain. Methods: A total of 59 patients were randomly allocated to 1 of 2 treatment groups and followed for 3 months after procedure. Each patient was subjected to C-arm guided transforaminal epidural injection (TFEI) of an affected nerve root. As assigned, patients received either morphine sulfate (2.5 mg/2.5 ml) or tramadol (25 mg/0.5 ml) in combination with 0.2% ropivacaine (1 ml). Using numeric rating scale was subsequently rates at 2 weeks and 3 months following injection for comparison with baseline. Results: Both groups had significantly lower mean pain scores at 2 weeks and at 3 months after treatment, but outcomes did not differ significantly between groups. Conclusions: TFEI of an opioid plus local anesthetic proved effective in treating radicular pain. Although morphine surpassed tramadol in pain relief scores, the difference was not statistically significant.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.4
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• pp.193-197
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• 2002

In spite of abundant anatomical evidences for the fiber connection between vestibular nuclei and inferior olivary (IO) complex, the transmission of vestibular information through the vestibulo- olivo-cerebellar climbing fiber pathway has not been physiologically established. The aims of the present study were to investigate whether there are IO neurons specifically responding to horizontal rotation and also in which subregions of IO complex these vestibularly-activated neurons are located. The extracellular recording was made in 68 IO neurons and responses of 46 vestibularly-activated cells were analyzed. Most of the vestibularly-activated IO neurons responded to signals of vertical rotation (roll), while a small number (13/46) of recorded cells were activated by horizontal canal signal (yaw). Regardless of yaw-sensitive or roll-sensitive, vestibular IO neurons were excited, when the animal was rotated to the side contralateral to the recording side. The gain and excitation phase were very similar to otolithic or vertical-canal responses. Histologic identification of recording sites showed that most of vestibular IO neurons were located in ${\beta}$ subnucleus. Electrical stimulation of a HSC evoked an inhibitory effect on the excitability of the ipsilateral IO neurons. These results suggest that IO neurons mainly in the ${\beta}$ subnucleus receive vestibular signals from semicircular canals and otolithic organs, encode them, and transmit vestibular information to the cerebellum.

• The Korean Journal of Physiology
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• v.4 no.2
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• pp.19-24
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• 1970

Since the discovery of the muscle spindle by Hassall (1831), an intensive studies of its anatomical and physiological characteristics had been undertaken. Recent morphological studies of Boyd (1962) demonstrated that the muscle spindles have two different intrafusal muscle fibers, nuclear bag and nuclear chain fiber, and these intrafusal fibers are under independent motor innervation by ${\gamma}_1$ and ${\gamma}_2$ motor neurone. Neurophysiological studies of Hunt and Kuffler (1951) showed regulatory effect of ${\gamma}$ motor neurone upon the excitability of the spindle afferents. Harvey and Mathews (1961) observed the dynamic and static characteristics of the two different spindle afferents, the primary and secondary ending. Furthermore, Mathews (1962) postulated the functional existance of two kind of ${\gamma}$ motor neurones, namely, the dynamic and static fusimotor fiber. Recent report of Kim and Partridge(1969) pointed out that the descending vestibular signals had increased the slope of the length-tension relationship in stretch reflex; Kim (1967) demonstrated that the descending vestibular impulses act upon the stretch reflex loop through the ${\gamma}$ motor pathway. These experimental evidences from the morphological and neurophysiological studies on the muscle spindles support the concept that the stretch reflex action of the skeletal muscle operates as a negative feedback control system. The author had discussed the way by which the f system participates in the control of stretch relfex feed back system. that was taken for a prototype of posture and movement.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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• pp.63-70
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• 2002

Cholinergic modulation of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) by the activation of muscarine receptors was investigated in mechanically dissociated rat nucleus basalis of the Meynert neurons using the conventional whole-cell patch recording configuration. Muscarine $(10{\mu}M)$ reversibly and concentration-dependently decreased mIPSC frequency without affecting the current amplitude distribution. Muscarine action on GABAergic mIPSCs was completely blocked by $1{\mu}M$ methoctramine, a selective $M_2$ receptor antagonist, but not by $1{\mu}M$ pirenzepine, a selective $M_1$ receptor antagonist. NEM $(10{\mu}M),$ a G-protein uncoupler, attenuated the inhibitory action of muscarine on GABAergic mIPSC frequency. Muscarine still could decrease GABAergic mIPSC frequency even in the $Ca^{2+}-free$ external solution. However, the inhibitory action of muscarine on GABAergic mIPSCs was completely occluded in the presence of forskolin. The results suggest that muscarine acts presynaptically and reduces the probability of spontaneous GABA release, and that such muscarine-induced inhibitory action seems to be mediated by G-protein-coupled $M_2$ receptors, via the reduction of cAMP production. Accordingly, $M_2$ receptor-mediated disinhibition of nBM neurons might play one of important roles in the regulation of cholinergic outputs from nBM neurons as well as the excitability of nBM neurons themselves.

• Journal of Magnetics
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• v.19 no.4
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• pp.353-356
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• 2014

The aim of the present study was to examine whether mental practice (MP) in conjunction with repetitive transcranial magnetic stimulation (rTMS) can improve the upper limb function of sub-acute stroke patients. This study was conducted with 32 subjects who were diagnosed with hemiparesis by stroke. The experimental group consisted of 16 members upon each of whom was performed MP in conjunction with rTMS, whreas the control group consisted of 16 members upon each of whom was performed MP and sham rTMS. Both groups received traditional physical therapy for 30 minutes a day, 5 days a week, for 6 weeks; additionally, they received mental practice for 15 minutes a day. The experimental group was instructed to perform rTMS, and the control group was instructed to apply sham rTMS for 15 minutes. A motor cortex excitability analysis was performed by motor evoked potentials (MEPs), and upper limb function was evaluated by Fugl-Meyer Assessment (FMA) and the Box and Block test (BBT). Results showed that the amplitude, latency, FMA, and BBT of the experimental group and the latency, FMA, and BBT of the control group were significantly improved after the experiment (p<0.05). Significant differences were found between the groups in amplitude and latency after the experiment (p<0.05). The results showed that MP in conjunction with rTMS is more effective in improving upper limb function than MP alone.

• Biomolecules & Therapeutics
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• v.18 no.1
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• pp.24-31
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• 2010

Taurine, 2-aminoethanesulfonic acid, is an abundant free amino acid present in brain cells and exerts many important biological functions such as anti-convulsant, modulation of neuronal excitability, regulation of learning and memory, anti-aggressiveness and anti-alcoholic effects. In the present study, we investigated to explore whether taurine has any protective actions against oxidative stress-induced damages in neuronal cells. ERK I/II regulates signaling pathways involved in nitric oxide (NO) and reactive oxygen species (ROS) production and plays a role in the regulation of cell growth, and apoptosis. We have found that taurine significantly inhibited AMPA induced cortical depolarization in the Grease Gap assays using rat cortical slices. Taurine also inhibited AMPA-induced neuronal cell damage in MTT assays in the differentiated SH-SY5Y cells. When the neuronal cells were treated with $H_2O_2$, levels of NO were increased; however, taurine pretreatment decreased the NO production induced by $H_2O_2$ to approximately normal levels. Interestingly, taurine treatment stimulated ERK I/II activity in the presence of AMPA or $H_2O_2$, suggesting the potential role of ERK I/II in the neuroprotection of taurine. Taken together, taurine has significant neuroprotective actions against AMPA or $H_2O_2$ induced damages in neuronal cells, possibly via activation of ERK I/II.

• BMB Reports
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• v.46 no.2
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• pp.80-85
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• 2013

We investigated the temporal alterations of adrenocorticotropic hormone (ACTH) immunoreactivity in the hippocampus after seizure onset. Expression of ACTH was observed within inter-neurons in the pre-seizure group of seizure sensitive gerbils, whereas its immunoreactivities were rarely detected in seizure resistant gerbil. Three hr after the seizure, ACTH immunoreac-tivity was significantly increased in interneurons within all hippocampal regions. On the basis of their localization and morphology through immunofluorescence staining, these cells were identified as $GABA_A$ ${\alpha}1$-containing interneurons. At the 12 hr postictal period, ACTH expression in these regions was down-regulated, in a similar manner to the pre-seizure group of gerbils. These findings support the increase in ACTH synthesis that contributes to a reduction of corticotrophin-releasing factor via the negative feedback system which in turn provides an opportunity to enhance the excitability of GABAergic interneurons. Therefore, ACTH may play an important role in the reduction of excitotoxicity in all hippocampal regions.

• International Journal of Oral Biology
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• v.40 no.4
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• pp.211-216
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• 2015

Nitric Oxide (NO) is an important signaling molecule in the nociceptive process. Our previous study suggested that high concentrations of sodium nitroprusside (SNP), a NO donor, induce a membrane hyperpolarization and outward current through large conductances calcium-activated potassium ($BK_{ca}$) channels in substantia gelatinosa (SG) neurons. In this study, patch clamp recording in spinal slices was used to investigate the sources of $Ca^{2+}$ that induces $Ca^{2+}$-activated potassium currents. Application of SNP induced a membrane hyperpolarization, which was significantly inhibited by hemoglobin and 2-(4-carboxyphenyl) -4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), NO scavengers. SNP-induced hyperpolarization was decreased in the presence of charybdotoxin, a selective $BK_{Ca}$ channel blocker. In addition, SNP-induced response was significantly blocked by pretreatment of thapsigargin which can remove $Ca^{2+}$ in endoplasmic reticulum, and decreased by pretreatment of dentrolene, a ryanodine receptors (RyR) blocker. These data suggested that NO induces a membrane hyperpolarization through $BK_{ca}$ channels, which are activated by intracellular $Ca^{2+}$ increase via activation of RyR of $Ca^{2+}$ stores.