• The Korean Journal of Physiology and Pharmacology
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• v.3 no.4
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• pp.365-373
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• 1999

Somatostatin (SOM) is one of the major neuropeptides in dorsal root ganglion cells, but its role in spinal nociceptive process has not been well known. In present study we aimed to investigate the effect of SOM on the response of dorsal horn neurons to the various types of peripheral nociceptive stimuli in anesthetized cats. Using carbon-filament microelectrode, the single cell activities of wide dynamic range neurons were recorded from the lumbosacral enlargement after noxious mechanical (squeeze), thermal (radiant heat lamp) and cold (dry ice) stimulation to the receptive field. Sciatic nerve was stimulated electrically to evoke $A\;{\delta}-$ and C-nociceptive responses. SOM analogue, octreotide $(10\;{\mu}g/kg),$ was applied intravenously and the results were compared with those of morphine (2 mg/kg, MOR). Systemic SOM decreased the cellular responses to the noxious heat and the mechanical stimulation, but increased those to the cold stimulation. In the responses to the electric stimuli of sciatic nerve, $A\;{\delta}-nociceptive$ response was increased by SOM, while C-nociceptive response was decreased. On the other hand, MOR inhibited the dorsal horn cell responses to all the noxious stimuli. From the above results, it is concluded that SOM suppresses the transmission of nociceptive heat and mechanical stimuli, especially via C-fiber, while it facilitates those of nociceptive cold stimuli via $A\;{\delta}-fiber$.

• Journal of Korean Medicine Rehabilitation
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• v.18 no.4
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• pp.39-61
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• 2008

Objectives : The present study was performed to investigate whether acupuncture stimulation in the rats affected regeneration properties of the injured sciatic nerve. A differential effect of acupuncture stimulation on the one point near the spinal nerve root controlling sciatic nerve activity and the other point in the peripheral area subordinated by injured nerve was compared. Materials and Methods: Rat sciatic nerves were injured by crush, and the effects on axonal regeneration on injured sciatic nerves were evaluated by acupuncture stimulation at two different regions. In proximal acupuncture stimulation group, acupuncture stimulation was performed on Huatuo Jiaji(EX B2) points located from L5 to S1 vertebral levels to stimulate the nearest spinal nerve root that innervates sciatic nerves. In distal acupuncture stimulation group, acupuncture stimulation was performed on Zusanli(ST 36) and Weizhong(BL 40) points to stimulate at peripheral area dominated by injured sciatic nerves. Acupuncture stimulation was given every other days for 1 or 2 weeks. Sciatic nerve tissues collected from acupuncture stimulation experimental groups, injury control group, and intact animal group were used for protein analysis by Western blotting or Hoechst nuclear staining. To determine axonal regeneration, Dil fluorescence dye was injected into the sciatic nerve 0.5 cm distal to the injury site in individual animal groups and Dil-labeled cells by retrograde tracing were measured in the DRG at lumbar 5 or in the spinal cord. DRG sensory neurons prepared from individual animal groups were used to measure the extent of neurite outgrowth and for immunofluorescence staining with anti-GAP-43 antibody. Results : Animal groups given proximal or distal acupuncture stimulation showed upregulation of GAP-43 and Cdc2 protein levels in the sciatic nerve at 7 days after injury. Cdk2 protein levels were strongly induced by nerve injury, but did not show changes by acupuncture stimulation. Phospho-Erk1/2 protein levels were elevated by acupuncture stimulation above those present in the injury control animals. These increase in regeneration-associated protein levels appeared to be related with increase cell proliferation in the injured sciatic nerves. Hoechst 33258 staining of sciatic nerve tissue to visualize nuclei of individual cells showed increased Schwann cell number in the distal portion of the injured nerve 7 and 14 days after injury and further increases by acupuncture stimulation particularly at the proximal position. Measurement of axonal regeneration by retrograde tracing showed significantly increased Dil-labeled cells in proximal acupuncture stimulation group compared to distal acupuncture stimulation group and injury control group. Finally, an evaluation of axonal regeneration by retrograde tracing showed increased number of Dil labeled cells in the DRG at lumbar 5 or in the ventral horn of the spinal cord at lower thoracic level at 7 days after nerve injury. Conclusions : The present data show that the proximal acupuncture stimulation at Huatuo Jiaji(EX B2) points governing injured sciatic nerves was more effective for axonal regeneration than the distal acupuncture stimulation. Further studies on functional recovery or associated molecular mechanisms should be critical for developing animal models and clinical applications.

• Annals of Clinical Neurophysiology
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• v.13 no.1
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• pp.1-12
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• 2011

Transcranial magnetic stimulation (TMS) is a non-invasive tool used to study aspects of human brain physiology, including motor function and the pathophysiology of various brain disorders. A brief electric current passed through a magnetic coil produces a high-intensity magnetic field, which can excite or inhibit the cerebral cortex. Although various brain regions can be evaluated by TMS, most studies have focused on the motor cortex where motor evoked potentials (MEPs) are produced. Single-pulse and paired-pulse TMS can be used to measure the excitability of the motor cortex via various parameters, while repetitive TMS induces cortical plasticity via long-term potentiation or long-term depression-like mechanisms. Therefore, TMS is useful in the evaluation of physiological mechanisms of various neurological diseases, including movement disorders and epilepsy. In addition, it has diagnostic utility in spinal cord diseases, amyotrophic lateral sclerosis and demyelinating diseases. The therapeutic effects of repetitive TMS on stroke, Parkinson disease and focal hand dystonia are limited since the duration and clinical benefits seem to be temporary. New TMS techniques, which may improve clinical utility, are being developed to enhance clinical utilities in various neurological diseases.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.16 no.3
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• pp.2029-2037
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• 2015

The purpose of this study was to investigate the effect the interferential current (IFC) stimulation level according to autonomic nerve system (ANS) of healthy adults. IFC measured with adhesive 2-pole electrodes pad on T1~T4 spinal cord segment level that electrode stimulation of 20 min after. A total of 45 healthy adults participated in the study, who were randomly divided into three groups: 15 of sensory level stimulus group (100 bps, 10~12 mA), 15 of exercise level stimulus group (5 bps, 45~50 mA), 15 of noxious level stimulus group (100 bps, 80~90 mA). Measured items were sympathetic activity and parasympathetic activity. In order to identify the changes in measurement variables before electrode stimulation and after and 30 min stimulation. The comparison of sympathetic and parasympathetic activity in each group revealed that they was changes of after vs 30 min in after electrical stimulation time(p<.05).

• Korean Journal of Veterinary Research
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• v.40 no.3
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• pp.431-437
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• 2000

The aim of this study was to evaluate the involvement of CPP32 (caspase-3), one of the death-related enzymes, in the course of experimental autoimmune encephalomyelitis (EAE). EAE was induced in Lewis rats immunized with an emulsion of rat spinal cord homogenate with complete Freunds adjuvant supplemented with Mycobacterium tuberculosis (H37Ra, 5mg/ml). The expression of CPP32 in the spinal cords of rats with EAE was studied. In normal rat spinal cords, CPP32 is constitutively, but weakly, expressed in neurons and some neuroglial cells. In the EAE spinal cords, many inflammatory cells were positive for CPP 32, and the majority of CPP32(+) cells were identified as ED1(+) macrophages. During this stage of EAE, the number of CPP32(+) cells in brain cells, including neurons and astrocytes, increased, and these cells also had increased CPP32 immunoreactivity. CPP32 immunor eactivity was not always matched with apoptosis of inflammatory cells in EAE lesions. We speculate that CPP32, which is constitutlvely expressed in brain cells, increases in response to neuroimmunological stimulation in both brain neuronal cells and inflammatory cells. The functional role of CPP32 in neuroimmunological disorders is discussed.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.625-637
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• 1997

Calcium ions are implicated in a variety of physiological functions, including enzyme activity, membrane excitability, neurotransmitter release, and synaptic transmission, etc. Calcium antagonists have been known to be effective for the treatment of exertional angina and essential hypertension. Selective and nonselective voltage-dependent calcium channel blockers also have inhibitory action on the acute and tonic pain behaviors resulting from thermal stimulation, subcutaneous formalin injection and nerve injury. This study was undertaken to investigate the effects of iontophoretically applied $Ca^{++}$ and its antagonists on the responses of WDR (wide dynamic range) cells to sensory inputs. The responses of WDR cells to graded electrical stimulation of the afferent nerve and also to thermal stimulation of the receptive field were recorded before and after iontophoretical application of $Ca^{++}$, EGTA, $Mn^{++}$, verapamil, ${\omega}-conotoxin$ GVIA, ${\omega}-conotoxin$ MVIIC and ${\omega}-agatoxin$ IVA. Also studied were the effects of a few calcium antagonists on the C-fiber responses of WDR cells sensitized by subcutaneous injection of mustard oil (10%). Calcium ions and calcium channel antagonists ($Mn^{++}$, verapamil, ${\omega}-conotoxin$ GVIA & ${\omega}-agatoxin$ IVA) current-dependently suppressed the C-fiber responses of WDR cells without any significant effects on the A-fiber responses. But ${\omega}-conotoxin$ MVIIC did not have any inhibitory actions on the responses of WDR cell to A-fiber, C-fiber and thermal stimulation. Iontophoretically applied EGTA augmented the WDR cell responses to C-fiber and thermal stimulations while spinal application of EGTA for about $20{\sim}30\;min$ strongly inhibited the C-fiber responses. The augmenting and the inhibitory actions of EGTA were blocked by calcium ions. The WDR cell responses to thermal stimulation of the receptive field were reduced by iontophoretical application of $Ca^{++}$, verapamil, ${\omega}-agatoxin$ IVA, and ${\omega}-conotoxin$ GVIA but not by ${\omega}-conotoxin$ MVIIC. The responses of WDR cells to C-fiber stimulation were augmented after subcutaneous injection of mustard oil (10%, 0.15 ml) into the receptive field and these sensitized C-fiber responses were strongly suppressed by iontophoretically applied $Ca^{++}$, verapamil, ${\omega}-conotoxin$ GVIA and ${\omega}-agatoxin$ IVA. These experimental findings suggest that in the rat spinal cord, L-, N-, and P-type, but not Q-type, voltage-sensitive calcium channels are implicated in the calcium antagonist-induced inhibition of the normal and the sensitized responses of WDR cells to C-fiber and thermal stimulation, and that the suppressive effect of calcium and augmenting action of EGTA on WDR cell responses are due to changes in excitability of the cell.

• The Korean Journal of Physiology
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• v.26 no.1
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• pp.75-88
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• 1992

It is well established that neurons in ventrolateral medulla play a key role in determining the vasomotor tone. The purpose of present study is to identify sympathetic related, medullospinal tract neurons in ventrolateral medulla and to show that these mediate somato-sympathetic reflex. Medullospinal tract cells were identified by antidromic stimulation to intermediolateral nucleus (IML) of the second thoracic ($T_2$) spinal cord in anesthetized cats. Peripheral nerves were stimulated for orthodromic activation of these cells and peripheral receptive fields were determined. Post R wave histogram of unit and spike triggered averaging of sympathetic nerve discharge (SND) were used to define sympathetic related cell. A total of 113 neurons was recorded in ventrolateral medulla that had the axonal projections to $T_2$ spinal cord. Thirty four of these medullospinal cells showed spontaneous discharges and the others not. Between these two groups, rostro-caudal coordinate of the distribution from obex [$4.7{\pm}0.2\;$ (mean S.E.) mm, 4.1 0.1 mm], depth from dorsal surface ($5.5{\pm}0.2mm,\;4.9{\pm}0.1mm$ and conduction velocity ($9.9{\pm}1.7m/sec,\;16.7{\pm}1.9\;m/sec$) were significantly different (p<0.05). In spontaneously discharging group, characteristics of rostral and caudal groups were significantly different and we demonstrated that cells in rostral group mediate somatosympathetic reflex. From these results, we conclude that a certain portion of spontaneously discharging medullospinal tract cells in rostral ventrolateral medulla comprise the efferent outputs of somatosympathetic reflex to sympathetic preganglion neurons.

• The Korean Journal of Physiology
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• v.21 no.1
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• pp.67-77
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• 1987

Effect of intravenously injected clonidine on the flexion reflex was studied in 15 decerebrated and spinalized cats. The flexion reflex was elicited by electrical stimulation of the tibial nerve or the common peroneal nerve and it was recorded as single unit activity from filaments of the L6 or L7 ventral roots. In order to obtain the late flexion reflex discharges, $A{\delta}$ and C afferent fibers were stimulated with single or train electrical pulses respectively. The flexion reflex, especially the late component, was markedly inhibited after intravenous administration of clonidine. The clonidine-induced inhibition of the flexion reflex was compared before and after treatment of the animals respectively with yohimbine and naloxone. The inhibitory effect on the flexion reflex of clonidine was not altered by naloxone, a ${\mu}-opioid$ receptor blocker, whereas it was completely blocked by yohimbine, an ${\alpha}_2-adrenergic$ antagonist. These results indicate that clonidine inhibits the flexion reflex through excitation of ${\alpha}_2-adrenoceptors$ even at the spinal cord level.

• Journal of Acupuncture Research
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• v.17 no.2
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• pp.153-168
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• 2000

Introduction : In spite of the use of Bee Venom aqua-acupuncture in the clinics, the scientific evaluation on effects is not enough. Bee Venom aqua-acupuncture is used according to the stimulation of acupuncture point and the chemical effects of Bee Venom. The aims of this study is to investigate the analgegic effects of the Bee Venom aqua-acupuncture, through the change of writhing reflex and the change of c-fos in secondary neurons in the spinal cord. Materials and Methods : Pain animal model was used acetic acid method. The changes of writhing reflex of the mice which were derived pain by injecting acetic acid into the abdomen, after stimulating Bee Venom aqua-acupuncture on Chungwan(CV12) were measured. We used Fos immunohistochemical technique to study the neuronal activity in the spinal cord. Results : 1. Expression of c-fos in superficial dorsal horn(SDH), nucleus proprius(NP) and neck of dorsal hom(N) on 6~9th thoracic spine decreased significantly at $2.5{\times}10-4$g/kg Bee Venom aqua-acupuncture, compared with saline-acetic acid group. 2. The numeral change of Fos-LI neurons on the NP, N, and ventral gray(V) on 6-9th thoracic spine, SDH on 9-11th thoracic spine, and SDH and V on 11~13th thoracic spine decreased significantly at Chungwan(CV12) Bee Venom aqua-acupuncture, compared with saline-acetic acid group. 3. The correlation between the numbers of writhing refleax and Fos-LI neurons in T6-13 segment was statistically statistically significant at Chungwan(CV12) Bee Venom aqua-acupuncture. Conclusion : This study shows that the Bee Venom aqua-acupuncture on Chungwan(CV12) decreases the numbers of Fos-LI neurons. As the analgegic effects of Bee Venom aqua-acupuncture is recognized. Bee Venom aqua-acupuncture treatment is expected for pain modulation. In order to use it in many ways, more researches are needed for the dose and stability of Bee Venom aqua-acupuncture.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.29-37
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• 1994

Inhibition of the nociceptive Tail Flick Reflex (TFR) was observed with electrical stimulation of the locus coeruleus/subcoeruleus (LC/SC) in the male Sprague - Dawley rats under light anesthesia, and the involved neurotransmitter (s) were characterized. Electrical stimulation of LC/SC induced the analgesia with the stimulation threshold (intensity of the current, given for 100 usec and in 100 Hz frequency, which caused the TF latency longer than 6.5 sec) around 55 uA. Intrathecal administrations of ${\alpha}_2$ antagonist, yohimbine (30 ug) or opioid antagonist, naloxone (20 ug) increased the stimulation threshold by 147% and 123% respectively (from 55 uA to 135 uA,9 and from 54 uA to 123 uA;P0.01, n=5, each). The basal TF latency without stimulation (3.1 sec) was reduced by the antagonists (to 2.5 sec by yohimbine, p<0.05, n=5; to 2.6 sec by naloxone, p<0.1, n=5), vehicle only did not show any effect. Noradrenaline(NA) in the spinal cord superfusates measured with HPLC was increased by the LC/SC stimulation, from 4.18 ng/ml before to 7.74 ng/ml after stimulation (P<0.05, n=10). The result suggest that analgesia induced by LC/SC stimulation is mediated, at least in part, by the noradrenergic system in which ${\alpha}_2$ receptor is involved, as well as the opioid system.