• 동의생리병리학회지
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• 제17권2호
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• pp.457-460
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• 2003

It has been suggested that oxidative stress of reactive oxygen species(ROS) may play an important role in the pathogenesis of neurological disorder. The aim of this study was to elucidate the oxidative stress of glucose oxidase(GO) in the cultured mouse spinal motor neurons and the preventing effect of Benincasae Semen(BS) on ROS-induced neurotoxicity. Cytotoxic effect of GO and protective effect of BS were performed by MTT assay. 30mU/ml GO decreased cell viability in dose-and time-dependent mannner, and BS diminished GO-induced neurotoxicity in these cultures. From above the results, ROS such as GO has toxic effect, and herb extract of BS is very effective against GO-induced neurotoxicity in cultured spinal motor neurons of neonatal mouse.

• The Korean Journal of Physiology
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• 제30권1호
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• pp.117-124
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• 1996

This study evaluated the hypothesis that motoneuron collaterals modulate the excitability of ventral spinocerebellar tract neurons. In acute cats, 128 ventral cerebellar tract cells were studied extracellularly to determine the effects of ventral root stimuli. The majority of the cells responded to ventral root stimulation with either short or long latency increases in spike discharge. In many cells with sufficient spontaneous activity ventral root stimulation also evoked a long lasting reduction in activity. In preparations with the dorsal root ganglion removed VSCT neurons had similar response properties. In some cells contralateral ventral root stimulation also evoked excitatory responses. These findings indicate the VSCT can provide the cerebellum with information regarding activity in the final output neurons of the motor system, the alpha motoneurons.

• 한방재활의학과학회지
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• 제23권1호
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• pp.1-13
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• 2013

Objectives : The pathophysiology of acute spinal cord injury(SCI) may be divided into primary and secondary mechanisms of injury. The secondary mechanism involves free radical formation, excitotoxicity, inflammation and apoptotic cell death, and sets in minutes after injury and lasts for weeks or months. During this phase the spinal tissue damages are aggravated. Therefore, secondary mechanisms of injury serve as a target for the development of neuroprotective drug against SCI. The present study investigated the effect of tetramethylpyrazine(TMP), an active ingredient purified from the rhizome of Ligusticum wallichii(川芎, chuanxiong), on neuronal apoptosis in spinal cord compression injury in rats. Methods : SCI was subjected to rats by a static compression method(35 g weight, 5 mins) and TMP was treated 3 times(30 mg/kg, i.p.) during 48 hours after the SCI. Results : TMP ameliorated the tissue damage in peri-lesion of SCI and reduced TUNEL-labeled cells both in gray matter and in white matter significantly. TMP also attenuated Bax-expressed motor neurons in the ventral horn and preserved Bcl-2-expressed motor neurons. Conclusions : These results indicate that TMP plays a protective role in apoptotic cell death of neurons and oligodendrocytes in spinal cord injury. Moreover, it is suggested that TMP and TMP-containing chuanxiong may potentially delay or protect the secondary spinal injury.

• Journal of Korean Neurosurgical Society
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• 제42권6호
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• pp.462-469
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• 2007

Objective : This study characterized the neurons in the lumbosacral cord that express phospho ERK (pERK) after distension or irritation of the bladder, and their relation to the vanilloid receptor 1 (VR1) positive primary afferents. Methods : Mechanical distension and chemical irritation of the bladder were induced by intravesical injection of the saline and mustard oil, respectively. Spinal neurons expressing pERK and the primary afferent fibers were characterized using multiple immunofluorescence for neurokinin 1 (NK1), neuronal nitric oxide synthetase (nNOS) and VR1. Results : Neurons in lamina I, medial dorsal horn (MDH), dorsal gray commissure (DGC) and sacral parasympathetic nucleus (SPN) were immunoreactive for pERK after either mechanical or chemical stimulation. The majority of pERK positive cells were positive for NK1 in lamina I and SPN, but not in the DGC. Most of pERK positive cells are not stained for nNOS except in a small population of the cells in the SPN and DGC. Contacts between perikarya and dendrites of pERK-positive cells and terminals of primary afferents expressing VR1 were identified in lamina I. lateral collateral path (LCP) and SPN. Conclusion : In this study, the lumbosacral neurons activated by mechanical and chemical stimulation of the urinary bladder were identified with expression of the pERK, and also provided the evidence that VR1-positive primary afferents may mediate the activation of these neurons.

• The Korean Journal of Pain
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• 제9권1호
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• pp.26-38
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• 1996

In a normal state, sympathetic efferent activity does not elicit discharges of sensory neurons, whereas it becomes associated with and excites sensory neurons in a pathophysiological state such as injury to a peripheral nerve. Although this sympathetic-sensory interaction is reportedly adrenergic, involved subtypes of adrenoreceptors are not yet clearly revealed. The purpose of this study was to determine which adrenorceptor subtypes were involved in sympathetic-sensory interaction that was developed in rats with an experimental peripheral neuropathy. Using rats that received a tight ligation of one or two of L4-L6 spinal nerves 10~15 days previously, a recording was made from afferent fibers in microfilaments teased from the dorsal root that was in continuity with the ligated spinal nerve. Electrical stimulation of sympathetic preganglionic fibers in T13 or L1 ventral root (50 Hz, 2-5 mA. 0.5 ms pulse duration, 10 sec) was made to see if the activity of recorded afferents was modulated. About half of afferents showing spontaneous discharges responded to sympathetic stimulation, and had the conduction velocities in the A-fiber range. Most of the sympathetically induced afferent responses were excitation. This sympathetically induced excitation occurred in the dorsal root ganglion (DRG), and was blocked by yohimbine (${\alpha}_2$ blocker), neither by propranolol ($\beta$ blocker) not by prazosine (${\alpha}_1$ blocker). The results suggest that after spinal nerve ligation, sympathetic efferents interact with sensory neurons having A-fiber axons in DRG where adrenaline released from sympathetic nerve endings excites the activity of sensory neurons by acting on 2-adrenoreceptors. This 2-adrenoreceptor mediated excitation of sensory neurons may account for sympathetic involvement in neuropathic pain.

• The Korean Journal of Physiology
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• 제27권2호
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• pp.185-197
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• 1993

The rostral ventrolateral medulla (RVLM) includes vasopressor neurons, which transmit activation signals to the intermediolateral nucleus (IML) of the spinal cord, where the preganglionic sympathetic nucleus is located, to raise arterial blood pressure (BP). However, controversy exists as to the possible depressor area in the RVLM and the pathway involved. The present study persued evidence far the location of depressor neurons and the pathway by simultaneously observing changes in BP and the firing rate (FR) of cardiovascular neurons (CVNs) in the RVLM during the somatosympathetic reflex (SSR) elicited by peripheral nerve stimulation, since CVNs are known to contribute to the generation of the sympathetic nerve discharge. In 42 cats, anaesthetized with $\alpha-chloralose$, single unit recording was performed, using carbon filament electrodes inserted into the RVLM, enabling estimation of the post R wave unit histogram (PR-UNlT) and the spike triggered average of sympathetic nerve discharge (STA-SND), allowing identification of CVNs. Antidromic stimulation of spinal $T_2$ segment was followed to determine whether the identified CVN projects axonal endings to the spinal cord (reticulospinal neuron). The sciatic nerve was electrically stimulated at $A\delta-intensity$ (1 mA, 0.1 ms), 1 Hz and C-intensity (10 mA, 0.5 ms), 20 Hz to elicit the depressor, and pressor responses of the SSR, respectively. Simultaneous measurement of CVN firing rate was made. Experimental results are summarized as follows. 1) 20 out of 98 CVNs had axonal projections to the spinal cord and 17 out of 98 CVNs showed FR changes during SSR. 2) Response patterns of FR and BP during SSR were classified into 8 types. 3) These 8 different response patterns could be further classified into those from pressor and depressor neurons. These results demonstrate that some CVNs were identifiable as reticulospinal neurons responding to anti-dromic stimulation and that CVNs operating as depressor neurons as well as pressor neurons exist in the RVLM, both of which are involved with SSR mediation. Therefore, evidence was found that an independent depressor pathway might be involved in the mediation of SSR.

• 동의생리병리학회지
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• 제16권1호
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• pp.117-123
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• 2002

To investigate the antiinflammatory and analgesic effects of Sophorae radix extracts administered to the arthritic rat model, immunohistochemical stains for CGRP in the L4, L5 and L6 spinal cord and ganglia were done, and paw swelling thickness were measured. Complete Freund,s Adjuvant(CFA) were injected to subcutaneous tissue of left foot paw of rats to induce arthritis. Sophorae radix extracts was administered immediately after CFA injection for 10 days. The spinal cord and ganglia were frozen sectioned(30㎛). These sections were stained by CGRP immunohistochemical staining method, and observed with light microscope. The results were as follows : 1. The change of paw swelling thickness of experimental group decreased from 4 day to 10day after CFA injection compared to control group. 2. The change of differential leukocytes counts of experimental group increased the ratio of lymphocytes. and decreased the ratio of neutrophils compared to control group. 3. The change of CGRP immunoreactive nerve fiber of dorsal horn of experimental group was dense stained compared to control group. 4. The number of CGRP immunoreactive neurons of L4 and L5 spinal cord of experimental group was less than in those control group. These results suggested that Sophorae radix extracts reduces the number of CGRP immunoreactive neurons and nerve fibers of spinal cord and ganglia, and decrease paw swelling thickness in arthritic rat model, which may be closely related to analgesic and antiinflammatory effects of Sophorae radix.

• The Korean Journal of Pain
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• 제14권2호
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• pp.142-149
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• 2001

Background: The expression of the proto-oncogene c-fos in spinal cord neurons following various noxious stimuli has been demonstrated in numerous studies. However, the pattern of expression of c-fos after incisional stimulus has not been evaluated. This study was designed to examine c-fos expression in an incisional pain model of rats. Methods: A 1 cm longitudinal incision was made through the skin, fascia and muscle of the plantar aspect of the hindpaw in enflurane-anesthetized rats. Withdrawal responses were measured using von Frey filaments at areas around the wound before surgery and for the next 48 hours. The expression of c-fos protein in the lumbar spinal cord was examined by immunohistochemistry. Results: After incision, c-fos was strongly expressed within laminae I, II, III, IV, V and VI ipsilateral to the incision. C-fos positive neurons were detected in the controlateral site, as well. Conclusions: These studies suggest that spinal c-fos protein may not be used as a specific marker for spinal nociceptive processing in an incisional pain model.

• The Korean Journal of Pain
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• 제11권1호
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• pp.23-29
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• 1998

Background: The present study was conducted to investigate effects of microinjection of bicuculline, GABA-A receptor antagonist, into the brain stem nuclei on the dorsal horn neuron responsiveness in rats with an experimental peripheral neuropathy. Methods: An experimental neuropathy was induced by a unilateral ligation of L5~L6 spinal nerves of rats. After 2~3 weeks after the surgery, single-unit recording was made from wide dynamic range (WDR) neurons in the spinal cord dorsal horn. Results: Responses of WDR neurons to both noxious and innocuous mechanical stimuli applied to the somatic receptive fields were enhanced on the nerve injured side. These enhanced responsiveness of WDR neurons were suppressed by microinjection of bicuculline into periaqueductal gray(PAG) or nucleus reticularis gigantocellularis(Gi). A similar suppression was also observed when morphine was microinjected into PAG or Gi. Suppressive action by Gi-bicuculline was reversed by naloxonazine, ${\mu}$-opioid receptor antagonist, microinjected into PAG whereas PAG-bicuculline induced suppression was not affected by naloxonazine injection into Gi. Gi-bicuculline induced suppression were reversed by a transection of dorsolateral funiculus(DLF) of the spinal cord. Conclusions: The results suggest that endogenous opioids, via acting on GABAergic interneurons in PAG and Gi, may be involved in the control of neuropathic pain by activating the descending inhibitory pathways that project to the spinal dorsal horn through DLF to inhibit the responsiveness of WDR neurons.

• The Korean Journal of Pain
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• 제14권2호
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• pp.136-141
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• 2001

Background: Sodium salicylate (SS) is a nonsteroidal anti-inflammatory drug (NSAID) for the treatment of neuralgia or pain from rheumatoid arthritis. When abused or used in excess, SS can induce cytotoxicity. The present study examined whether SS has a neurotoxic effect. Methods: Cell viability was examined by MTT [3-(4,5-dimethylthiazol-2,5-dipheny ltetrazolium bromide] assay and Sulforhodamine (SRB) assay after cultivating dorsal root ganglion (DRG) neurons derived from neonatal mouse. These cells were treated with various concentrations of SS for 24 hours. In addition, the amount of protein synthesis against SS was measured in these cultures. Results: Cell viability (20, $40{\mu}g/ml$ SS) significantly decreased in a dose-dependent manner. Additionally, SS inhibited protein synthesis after the exposure of cultured mouse DRG neurons to $30{\mu}g/ml$ of SS for 24 hours. Conclusions: The present study suggests that SS is toxic in cultured DRG neurons derived from neonatal mouse by decreasing cell viability and the amount of protein synthesis.