• The Korean Journal of Physiology
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• v.28 no.2
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• pp.133-141
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• 1994

The discharge patterns and peripheral nerve inputs to cardiovascular neurons were investigated in rostral ventrolateral medulla (RVLM) and raphe nucleus of cats. The data from the two were compared to determine their roles in cardiovascular regulation and the endogenous analgesic system. Animals were anesthetized with ${\alpha}-chloralose$ and single cell activities were recorded by carbon-filament microelectrode and their relationships with cardiovascular activity were analyzed. In RVLM area, a total of thirty-three cells were identified as cardiovascular neurons. During one cardiac cycle, the mean discharge rate of the neurons was $1.96{\pm}0.29$ and the peak activity was observed 45 ms after the systolic peak of arterial blood pressure. Thirteen cells could be activated antidromically by stimulation of the the $T_2$ intermediolateral nucleus. Forty-three raphe neurons were identified as cardiovascular neurons whose mean discharge rate during one cardiac cycle was $1.02{\pm}0.12$. None of these cells could be activated antidromically. Study of the interval time histogram of RVLM neurons revealed that the time to the first peak was $128{\pm}20.0\;ms$, being shorter than the period of a cardiac cycle. The same parameter found from the raphe neurons was $481{\pm}67.2\;ms$, which was much longer than the cardiac cycle length. Of seventeen RVLM neurons examined ten received only the peripheral $A{\delta}-afferent$ inputs, whereas six RVLM neurons received both $A{\delta}-$ and C-inputs; the remaining one cell received an inhibitory peripheral C-input. In contrast, nine of eleven raphe neurons were found to receive $A{\delta}-inputs$ only. We conclude that the main output of cardiovascular regulatory influences are mediated through the RVLM neurons. The cardiovascular neurons in the raphe nucleus appear to serve as interneurons transferring cardiovascular afferent information to the raphespinal neurons mediating the endogenous analgesic mechanisms.

• The Korean Journal of Pain
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• v.11 no.1
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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 Journal of Korean Medicine
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• v.29 no.5
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• pp.14-28
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• 2008

Objective : This study was carried out to understand effects of ginseng(hearinafter ; GS, Panax Ginseng) extract on regeneration responses on injured sciatic nerves in rats. Methods :Using white mouse, we damaged sciatic nerve & central nerve, and then applied GS to the lesion. Then we observed regeneration of axon and non-neuron. Results : 1. NF-200 protein immunostaining for the visualization of axons showed more distal elongation of sciatic nerve axons in GS-treated group than saline-treated control 3 and 7 days after crush injury. 2. GAP-43 protein was increased in the injured sciatic nerve and further increased by GS treatment. Enhanced GAP-43 protein signals were also observed in DRG prepared from the rats given nerve injury and GS treatment. 3. GS treatment in vivo induced enhanced neurite outgrowth in preconditioned DRG sensory neurons. In vitro treatment of GS on sensory neurons from intact DRG also caused increased neurite outgrowth. 4. Phospho-Erk1/2 protein levels were higher in the injured nerve treated with GS than saline. Phospho-Erk1/2 protein signals were mostly found in the axons in the injured nerve. 5. NGF and Cdc2 protein levels showed slight increases in the injured nerves of GS-treated group compared to saline-treated group. 6. The number of Schwann cell population was significantly increased by GS treatment in the injured sciatic nerve. GS treatment with cultured Schwann cells increased proliferation and Cdc2 protein signals. 7. GS pretreatment into the injured spinal cord generated increased astrocyte proliferation and oligodendrocytes in culture. In vitro treatment of GS resulted in more differentiated pericytoplasmic processes compared with saline treatment. 8. More arborization around the injury cavity and the occurrence at the caudal region of CST axons were observed in GS-treated group than in saline-treated group. Conclusion :GS extract may have the growth-promoting activity on regenerating axons in both peripheral and central nervous systems.

• The Journal of Pediatrics of Korean Medicine
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• v.14 no.1
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• pp.197-204
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• 2000

Neuromuscular disorders are common causes of weakness and hypotonia in the infantile period and in childhood. Accurate diagnosis of specific neuromuscular disorders depends first on identification of which aspect of the peripheral neuromuscular system is affected-the motor neuron in the spinal cord, the nerve root or peripheral nerve, the neuromuscular junction, or the muscle-and then on the determination of the etiology and specific clinical entity. Spinal muscular atrophy(SMA) is the most common autosomal-recessive genetic disorder lethal to infants. The three major childhood-onset forms of SMA are now usually called type I, type II and typeⅢ. Progression of the disease is due to loss of anterior horn cells, thought to be caused by apoptosis. Diagnosis is based on the course of the illness, as well as certain changes seen on nerve and muscle biopsy and electrodiagnostic studies. More recently, our understanding of the genetics of this disorder has provided a noninvasive approach to diagnosis. We report on a 3-year-old male patient with spinal muscular atrophy type II. He had progressive muscular weakness since 18 months of age. The upper arms were slightly, and the thighs moderately atrophic. There was muscle weakness of both the upper and lower limbs, being more proximal in distribution. Electromyogram revealed a neurogenic pattern.

• The Korean Journal of Cytopathology
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• v.1 no.1
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• pp.111-120
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• 1990

Small cell neuroendocrine carcinoma of the uterine cervix is a distinct subtype of cervical cancer that appears analogous to oat cell carcinoma and carcinoid tumors of the lung. It has been assumed to be derived from the neural crest via argyrophilic cells in the normal endocervix. We have recently encountered a case of small cell neuroendocrine carcinoma of the uterine cervix coexisting with adenocarcinoma which was argyrophil negative. A 66-year-old multiparous woman was admitted because of vaginal bleeding for 2 months. Cervicovaginal smear revealed several scattered clusters and sheets of monotonous small cells with some peripheral palisading in the background of hemorrhage and necrosis. Radical hysterectomy specimen revealed an ulcerofungating tumor on endocervical canal which was composed of two components. Major component of the tumor was made up of monomorphic population of small oval-shaped tumor cells arranged in sheets and partly in acinar structures or trabecular fashion. Other component was adenocarcinoma, endocervical well-differentiated type. Argyrophilia was present on the Grimelius stain and immunohistochemical studies revealed diffuse positivity to neuron-specific enolase and carcinoembryonic antigen. Electron microscopic examination showed clusters of small round to oval cells, which had a few well-formed desmosomes and several membrane-bound, dense-core neurosectetory granules.

• Journal of Oriental Neuropsychiatry
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• v.10 no.2
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• pp.29-45
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• 1999

As the average life span has been lengthened and the rate of senile population has been raised, chronic degenerative diseases incident to aging have been increased rapidly and become a social problem. With this social background, recently, oxygen radicals(OR) have toxic effects on Central Nervous System and Peripheral Nervous System and cause neuropathy such as Parkinson's Disease, Alzheimer Disease. The purpose of this study is to examine the toxic effects caused by Xanthine Oxidase(XO) and the effects of herbal extracts such as Jokihaeatang(JHT) on the treatment of the toxic effects. For this purpose, experiments with the cultured cell from the cerebrums of new born mice were done. The results of these experiments were as follows. 1. X0, an oxygen radical, decreased the survival rate of the cultured cells on NR assay, MTT assay and amount of neurofilaments and increased the amount of lipid peroxidation. 2. JHT have efficacy of increasing the amount of neurofilaments.

• The Journal of Korean Physical Therapy
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• v.13 no.1
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• pp.219-227
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• 2001

Capsaicin. a vanillyl amide(8-methy1-N-vanilly1-6-nonenamide) with a molecular weight of 305.42, was substance, interrupting the pain conducting pathway Until recently the neurotoxic effects of Capsaicin to adult animals were thought to be limited to the peripheral nervous system. But several reports suggest the possibility of central nervous system changes after Capsaicin administration to the adult rat. Capsaicin desensitization is defined as long lasting, reversible suppression of sensory neuron activity. How fast and for how long the desensitization develops is related to the dose and time of exposure to Capsaicin, and the interval between consecutive dosing. In the long term Capsaicin treatment can lead to morphological degeneration and changes in some small sensory neurons, predominantly unmyelinated C fiber afferent nerve fibers. Clinical interest has recently been roused by evidence that Capsaicin's desensitizing action may be of therapeutic value and that an endogenous Capsaicin-1 ike substance may exist. This study summarizes the fundamental knowledge(mechanism, receptors, et al of Capsaicin) of Capsaicin for physical therapists.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.3
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• pp.211-217
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• 2012

Recent studies have demonstrated that nitric oxide (NO) activates transient receptor potential vanilloid subtype 1 (TRPV1) via S-nitrosylation of the channel protein. NO also modulates various cellular functions via activation of the soluble guanylyl cyclase (sGC)/protein kinase G (PKG) pathway and the direct modification of proteins. Thus, in the present study, we investigated whether NO could indirectly modulate the activity of TRPV1 via a cGMP/PKG-dependent pathway in cultured rat dorsal root ganglion (DRG) neurons. NO donors, sodium nitroprusside (SNP) and S-nitro-N-acetylpenicillamine (SNAP), decreased capsaicin-evoked currents ($I_{cap}$). NO scavengers, hemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO), prevented the inhibitory effect of SNP on $I_{cap}$. Membrane-permeable cGMP analogs, 8-bromoguanosine 3', 5'-cyclic monophosphate (8bromo-cGMP) and 8-(4chlorophenylthio)-guanosine 3',5'-cyclic monophosphate (8-pCPT-cGMP), and the guanylyl cyclase stimulator YC-1 mimicked the effect of SNP on $I_{cap}$. The PKG inhibitor KT5823 prevented the inhibition of $I_{cap}$ by SNP. These results suggest that NO can downregulate the function of TRPV1 through activation of the cGMP/PKG pathway in peripheral sensory neurons.

• The Journal of The Korea Institute of Intelligent Transport Systems
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• v.11 no.4
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• pp.63-69
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• 2012

This paper describes novel scheme of a gray scale capacitive fingerprint image for high-accuracy capacitive sensor chip. The typical gray scale image scheme used a DAC of big size layout or charge-pump circuit of non-volatile memory with high power consumption and complexity by a global clock signal. A modified capacitive detection circuit of charge sharing scheme is proposed, which uses DLC(down literal circuit) based on a neuron MOS(vMOS) and analog simple multiplexor. The detection circuit is designed and simulated in 3.3V, $0.35{\mu}m$ standard CMOS process. Because the proposed circuit does not need a comparator and peripheral circuits, a pixel layout size can be reduced and the image resolution can be improved.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2018.05a
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• pp.584-587
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• 2018

Many viruses including mouse hepatitis virus, corona, measles, and sidbis viruses are known as causative virus of inducing demyelination which means destruction of myelination in nervous system of mice. The purpose of this study is to investigate processing of myelination by co-culture of Schwann cells and neuronal cells and demyelination induced by infection of sindbis virusin rat. Schwann cells and neuronal cells from dorsal root ganglion (DRG) in embryos (E16) of rat were cultured in vitro respectively. The purified neuronal cells with anti-mitotic agents and purified Schwann cells were co-cultured. After that, infection of sindbis virus into this myelinated co-culture system was performed. Myelination and demyelination process were observed using antibody of myelin basic protein meaning presence of myelination.We identified myelination and demyelination processing using antibody of peripheral myelin protein 22 (PMP 22) meaning presence of myelinated neuron. This study was supported by the Basic Research Program through the National Research Foundation (NRF) funded by the Ministry of Science, ICT & Future Planning (NRF-2015R1C1A1A01053484 and 2017R1A2B3005753).