• Journal of Dental Anesthesia and Pain Medicine
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• v.19 no.2
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• pp.77-82
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• 2019

It is well known that trigeminal nerve injury causes hyperexcitability in trigeminal ganglion neurons, which become sensitized. Long after trigeminal nerve damage, trigeminal spinal subnucleus caudalis and upper cervical spinal cord (C1/C2) nociceptive neurons become hyperactive and are sensitized, resulting in persistent orofacial pain. Communication between neurons and non-neuronal cells is believed to be involved in these mechanisms. In this article, the authors highlight several lines of evidence that neuron-glial cell and neuron macrophage communication have essential roles in persistent orofacial pain mechanisms associated with trigeminal nerve injury and/or orofacial inflammation.

• International Journal of Industrial Entomology and Biomaterials
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• v.3 no.2
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• pp.177-185
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• 2001

This study has been carried out to determine localization of Manduca sexta allatotropin (Mas-AT) neuropeptide in developing ventral nerve cord of the silk moth Bombyx mori with polyclonal antisera against Mas-AT. Suboesophageal ganglion (SOG) of the second to fifth instar larvae and 3-day-old pupae showed two to ten Mas-AT-immunoreactive (Mas-AT-IR) cell bodies. There were two to three pairs of labeled cell bodies in each thoracic ganglion (TG) from third instar larvae to adults, with the exception of TG from prepupae. One pair of labeled cell bodies was localized in each abdominal ganglion (AG) 1 to 6 from third instar larvae to 3-day-old pupae, whereas in 5-day-old pupae to adults there was one pair in a similar location of AG 1 to 5. The seventh neuromeres of terminal abdominal ganglia (TAG) from third instar Iarvae to 3- day-old pupae contained four labeled large cell bodies. In each of AG 1 to 7, these cell bodies showed similar allatotropin-immunoreactivity in appearance. Some labeled axons, projected from Mas-AT-lR cells in each of those AG, were extended to the nerves N 1 and N 2.

• Animal cells and systems
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• v.3 no.3
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• pp.259-267
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• 1999

The expression of the neural cell adhesion molecule-180 (NCAM-180), which accumulates at contact sites between cells and may be responsible for the stabilization of cell contacts, was studied in the olfactory system and retina of developing and adult rats. From embryonic day 12 onwards, which was the earliest stage examined, the NCAM-180 pathway directing to the presumptive olfactory bulb was observed. In later stages, olfactory neurons and fasciculating axons in the olfactory epithelium and nerve fiber layer and glomeruli of the olfactory bulb expressed NCAM-180. From postnatal day 0, immunolabelling pattern of the olfactory epithelium and olfactory bulb were the same as that during later stages. NCAM-180 immunoreactivity was present on differentiating retinal cells and persisted on those cells throughout adulthood. However, contrary to the olfactory nerve which remained detectable in the adult, the optic nerve was only transiently expressed with NCAM-180 and was no longer detectable in the adult. The presence of NCAM-180 in olfactory tissues suggests their possible role in pathfinding, differentiation, fasciculation and synaptic plasticity. The continued presence of NCAM-180 in the olfactory system examined may underlie its continuous cell turnover and regenerative capacity. The continuous expression of NCAM-180 in ganglion cells, bipolar cells and photoreceptor cells, also suggests potential regenerating capability and some plastic functions for these cells in the adult. Since the expression of NCAM-180 by the optic nerve was restricted to the period of special histogenetic events, for example, during axonal growth and synaptogenesis, it is possible that the lack of NCAM-180 in the adult optic nerve might cause a nonpermissive environment for the regeneration and result in regenerative failure of this system.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.3
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• pp.143-147
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• 2005

Following peripheral nerve injury, excessive nociceptive inputs result in diverse physiological alterations in the spinal cord substantia gelatinosa (SG), lamina II of the dorsal horn. Here, I report the alterations of excitatory or inhibitory transmission in the SG of a rat model for neuropathic pain ('spared nerve injury'). Results from whole-cell recordings of SG neurons show that the number of distinct primary afferent fibers, identified by graded intensity of stimulation, is increased at 2 weeks after spared nerve injury. In addition, short-term depression, recognized by paired-pulse ratio of excitatory postsynaptic currents, is significantly increased, indicating the increase of glutamate release probability at primary afferent terminals. The peripheral nerve injury also increases the amplitude, but not the frequency, of spontaneous inhibitory postsynaptic currents. These data support the hypothesis that peripheral nerve injury modifies spinal pain conduction and modulation systems to develop neuropathic pain.

• Archives of Reconstructive Microsurgery
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• v.6 no.1
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• pp.9-28
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• 1997

Adequate vascularization is pivotally essential for a successful nerve graft. Theoretically, the immediate vascularization will inhibit fibroblast infiltration and stimulate nerve cell regeneration. In this study, histomorphological and electrophysiological studies were performed to determine if vascularized grafts are functionally superior. In rat model, a 4cm segment of the sciatic nerve was obtained and placed as a non vascularized graft on one side, and as a vascularized graft connected to the inferior gluteal vessels on the opposite side. To determine the compound action potential of the gastrocnemius muscle, electromyography was done after 2, 3 and 4 months. Histomorphologically, the distribution of myelinated nerve fibers and Schwann cell were evaluated after toluidine blue staining, The following resutls were obtained: 1. The electrophysiological studies showed no difference between the nonvascularized and vascularized grafts. 2. Two and three months after grafting, myelinated nerve fibers were more abundant in the vascularized proximal, middle and distal areas in all nerve fibers of varying diameters. 3. In the post-nonvascularized graft 2-month group, a few myelinated nerve fibers were present in the proximal and middle areas, but none distally. In the post-vascularized graft 2 month group, myelinated nerve fibers ranging $2-8{\mu}m$ were present in all three areas. 4. In the post-nonvascularized graft 3 month group, a few myelinated nerve fibers ranging in $2-6{\mu}m$ were present in all three areas, but in the post-vascularized graft 3 month group, many myelinated nerve fibers ranging in $2-10{\mu}m$ were present in all three areas. 5. In the post-graft 4-month group, more myelinated nerve fibers were present in all three areas of the vascularized grafts. However, nerve fibers of less than $2{\mu}m$ in diameter were more abundant in the non vascularized grafts. 6. Schwann cells were more abundant in the proximal, middle and distal areas of the post-vascularized 2, 3 and 4-month grafts. Based on these findings, the immediate restoration of circulation in vascularized nerve grafts allows for the increased number of surviving Schwann cells, rapid healing of the axon and myelin sheath changes which occur during Wallerian degeneration, and thus is able to stimulate a morphologically optimal regeneration.

• 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 Internal Korean Medicine
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• v.27 no.3
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• pp.737-744
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• 2006

Guillain-Barre Syndrome is a disorder caused by nerve inflammation. The inflammation damages portions of the nerve cells, resulting in pain, numbness, muscle weakness or paralysis and sensory loss. The damage can also leads to denervation (killing the axon part of the nerve cell), which stops nerve function entirely. Without the axon, messages cannot be transferred from one nerve cell to another, but the causes and mechanism of this syndrome are unknown. This is a clinical report about two patients diagnosed with Guillain-Barre Syndrome. The patients, a 54-year-old woman and a 37-years-old man, had pain, and weakness in both legs and arms. After about 4 weeks of Korean medicine and acupuncture treatment, most of their symptoms improved. Therefore, Korean traditional therapy has potential for treatment of Guillain-Barre Syndrome.

• The Korean Journal of Pain
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• v.20 no.2
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• pp.255-257
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• 2007

Giant cell arteritis, which is also referred to as temporal arteritis, is defined as a systemic vasculitis in individuals over 50 years of age. Here, we report a case of giant cell arteritis combined with oculomotor nerve palsy. An 81-year old female patient experienced a headache for 10 days in her left temporoparietal area, that was characterized by a continuous dull ache and heaviness with intermittent shooting and lancinating pain. Her symptoms persisted in spite of receiving strong analgesics in another hospital. Upon physical examination, she was found to have marked tenderness over the left temporal area, especially along the path of the temporal artery as well as limitation of adduction, supraduction and infraduction of the left eyeball. At the time of admission, her erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were 52 mm/hr and 3.94 mg/dl. In addition her brain MRI revealed no specific findings. Giant cell arteritis was suspected based on the clinical symptoms and signs as well as the elevated ESR and CRP. Oral steroid therapy started was started with an initial dose of 40 mg of prednisolone per day that was gradually tapered to 5 mg a day for 2 weeks. Her headache subsided one day after the steroid therapy and oculomotor nerve palsy was markedly improved after 2 weeks of the therapy. After 2 months she had recovered completely from her symptoms.

• Proceedings of the Korean Society of Life Science Conference
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• 2008.10a
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• pp.97.1-97.1
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• 2008

• The Journal of Korean Medicine
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• v.29 no.2
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• pp.133-150
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• 2008

Objective: This study was performed to examine Danggui (DG, Angelica gigas Nakai)'s potential activity for promoting axonal regeneration in the injured peripheral nerve. Methods: Using the sciatic nerve in the rats, DG extract 5 ${\mu}l$(10 mg/ml in 0.5% saline) was dripped into the injury site of the nerve. Results: DG treatment facilitated axonal elongation responses in the distal portion to the injury site. GAP-43 protein levels were upregulated by DG treatment in the injured nerve and also in the DRG, suggesting the induction of GAP-43 expression at gene expression level after nerve injury. Phospho-Erk1/2 protein levels were upregulated in the injured nerve area and also in the DRG, suggesting retrograde transport of phospho-Erk1/2 protein from the injury area to the cell body. Cdc2 protein levels were slightly upregulated by DG treatment. DG treatment increased the number of non-neuronal cells in the distal portion to the injury site. Conclusions: The present data suggest that DG is effective for enhanced axonal regrowth after sciatic nerve injury.