• Title/Summary/Keyword: neuromuscular junction

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The Effects of Neuromuscular Electrical Stimulation on Synaptic Reorganization of Neuromuscular Junctions in Rat Atrophic Muscle (신경근 전기자극이 흰쥐 위축근 신경근 연접부의 연접재형성에 미치는 영향)

  • Nam, Ki-Won;Kim, Young-Eok
    • The Journal of Korean Physical Therapy
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    • v.19 no.3
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    • pp.19-30
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    • 2007
  • Purpose: This study was performed to investigate the effects of NMES for recovery of skeletal muscle. Methods: The normal group consisted of healthy rat without cast immobilization. The control group was breeding at standard cage during 7 days after 2 weeks-cast immobilization on hind limb. The experimental group. I. received NMES application during days after 2 weeks-cast immobilization on hind limb. The effects were measured with NT-3 immunoreactivity in neuromuscular junction by light microscope. Results: Immunoreactivity of NT-3 at the neuromuscular junction was higher appeared experimental groups than control group. Then, There was a little detection in the normal and control group. Conclusion: These therapeutic interventions enhance expression of NT-3 at the neuromuscular junction. Also, NMES is considered to effect on a normal structural formation and NT-3 expression at the neuromuscular junction.

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The Ultrastructure and Function of Neuromuscular Junction (신경근 연접부의 미세구조와 기능)

  • Nam Ki-Won;Hwang Bo-Gak;Koo Hyun-Mo;Kim Jin
    • The Journal of Korean Physical Therapy
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    • v.14 no.4
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    • pp.163-171
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    • 2002
  • Neuromuscular junction consist of presynaptic membrane, synaptic cleft and postsynaptic membrane. In the neuromuscular junction, presynaptic membrane is the motor nerve terminal, have many synaptic vesicle. Postsynaptic membrane is the motor end plate of muscle fiber and the most striking structural features are the deep infolding of the sarcolemma. Between the nerve and muscle cells, there is a synaptic cleft of some 50-100nm. This review shows the ultrastructure and function of neuromuscular junction, summarizes the current knowledge.

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Fine Structural Analysis of the Neuromuscular Junction in the Venomous Organ of the Spider, Agelena limbata (Araneae: Aselenidae) (거미(agelena Limbata Thorell) 독 분비기관의 신경근육간 연접장치의 미세구조적 분석)

  • 문명진
    • The Korean Journal of Zoology
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    • v.39 no.2
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    • pp.223-230
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    • 1996
  • Fine structure of the neuromuscular junction in the venomous organ of the spider, Agelena li'mbutq, was studied using high magnification electron microscope. The motor nerve endings at neuromuscular contact area composed of neurons and neuroslial cells were located between musculature and extracellular sheath of the venom gBand. At the synaptic contact between a motor axon and a muscle fiber in the musculature, spherical synaptic vesicles were prominent in the nerve terminal. The sarcoplasm beneath the neuromuscular synapse has a granular appearance and lacks mvofilaments. And the main axon gives off a branch between the muscle fibers. The synaptic regions of this organ are located close to the myofilaments unlike to other chelicerate classes. Moreover the postsvnaptic complex of vesicles and membrane invasinations present in other synaptic legions are absent from these legions in this venomous organ.

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The effects of Electrical Stimulation Therapy on NT-3 Expression in the Denervated Neuromuscular Junction in Rat (전기자극치료가 흰쥐 탈 신경근연접부에서 NT-3의 발현에 미치는 영향)

  • Nam Ki-Won;Koo Hyun-Mo;Cheon Song-Hee;Lee Yun-Seop;Kang Jong-Ho;Kim Jin-Sang
    • The Journal of Korean Physical Therapy
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    • v.16 no.2
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    • pp.63-71
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    • 2004
  • Denervated skeletal muscle produces muscle atrophy as well as changes at the neuromuscular junction which leads to terminal axonal sprouting and an ultrastructural remodeling. NT-3 is expressed in adult muscle and motoneurons. Normally NT-3 has a potential role in regulating adult neuromuscular jungtion and recovering following muscle atrophy. Also, it could influence synaptic neurotransmission between motoneurons and skeletal muscle cells. The purpose of this study was to investigate the effect of electrical stimulation therapy(EST) on NT-3 expression in neuromuscular junction following sciatic nerve transsection in rats. After EST application during 7 days, the immunoreactivity of NT-3 was increased in neuromuscular junction

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Review of neuromuscular junction to understand myasthenia gravis (중증근무력증의 이해를 위한 신경근 연접부에 대한 고찰)

  • Song, Ju-Min;Nam, Ki-Won;Kim, Souk-Boum;Chae, Yun-Won;Kwon, Young-Shil;Kim, Jin-Sang
    • The Journal of Korean Physical Therapy
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    • v.13 no.3
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    • pp.761-767
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    • 2001
  • Myasthenia gravis is an autoimmune disorder mainly caused by antibodies to the muscle acetylcholine receptors at the neuromuscular junction Loss of these receptors leads to a defect in neuromuscular transmission with muscle weakness and fatigue. In this study, to understand of myasthenia gravis, were viewed about anatomical and physiological view of neuromuscular junction.

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Therapeutic Potential of CKD-504, a Novel Selective Histone Deacetylase 6 Inhibitor, in a Zebrafish Model of Neuromuscular Junction Disorders

  • Jeong, Hui Su;Kim, Hye Jin;Kim, Deok-Ho;Chung, Ki Wha;Choi, Byung-Ok;Lee, Ji Eun
    • Molecules and Cells
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    • v.45 no.4
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    • pp.231-242
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    • 2022
  • The neuromuscular junction (NMJ), which is a synapse for signal transmission from motor neurons to muscle cells, has emerged as an important region because of its association with several peripheral neuropathies. In particular, mutations in GARS that affect the formation of NMJ result in Charcot-Marie-Tooth disease and distal hereditary motor neuropathy. These disorders are mainly considered to be caused by neuronal axon abnormalities; however, no treatment is currently available. Therefore, in order to determine whether the NMJ could be targeted to treat neurodegenerative disorders, we investigated the NMJ recovery effect of HDAC6 inhibitors, which have been used in the treatment of several peripheral neuropathies. In the present study, we demonstrated that HDAC6 inhibition was sufficient to enhance movement by restoring NMJ impairments observed in a zebrafish disease model. We found that CKD-504, a novel HDAC6 inhibitor, was effective in repairing NMJ defects, suggesting that treatment of neurodegenerative diseases via NMJ targeting is possible.

Critical Illness Myopathy (위험질병 근병증)

  • Lee, Dong Kuck
    • Annals of Clinical Neurophysiology
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    • v.4 no.2
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    • pp.91-97
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    • 2002
  • The field of critical care medicine has flourished, but an unfortunate result of improved patient survival in the intensive care unit is the occurrence of certain acquired neuromuscular disorders. During the last two decades, various neuromuscular disorders were recognized as common causes of weakness occurring in critically ill patients. The two most common disorders are an acute quadriplegic myopathy predominantly associated with the use of intravenous corticosteroids and neuromuscular junction blocking agents and severe systemic illness termed critical illness myopathy(CIM), and an axonal sensorimotor polyneuropathy termed critical illness polyneuropathy. I will review briefly about general components of the CIM.

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Ultrastructure of the neuromuscular Junction in the Mantle Edge of the African Giant Snail, Achatina fulica (아프리카 왕달팽이(Achatina fulica) 외투막내 신경근연접의 미세구조)

  • 장남섭;한종민;황선종
    • The Korean Journal of Malacology
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    • v.14 no.2
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    • pp.75-83
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    • 1998
  • 아프리키 왕달팽이(Achatina fulica) 외투막(mantle edge) 내 근육 속의 신경근연접에 관한 미세구조 연구결과는 다음과 같았다. 신경근연접종말의 형태는 방추형이거나 불규칙형이었으며, 연접막과 근형질막상이 연접간극(synaptic cleft)의 넓이는 30mm 정도로 나타났다. 연접강속에는 전자밀도가 높은 둥근 과립(직경 100mm)과 중등도는 과립(직경 70mm)그리고 전자밀도가 낮은 소포(직경70mm)등 3종류가 관찰되었으며, 연접종말의 외측에는 0.2 - 0.4$\mu\textrm{m}$ 정도크기의 전자밀도가 높은 둥근 과립들이 존재하였다. 전자밀도가 중등도인 둥근 과립 중 일부는 연접막 밖으로 배출(exocytosis) 되었으며, 근형질막과 연접막이 합체되는 현상도 관찰되었다. 근형질(sarcoplasm)내에서 수축성단백질인 액틴과 미오신섬유의 배열은 불규칙하였으며, 세포질성 치밀체(cytoplasmic dense body)도 관찰되었다.

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A Study on Estimation of Numbers of Motor Unit related to the Widths and Distribution of Endplate in Neuromuscular Junction (신경근육 접합부의 종판 폭과 분포에 따른 운동단위 수의 추정에 관한 연구)

  • Lee, Ho-Yong;Kim, Duck-Young;Park, Jung-Ho;Jung, Chul-Ki;Kim, Sung-Hwan
    • Journal of the Institute of Electronics Engineers of Korea SC
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    • v.48 no.5
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    • pp.81-92
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    • 2011
  • In this paper, a new method to estimate the number of MU (motor unit) related to the widths and distribution of end plate in NMJ (neuromuscular junction) of biceps brachii is proposed by varying muscle parameter statistically in EMG model. This work is done by designing MU-simulator and EPZ-simulator. The proposed method was compared with the results of previous researchers. The proposed MU-simulator generates SMUAP (single motor unit action potential) and CMAP (compound muscle action potential) signal similar to detected SMUAP and CMAP signal obtained from muscle. The EPZ-simulator estimate the numbers of MU by varying the widths and distribution of end plate in neuromuscular junction of muscle. The results shows that the numbers of MU was estimated about 450 ea. and muscle fibers was about 340 ea., end plate widths was about 6 mm, and end plate was randomly distributed. The proposed method may be comparable with the method of anatomical studies.

MICAL-like Regulates Fasciclin II Membrane Cycling and Synaptic Development

  • Nahm, Minyeop;Park, Sunyoung;Lee, Jihye;Lee, Seungbok
    • Molecules and Cells
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    • v.39 no.10
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    • pp.762-767
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    • 2016
  • Fasciclin II (FasII), the Drosophila ortholog of neural cell adhesion molecule (NCAM), plays a critical role in synaptic stabilization and plasticity. Although this molecule undergoes constitutive cycling at the synaptic membrane, how its membrane trafficking is regulated to ensure proper synaptic development remains poorly understood. In a genetic screen, we recovered a mutation in Drosophila mical-like that displays an increase in bouton numbers and a decrease in FasII levels at the neuromuscular junction (NMJ). Similar phenotypes were induced by presynaptic, but not postsynaptic, knockdown of mical-like expression. FasII trafficking assays revealed that the recycling of internalized FasII molecules to the cell surface was significantly impaired in mical-like-knockdown cells. Importantly, this defect correlated with an enhancement of endosomal sorting of FasII to the lysosomal degradation pathway. Similarly, synaptic vesicle exocytosis was also impaired in mical-like mutants. Together, our results identify Mical-like as a novel regulator of synaptic growth and FasII endocytic recycling.