Sequences and Phylogenic Analysis of Squid New Kinesin Superfamily Proteins(KIFs)

Sang-Jin Kim(김상진),Dae-Hyun Seog(석대현) 한국생명과학회 2012 생명과학회지 Vol.22 No.3

분자 운동 단백질은 신경세포 내의 세포체에서 특정 목적지까지 소포를 이동시키는데 관여한다. 오징어의 거대 축삭은 간단한 제거조작으로 축삭을 분리 가능하기 때문에 신경세포내 물질이동기전 연구의 좋은 모텔로 활용 가능하다. 이전연구에서 오징어 거대축삭의 소포들은 미세소관을 따라 이동하는 키네신 항체에 의하여 운반됨이 확인되었다. 본 연구는 오징어 뇌에 존재하는 키네신들을 크로닝하고, 분리된 유전자의 분석을 행하기 위하여 키네신 운동 도메인에서 잘 보존된 아미노산 배열에 해당되는 영역에 DNA primer을 이용하여 새로운 6종류의 키네신을 분리하였다. 오징어의 키네신들과 생쥐의 키네신들의 motor 영역의 아미노산분석에서 보존된 영역이 존재하며, Maximum Parsimony (MP) 방법, Neighbor-Joining (NJ) 방법, Minimum Evolution (ME) 방법, 그리고 Maximum likelihood (ML) 방법을 기초로 한 계통분석에서 생쥐의 키네신과 높은 상동성을 나타내었으며, 또한 계통수에서도 높은 상관관계가 확인되었다. The movement of vesicles from the neuronal cell body to specific destinations requires molecular motors. The squid giant axon represents a powerful model for studies of the axonal transport mechanism because the axoplasm can readily be separated from the sheath by simple extrusion. In a previous study, vesicular movements in the axoplasm of the squid giant axon were inhibited by the kinesin antibody. In the present study, we cloned and sequenced the cDNAs for squid brain KIFs. Amplification of the conserved nucleotide sequences of the motor domain by polymerase chain reaction (PCR) using first-strand cDNAs of the squid optic lobe identified six new KIF proteins. Motif analysis of the motor domains revealed that the squid KIFs are homologous to the consensus sequences of the mouse KIFs. The phylogenetic tree generated by using the maximum parsimony (MP) method, the neighbor-joining (NJ) method, the minimum evolution (ME) method, and the maximum likelihood (ML) method showed that squid KIFs are closest to mouse KIFs. These data prove the phylogenetic relationships between squid KIFs and mouse ones.

Concomitant Acute Transverse Myelitis and Sensory Motor Axonal Polyneuropathy in Two Children: Two Case Reports

정형,좌경림,김효상,김창환,정한영,김명옥 대한재활의학회 2015 Annals of Rehabilitation Medicine Vol.39 No.1

Acute transverse myelitis (ATM) is an upper motor neuron disease of the spinal cord, and concomitant association of peripheral polyneuropathy, particularly the axonal type, is rarely reported in children. Our cases presented with ATM complicated with axonal type polyneuropathy. Axonal type polyneuropathy may be caused by acute motor-sensory axonal neuropathy (AMSAN) or critical illness polyneuropathy and myopathy (CIPNM). These cases emphasize the need for nerve and muscle biopsies to make the differential diagnosis between AMSAN and CIPNM in patients with ATM complicated with axonal polyneuropathy.

Sensory and motor axons are different: implications for neurological disease

David Burke,James Howells,Matthew C. Kiernan 대한임상신경생리학회 2017 Annals of Clinical Neurophysiology Vol.19 No.1

Using threshold tracking, differences have been established between large myelinated sensory and α motor axons in humans. Major differences are that sensory axons are relatively depolarised at rest such that they have a greater persistent Na+ current, and have greater activity of hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels. Sensory axons may thereby be protected from hyperpolarising stresses, and are less likely to develop conduction block. However, the corollary is that sensory axons are more excitable and more likely to become ectopically active.

Effects of Treadmill Training on Axonal Regeneration, Spinal Cord Motor Neuron, GAP-43 & GLUT-4 Protein Expression after Sciatic Nerve Injury in the Streptozotocin-Induced Diabetic Rats

( Jong Oh Kim ),( Tae Beom Seo ),( Jin Hwan Yoon ) 한국스포츠정책과학원(구 한국스포츠개발원) 2007 International Journal of Applied Sports Sciences Vol.19 No.1

Nerve regeneration in diabetes is essential for reversal of neuropathy as well as the recovery of nerves from injury due to acute nerve compression. Here, we investigated the effects of treadmill training (TMT) on nerve regeneration and myelination of injured nerve, restoration of spinal cord motor neuron, glucose metabolism and functional recovery of innervated muscles after sciatic nerve injury in the streptozotocin-induced diabetic rats. Using immunofluorescenestaining, anterograde and retrogradetracing techniques, we identified enhanced axonal regrowth in the sciatic nerve and number of DiI-labeled spinal cord motor neurons after crush injury in diabetes rats with low intensity treadmill exercise. Primary DRG cell culture cells were Immunofluorescence stained with tubulin, neuron-specific antibody and Hoechst staining for nuclear visualization. We also carried out western blot analysis to investigate axonal growth-associated protein, GAP-43 expression in injured sciatic nerve and glucose transporter (GLUT) 4 expression in innervated muscles. The neural functional assessment was determined by the Sciatic Functional Index (SFI) for hind-foot prints. The numbers of total myelinated axon and degenerated myelin in the sciatic nerves were measured by the examination of semithin sections made from epon-embedded tissue blocks under light microscope and transmission electron microscope (TEM) with toluidine blue staining and analyzed with image analysis system to make a morphological analysis of the effect of TMT on injured nerves. GAP-43 levels were highly induced in DIE (diabetes + sciatic nerve injury + low intensity treadmill exercise) group compared with sedentary group. Total number of DiI-labeled motor neurons in the spinal cord was increased in DIE group compared with DI (diabetes + sciatic never injury) group. Total number of myelinated axons was increased in DIE group. GLUT-4 levels also were highly induced in DIE group compared with DI group. Neurite outgrowth of DRG sensory neurons was increased after TMT. SFI values in DIE group were increased more rapidly than DI group. We found that low intensity treadmill exercise promoted axonal regeneration and myelination of injured nerve, glucose metabolism and functional recovery of innervated muscles after sciatic nerve injury in the streptozotocin-induced diabetic rats. Thus, the present results suggest that low intensity treadmill exercise may be used for adjuvant therapy to the regeneration of the peripheral nerve injury with diabetes.

Sensory and motor axons are different: implications for neurological disease

Burke, David,Howells, James,Kiernan, Matthew C. The Korean Society of Clinical Neurophysiology 2017 Annals of Clinical Neurophysiology Vol.19 No.1

Using threshold tracking, differences have been established between large myelinated sensory and ${\alpha}$ motor axons in humans. Major differences are that sensory axons are relatively depolarised at rest such that they have a greater persistent $Na^+$ current, and have greater activity of hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels. Sensory axons may thereby be protected from hyperpolarising stresses, and are less likely to develop conduction block. However, the corollary is that sensory axons are more excitable and more likely to become ectopically active.

Acute Motor Axonal Neuropathy 1례

김선영(Sun Young Kim),이주은(Ju En Lee),양의준(Eu Jun Yang),남상욱(Sang Ok Nam) 대한소아신경학회 1999 대한소아신경학회지 Vol.7 No.2

저자들은 임상적으로나 뇌척수액 검사 소견상 Guillain-Barré 증후군과 유사하나 전기 생리학적 검사로 축삭 병변 소견을 보여 acute motor axonal neuropahty로 진단된 1례를 문헌고찰과 함께 보고하는 바이다. In northern China, annual epidemics of acute-onset flaccid paralysis diagnosed clinically Guillain-Barre syndrome have been observed for at least 20 years. These patients had a distinctive pattern that shares clinical and cerebrospinal fluid findings with demyelinating Guillain-Barré syndrome. But it was different from Guillain-Barré syndrome physiologically and pathologically. Electrodiagnostic studies showed normal motor distal latencies and limb conduction velocity, but reduced compound muscle action potential amplitude. When sensory nerve action potentials are elicitable, F waves are within the range of normal. This disorder was named acute motor axonal neuropathy characterized pathologically by motor nerve fiber degeneration of variable severity and by sparing of sensory fibers. Recovery is usually complete. We experienced a case of acute axonal motor neuropathy, and reported the case with a review of literature.

Identification of cis-Regulatory Region Controlling Semaphorin-1a Expression in the Drosophila Embryonic Nervous System

Hong, Young Gi,Kang, Bongsu,Lee, Seongsoo,Lee, Youngseok,Ju, Bong-Gun,Jeong, Sangyun Korean Society for Molecular and Cellular Biology 2020 Molecules and cells Vol.43 No.3

The Drosophila transmembrane semaphorin Sema-1a mediates forward and reverse signaling that plays an essential role in motor and central nervous system (CNS) axon pathfinding during embryonic neural development. Previous immunohistochemical analysis revealed that Sema-1a is expressed on most commissural and longitudinal axons in the CNS and five motor nerve branches in the peripheral nervous system (PNS). However, Sema-1a-mediated axon guidance function contributes significantly to both intersegmental nerve b (ISNb) and segmental nerve a (SNa), and slightly to ISNd and SNc, but not to ISN motor axon pathfinding. Here, we uncover three cis-regulatory elements (CREs), R34A03, R32H10, and R33F06, that robustly drove reporter expression in a large subset of neurons in the CNS. In the transgenic lines R34A03 and R32H10 reporter expression was consistently observed on both ISNb and SNa nerve branches, whereas in the line R33F06 reporter expression was irregularly detected on ISNb or SNa nerve branches in small subsets of abdominal hemisegments. Through complementation test with a Sema-1a loss-of-function allele, we found that neuronal expression of Sema-1a driven by each of R34A03 and R32H10 restores robustly the CNS and PNS motor axon guidance defects observed in Sema-1a homozygous mutants. However, when wild-type Sema-1a is expressed by R33F06 in Sema-1a mutants, the Sema-1a PNS axon guidance phenotypes are partially rescued while the Sema-1a CNS axon guidance defects are completely rescued. These results suggest that in a redundant manner, the CREs, R34A03, R32H10, and R33F06 govern the Sema-1a expression required for the axon guidance function of Sema-1a during embryonic neural development.

증예(症例) : 급성 파종성 뇌척수염에 동반된 급성 운동 축삭형 신경병증

유성용 ( Seong Yong Yu ),임의성 ( Eui Seong Lim ),신병수 ( Byoung Soo Shin ),서만욱 ( Man Wook Seo ),김영현 ( Young Hyun Kim ) 전북대학교 의과학연구소 2003 全北醫大論文集 Vol.27 No.2

Acute motor axonal neuropathy(AMAN) is a subtype of Guillain-Barre syndrome and characterized by selective involvement of motor fibers. Acute disseminated encephalomyelitis(ADEM) is a demyelinating disease of central nervous system. The coincidence of central and peripheral nervous system involvement has been reported rarely. We described a 37-year-old male patient presented with fever, altered consciousness. The examination of cerebrospinal fluid and brain magnetic resonance imaging was compatible with acute disseminated encephalomyelitis. Several days later, his mentality was improved but he showed quadriparesis and palsy of cranial nerves, areflexia. Electrophysiologic studies suggested axonal form of motor dominant polyneuropathy. We report a caute motor axonal neuropathy combined with ADEM. We consider that this case is an example of simultaneous immunologic process in the common pathogenic epitope of central nervous system and peripheral nervous system.

소뇌 손상에 의한 사지 마비 환자의 보행 및 운동 기능 회복 양상 연구

여상석,Sang-Seok Yeo 대한고유수용성신경근촉진법학회 2023 PNF and Movement Vol.21 No.3

Purpose: Cerebellar injury can be caused by a variety of factors, including trauma, stroke, and tumor. Cerebellar injury can manifest in different clinical symptoms and signs depending on the size and location of the injury. The purpose of this study was to examine and compare the recovery patterns of each motor function by tracking the motor levels of patients with cerebellar injury. Methods: This study recruited 11 patients with quadriplegia resulting from cerebellar injury. The motricity index (MI), modified Brunnstrom classification (MBC), and functional ambulation category (FAC) methods were used to evaluate motor levels. The motor function evaluation was performed immediately after the onset of the condition and at intervals of one month, two months, and six months after onset. Results: The MI values of the upper and lower extremities and hand function (MBC) indicated severe paralysis in the early stages of onset. Compared to the onset time, significant motor function recovery was observed after 1, 2, and 6 months (p < 0.05). In contrast, there was no significant pattern of recovery between 1, 2, and 6 months after onset (p > 0.05). FAC indicated showed significant recovery at one month compared to onset (p<0.05), and there was also a significant difference between 1 and 2 months (p < 0.05). On the other hand, there was no significant difference in FAC between 2 and 6 months (p > 0.05). Conclusion: Patients with cerebellar injury showed significant recovery in functions related to muscle strength and voluntary muscle control one month after onset and gradually recovered further over the next six months. On the other hand, gait function, which is closely related to balance, showed a relatively slow recovery pattern from the beginning of the disease to the six month follow-up.

트레드밀 운동이 스트렙토조토신으로 당뇨 유발 후 좌골신경 손상 쥐의 신경재생, 척수운동신경세포, GAP-43와 GLUT-4 단백질 발현에 미치는 영향

김종오 ( Jong Oh Kim ),서태범 ( Tae Beom Seo ),윤진환 ( Jin Hwan Yoon ) 한국스포츠정책과학원(구 한국스포츠개발원) 2006 체육과학연구 Vol.17 No.3

당뇨에 있어서 신경재생은 급성신경압박 으로 인해 손상된 신경의 회복 및 신경장애를 막는데 필수적인 요소이다. 본 연구에서 우리는 streptozotocin으로 당뇨유발 후 좌골신경에 압궤손상을 가하여 당뇨병성 신경증을 유발한 흰쥐의 손상된 신경부위의 신경재생 및 수초화, 척수 내 운동신경세포의 회복, 손상된 신경섬유 지배근육의 당대사와 기능회복에 트레드밀 운동이 어떠한 영향을 미치는지를 알아보고자 실시되었다. 당뇨유발 후 신경압궤 손상을 준 쥐를 대상으로 저강도 운동이 손상된 좌골신경의 축삭재생, 척수신경부위의 운동신경세포수의 변화를 관찰하기 위하여 면역형광염색법, 순방향 및 역방향 DiI추적 기법 등을 사용하였다. 세포배양 후 tubulin과 Hoechst 염색을 통해 신경세포 및 핵을 관찰하였다. 또한, 손상된 좌골신경부위의 축삭 성장관련단백질인 GAP-43 발현과 지배근육의 당수송체 4의 발현은 western blot 분석방법을 이용하여 분석하였다. 손상된 신경의 기능적 평가는 좌골신경 기능지수로 알아보았다. 손상된 좌골신경 부위의 축삭 수초화와 탈수초화의 형태학적 변화에 대한 관찰은 epon-embedded tissue blocks와 toludine blue 염색법을 수행 한 후 광학 및 전자현미경으로 관찰하였다. 결과적으로, 척수 내 DiI에 염색된 운동신경 세포 수는 DI 그룹에 비해 DIE 그룹에서 증가하는 것으로 나타났으며, 수초화된 축삭의수도 DIE 그룹에서 높은 것으로 나타났다. 또한, 지배근육의 GLUT-4 수준 역시 DI 그룹에 비해 DIE 그룹이 더욱 높은 것으로 나타났다. DIE 그룹이 DI그룹에 비해 축삭 성장이 증가하는 것으로 나타났다. 기능회복의 지표인 좌골신경기능 지수의 변화는 DI 그룹에 비해 DIE 그룹이 더 빠르게 증가하는 것으로 나타났다. 본 연구에서 우리는 저강도 트레드밀 운동이 당뇨유발후좌골신경 손상된 흰쥐의 축삭재생, 손상된 신경의 수초화, 지배근육의 당대사 및 기능회복을 촉진함을 확인하였다. 따라서, 본 연구 결과는 저강도 트레드밀 운동이 당뇨 환자의 말초신경손상 후 신경재생을 위한 보조적 치료수단으로서의 가능함을 확인하는결과라 생각된다. Nerve regeneration in diabetes is essential for reversal of neuropathy as well as the recovery of nerves from injury due to acute nerve compression. Here, we investigated the effects of treadmill training (TMT) on nerve regeneration and myelination of injured nerve, restoration of spinal cord motor neuron, glucose metabolism and functional recovery of innervated muscles after sciatic nerve injury in the streptozotocin-induced diabetic rats. Using immunofluorescenestaining, anterograde and retrogradetracing techniques, we identified enhanced axonal regrowth in the sciatic nerve and number of DiI-labeled spinal cord motor neurons after crush injury in diabetes rats with low intensity treadmill exercise. Primary DRG cell culture cells were Immunofluorescence stained with tubulin, neuron-specific antibody and Hoechst staining for nuclear visualization. We also carried out western blot analysis to investigate axonal growth-associated protein, GAP-43 expression in injured sciatic nerve and glucose transporter (GLUT) 4 expression in innervated muscles. The neural functional assessment was determined by the Sciatic Functional Index (SFI) for hind-foot prints. The numbers of total myelinated axon and degenerated myelin in the sciatic nerves were measured by the examination of semithin sections made from epon-embedded tissue blocks under light microscope and transmission electron microscope (TEM) with toluidine blue staining and analyzed with image analysis system to make a morphological analysis of the effect of TMT on injured nerves. GAP-43 levels were highly induced in DIE (diabetes + sciatic nerve injury + low intensity treadmill exercise) group compared with sedentary group. Total number of DiI-labeled motor neurons in the spinal cord was increased in DIE group compared with DI (diabetes + sciatic never injury) group. Total number of myelinated axons was increased in DIE group. GLUT-4 levels also were highly induced in DIE group compared with DI group. Neurite outgrowth of DRG sensory neurons was increased after TMT. SFI values in DIE group were increased more rapidly than DI group. We found that low intensity treadmill exercise promoted axonal regeneration and myelination of injured nerve, glucose metabolism and functional recovery of innervated muscles after sciatic nerve injury in the streptozotocin-induced diabetic rats. Thus, the present results suggest that low intensity treadmill exercise may be used for adjuvant therapy to the regeneration of the peripheral nerve injury with diabetes.