The Nodes of Ranvier: Molecular Assembly and Maintenance
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Nervous Tissue
Nervous Tissue Prof.Prof. ZhouZhou LiLi Dept.Dept. ofof HistologyHistology andand EmbryologyEmbryology Organization:Organization: neuronsneurons (nerve(nerve cells)cells) neuroglialneuroglial cellscells Function:Function: Ⅰ Neurons 1.1. structurestructure ofof neuronneuron somasoma neuriteneurite a.a. dendritedendrite b.b. axonaxon 1.11.1 somasoma (1)(1) nucleusnucleus LocatedLocated inin thethe centercenter ofof soma,soma, largelarge andand palepale--stainingstaining nucleusnucleus ProminentProminent nucleolusnucleolus (2)(2) cytoplasmcytoplasm (perikaryon)(perikaryon) a.a. NisslNissl bodybody b.b. neurofibrilneurofibril NisslNissl’’ss bodiesbodies LM:LM: basophilicbasophilic massmass oror granulesgranules Nissl’s Body (TEM) EMEM:: RERRER,, freefree RbRb FunctionFunction:: producingproducing thethe proteinprotein ofof neuronneuron structurestructure andand enzymeenzyme producingproducing thethe neurotransmitterneurotransmitter NeurofibrilNeurofibril thethe structurestructure LM:LM: EM:EM: NeurofilamentNeurofilament micmicrotubulerotubule FunctionFunction cytoskeleton,cytoskeleton, toto participateparticipate inin substancesubstance transporttransport LipofuscinLipofuscin (3)(3) CellCell membranemembrane excitableexcitable membranemembrane ,, receivingreceiving stimutation,stimutation, fromingfroming andand conductingconducting nervenerve impulesimpules neurite: 1.2 Dendrite dendritic spine spine apparatus Function: 1.3 Axon axon hillock, axon terminal, axolemma Axoplasm: microfilament, microtubules, neurofilament, mitochondria, -
Vocabulario De Morfoloxía, Anatomía E Citoloxía Veterinaria
Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) Servizo de Normalización Lingüística Universidade de Santiago de Compostela COLECCIÓN VOCABULARIOS TEMÁTICOS N.º 4 SERVIZO DE NORMALIZACIÓN LINGÜÍSTICA Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) 2008 UNIVERSIDADE DE SANTIAGO DE COMPOSTELA VOCABULARIO de morfoloxía, anatomía e citoloxía veterinaria : (galego-español- inglés) / coordinador Xusto A. Rodríguez Río, Servizo de Normalización Lingüística ; autores Matilde Lombardero Fernández ... [et al.]. – Santiago de Compostela : Universidade de Santiago de Compostela, Servizo de Publicacións e Intercambio Científico, 2008. – 369 p. ; 21 cm. – (Vocabularios temáticos ; 4). - D.L. C 2458-2008. – ISBN 978-84-9887-018-3 1.Medicina �������������������������������������������������������������������������veterinaria-Diccionarios�������������������������������������������������. 2.Galego (Lingua)-Glosarios, vocabularios, etc. políglotas. I.Lombardero Fernández, Matilde. II.Rodríguez Rio, Xusto A. coord. III. Universidade de Santiago de Compostela. Servizo de Normalización Lingüística, coord. IV.Universidade de Santiago de Compostela. Servizo de Publicacións e Intercambio Científico, ed. V.Serie. 591.4(038)=699=60=20 Coordinador Xusto A. Rodríguez Río (Área de Terminoloxía. Servizo de Normalización Lingüística. Universidade de Santiago de Compostela) Autoras/res Matilde Lombardero Fernández (doutora en Veterinaria e profesora do Departamento de Anatomía e Produción Animal. -
Pre-Oligodendrocytes from Adult Human CNS
The Journal of Neuroscience, April 1992, 12(4): 1538-l 547 Pre-Oligodendrocytes from Adult Human CNS Regina C. Armstrong,lJ Henry H. Dorn, l,b Conrad V. Kufta,* Emily Friedman,3 and Monique E. Dubois-Dalcq’ ‘Laboratory of Viral and Molecular Pathogenesis, and %urgical Neurology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892 and 3Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania 19104-3246 CNS remyelination and functional recovery often occur after Rapid and efficient neurotransmission is dependent upon the experimental demyelination in adult rodents. This has been electrical insulating capacity of the myelin sheath around axons attributed to the ability of mature oligodendrocytes and/or (reviewed in Ritchie, 1984a,b). Nerve conduction is impaired their precursor cells to divide and regenerate in response after loss of the myelin sheath and results in severe neurological to signals in demyelinating lesions. To determine whether dysfunction in human demyelinating diseases such as multiple oligodendrocyte precursor cells exist in the adult human sclerosis (MS). Remyelination can occur in the CNS of MS CNS, we have cultured white matter from patients under- patients but appears to be limited (Perier and Gregoire, 1965; going partial temporal lobe resection for intractable epilep- Prineas et al., 1984). Studies of acute MS cases have revealed sy. These cultures contained a population of process-bear- that recent demyelinating lesions can exhibit remyelination that ing cells that expressed antigens recognized by the 04 appears to correlate with the generation of new oligodendrocytes monoclonal antibody, but these cells did not express galac- (Prineas et al., 1984; Raine et al., 1988). -
Rabbit Anti-CASPR/FITC Conjugated Antibody-SL11128R-FITC
SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-CASPR/FITC Conjugated antibody SL11128R-FITC Product Name: Anti-CASPR/FITC Chinese Name: FITC标记的轴突蛋白4/少突胶质细胞抗体 Neurexin4; caspr 1; Caspr; Caspr1; Cntnap 1; Cntnap1; CNTP 1; CNTP1; CNTP1_HUMAN; Contactin associated protein 1; Contactin-associated protein 1; Alias: MHDNIV; NCP 1; NCP1; Neurexin 4; Neurexin IV; Neurexin-4; Nrxn 4; Nrxn4; p190; Paranodin. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat,Dog,Pig,Cow,Horse, Flow-Cyt=1:50-200ICC=1:50-200IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 154kDa Cellular localization: The cell membrane Form: Lyophilized or Liquid Concentration: 1mg/ml immunogen: KLH conjugated synthetic peptide derived from human CASPR/Neurexin4 Lsotype: IgGwww.sunlongbiotech.com Purification: affinity purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: Neurexins comprise a family of neuronal cell surface proteins, which include neurexin I (NRXN1), neurexin II (NRXN2), neurexin III (NRXN3) and CASPR (neurexin IV). Product Detail: Neurexins I-III are expressed as ? and ∫ isoforms. -
Acute Reduction of Microglia Does Not Alter Axonal Injury in a Mouse Model of Repetitive Concussive Traumatic Brain Injury Rachel E
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2014 Acute reduction of microglia does not alter axonal injury in a mouse model of repetitive concussive traumatic brain injury Rachel E. Bennett Washington University School of Medicine David L. Brody Washington University School of Medicine Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Bennett, Rachel E. and Brody, David L., ,"Acute reduction of microglia does not alter axonal injury in a mouse model of repetitive concussive traumatic brain injury." Journal of Neurotrauma.31,9. 1647-1663. (2014). https://digitalcommons.wustl.edu/open_access_pubs/4711 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. JOURNAL OF NEUROTRAUMA 31:1647–1663 (October 1, 2014) ª Mary Ann Liebert, Inc. DOI: 10.1089/neu.2013.3320 Acute Reduction of Microglia Does Not Alter Axonal Injury in a Mouse Model of Repetitive Concussive Traumatic Brain Injury Rachel E. Bennett and David L. Brody Abstract The pathological processes that lead to long-term consequences of multiple concussions are unclear. Primary mechanical damage to axons during concussion is likely to contribute to dysfunction. Secondary damage has been hypothesized to be induced or exacerbated by inflammation. The main inflammatory cells in the brain are microglia, a type of macrophage. This research sought to determine the contribution of microglia to axon degeneration after repetitive closed-skull traumatic brain injury (rcTBI) using CD11b-TK (thymidine kinase) mice, a valganciclovir-inducible model of macrophage depletion. -
Schwann Cells (Cell Culture/Laminin) SETH PORTER*T, Luis GLASER*T, and RICHARD P
Proc. Natl. Acad. Sci. USA Vol. 84, pp. 7768-7772, November 1987 Neurobiology Release of autocrine growth factor by primary and immortalized Schwann cells (cell culture/laminin) SETH PORTER*t, Luis GLASER*t, AND RICHARD P. BUNGEt Departments of *Biological Chemistry and tAnatomy and Neurobiology, Washington University School of Medicine, St. Louis, MO 63110; and tDepartments of Biology and Biochemistry, University of Miami, Coral Gables, FL 33156 Communicated by Gerald D. Fischbach, July 20, 1987 ABSTRACT Schwann cells derived from neonatal rat proliferation. Because Schwann cells secrete laminin and sciatic nerve are quiescent in culture unless treated with specific form a basement membrane at an initial stage of neuronal mitogens. The use of glial growth factor (GGF) and forskolin ensheathment (21), it is important to establish the role of has been found to be an effective method for stimulating these components in the control of proliferation and differ- proliferation of Schwann cells on a poly(L-lysine) substratum entiation. while maintaining their ability to myelinate axons in vitro. We We report that repetitive passaging of Schwann cells find that repetitive passaging of Schwann cells with GGF and derived from neonatal rat can result in a population of forskolin results in the loss of normal growth control; the cells immortalized cells that, depending upon their duration in are able to proliferate without added mitogens. The immor- culture, display all or most ofthe functional characteristics of talized cells grow continuously in the absence of added growth a primary Schwann cell. It was found that both immortalized factor and in the presence or absence of serum yet continue to and primary Schwann cells secrete growth-promoting activ- express distinctive Schwann cell-surface antigens. -
Clustering of Na+ Channels and Node of Ranvier Formation in Remyelinating Axons
The Journal of Neuroscience, January 1995, 15(l): 492503 Clustering of Na+ Channels and Node of Ranvier Formation in Remyelinating Axons Sanja Dugandgija-NovakoviC,’ Adam G. Koszowski,2 S. Rock Levinson,2 and Peter Shragerl ‘Department of Physiology, University of Rochester Medical Center, Rochester, New York 14642 and 2Department of Physiology, University of Colorado Health Sciences Center, Denver, Colorado 80262 Polyclonal antibodies were raised against a well conserved nodal regions(Black et al., 1990). The density of Na+ channels, region of the vertebrate Na+ channel and were affinity pu- in particular, is about 25 times higher at nodesof Ranvier than rified for use in immunocytochemistry. Focal demyelination at internodal sites (Shrager, 1989). There has been vigorous of rat sciatic axons was initiated by an intraneural injection debate over the mechanism of Na+ channel clustering during of lysolecithin and Na+ channel clustering was followed at myelination, particularly with respect to the role of Schwann several stages of myelin removal and repair. At 1 week post- cells, and studies have included both developing nerve and injection axons contained long, fully demyelinated regions. pathological conditions (Ellisman, 1979; Rosenbluth, 1979; Ro- Na+ channel clusters appeared only at heminodes forming senbluth and Blakemore, 1984; Le Beau et al., 1987; England the borders of these zones, and at widely spaced isolated et al., 1990, 1991; Joe and Angelides, 1992, 1993).There remain sites that may represent former nodes of Ranvier. Over the many interesting questions, particularly regarding remodeling next few days proliferating Schwann cells adhered to axons that occurs following myelin disruption. When axons are de- and began to extend processes. -
Schwann Cell Processes Guide Regeneration of Peripheral Axons
Neuron, Vol. 14, 125-132, January, 1995, Copyright © 1995 by Cell Press Schwann Cell Processes Guide Regeneration of Peripheral Axons Young-Jin Son and Wesley J. Thompson come immunoreactive (Astrow et al., 1994). There is a Center for Developmental Biology similar up-regulation of immunoreactivity in Schwann cells and Department of Zoology of the nerve following axonal degeneration. University of Texas Motor axons commonly reinnervate muscle fibers by Austin, Texas 78712 growing down the old endoneurial Schwann cell tubes leading to each endplate. Some axons continue to grow beyond their endplates (Tello, 1907; Ramon y Cajal, 1928; Summary Gutmann and Young, 1944; Letinsky et al., 1976; Gorio et al., 1983), forming so-called "escaped" fibers. In some Terminal Schwann cells overlying the neuromuscular cases these escaped fibers grow to reinnervate nearby junction sprout elaborate processes upon muscle de- endplates. Muscle fibers reinnervated by an escaped fiber nervation. We show here that motor axons use these from an adjacent endplate as well as by an axon regenerat- processes as guides/substrates during regeneration; ing down the old Schwann cell tube become polyneuro- in so doing, they escape the confines of endplates and nally innervated (Rich and Lichtman, 1989). We wondered grow between endplates to generate polyneuronal in- whether the processes extended by terminal Schwann nervation. We also show that Schwann cells in the cells play a role in the generation of escaped fibers and nerve provide similar guidance. Axons extend from the polyneuronal reinnervation. Using immunocytochemistry, cut end of a nerve in association with Schwann cell we found that motor axons use processes of terminal processes and appear to navigate along them. -
Was Not Reached, However, Even After Six to Sevenhours. A
PROTEIN SYNTHESIS IN THE ISOLATED GIANT AXON OF THE SQUID* BY A. GIUDITTA,t W.-D. DETTBARN,t AND MIROSLAv BRZIN§ MARINE BIOLOGICAL LABORATORY, WOODS HOLE, MASSACHUSETTS Communicated by David Nachmansohn, February 2, 1968 The work of Weiss and his associates,1-3 and more recently of a number of other investigators,4- has established the occurrence of a flux of materials from the soma of neurons toward the peripheral regions of the axon. It has been postulated that this mechanism would account for the origin of most of the axonal protein, although the time required to cover the distance which separates some axonal tips from their cell bodies would impose severe delays.4 On the other hand, a number of observations7-9 have indicated the occurrence of local mechanisms of synthesis in peripheral axons, as suggested by the kinetics of appearance of individual proteins after axonal transection. In this paper we report the incorporation of radioactive amino acids into the protein fraction of the axoplasm and of the axonal envelope obtained from giant axons of the squid. These axons are isolated essentially free from small fibers and connective tissue, and pure samples of axoplasm may be obtained by extru- sion of the axon. Incorporation of amino acids into axonal protein has recently been reported using systems from mammals'0 and fish."I Materials and Methods.-Giant axons of Loligo pealii were dissected and freed from small fibers: they were tied at both ends. Incubations were carried out at 18-20° in sea water previously filtered through Millipore which contained 5 mM Tris pH 7.8 and 10 Muc/ml of a mixture of 15 C'4-labeled amino acids (New England Nuclear Co., Boston, Mass.). -
Glial Cells Are Involved in Itch Processing
Acta Derm Venereol 2016; 96: 723–727 REVIEW ARTICLE Glial Cells are Involved in Itch Processing Hjalte H. ANDERSEN, Lars ARENDT-NIELSEN and Parisa GAZERANI SMI®, Department of Health Science and Technology, School of Medicine, Aalborg University, Denmark Recent discoveries in itch neurophysiology include itch- worsening the skin lesions and leading to more or pro- selective neuronal pathways, the clinically relevant non- longed pruritus (5, 6). This phenomenon, known as the histaminergic pathway, and elucidation of the notable itch–scratch–itch vicious cycle, is physiologically com- similarities and differences between itch and pain. Po- plex and is likely to involve: local inflammatory medi- tential involvement of glial cells in itch processing and ators and structural changes, reward components, and the possibility of glial modulation of chronic itch have the autonomic nervous system (5, 7). In most conditions recently been identified, similarly to the established glial associated with chronic itch, very limited or ambiguous modulation of pain processing. This review outlines the evidence is found for the effectiveness of pharmaceutical similarities and differences between itch and pain, and interventions, and the evidence is often characterized by how different types of central and peripheral glial cells off-label small-scale trials or case series. Histamine is may be differentially involved in the development of ch- now widely accepted not to have a key role in evoking ronic itch akin to their more investigated role in chronic itch in most of the clinical conditions characterized by pain. Improvements are needed in the management of chronic pruritus (for an overview of itch neurobiology chronic itch, and future basic and interventional studies and mechanisms, see recent reviews in the field [8, 9]). -
(Caspr) and Contactin Form a Complex That Is Targeted to the Paranodal Junctions During Myelination
The Journal of Neuroscience, November 15, 2000, 20(22):8354–8364 Contactin-Associated Protein (Caspr) and Contactin Form a Complex That Is Targeted to the Paranodal Junctions during Myelination Jose C. Rios,1 Carmen V. Melendez-Vasquez,1 Steven Einheber,1 Marc Lustig,2 Martin Grumet,2 John Hemperly,5 Elior Peles,6 and James L. Salzer1,3,4 Departments of 1Cell Biology, 2Pharmacology, 3Neurology, and the 4Kaplan Cancer Center, New York University School of Medicine, New York, New York 10016, 5BD Technologies, Research Triangle Park, North Carolina 27709, and 6Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel Specialized paranodal junctions form between the axon and the associated specifically with Caspr in the paranodes, whereas a closely apposed paranodal loops of myelinating glia. They are higher-molecular-weight form of contactin, not associated with interposed between sodium channels at the nodes of Ranvier Caspr, is present in central nodes of Ranvier. These results and potassium channels in the juxtaparanodal regions; their suggest that the targeting of contactin to different axonal do- precise function and molecular composition have been elusive. mains may be determined, in part, via its association with Caspr. We previously reported that Caspr (contactin-associated protein) Treatment of myelinating cocultures of Schwann cells and neu- is a major axonal constituent of these junctions (Einheber et al., rons with RPTP–Fc, a soluble construct containing the carbonic 1997). We now report that contactin colocalizes and forms a cis anhydrase domain of the receptor protein tyrosine phosphatase complex with Caspr in the paranodes and juxtamesaxon. -
Regulation of Myelin Structure and Conduction Velocity by Perinodal Astrocytes
Correction NEUROSCIENCE Correction for “Regulation of myelin structure and conduc- tion velocity by perinodal astrocytes,” by Dipankar J. Dutta, Dong Ho Woo, Philip R. Lee, Sinisa Pajevic, Olena Bukalo, William C. Huffman, Hiroaki Wake, Peter J. Basser, Shahriar SheikhBahaei, Vanja Lazarevic, Jeffrey C. Smith, and R. Douglas Fields, which was first published October 29, 2018; 10.1073/ pnas.1811013115 (Proc. Natl. Acad. Sci. U.S.A. 115,11832–11837). The authors note that the following statement should be added to the Acknowledgments: “We acknowledge Dr. Hae Ung Lee for preliminary experiments that informed the ultimate experimental approach.” Published under the PNAS license. Published online June 10, 2019. www.pnas.org/cgi/doi/10.1073/pnas.1908361116 12574 | PNAS | June 18, 2019 | vol. 116 | no. 25 www.pnas.org Downloaded by guest on October 2, 2021 Regulation of myelin structure and conduction velocity by perinodal astrocytes Dipankar J. Duttaa,b, Dong Ho Wooa, Philip R. Leea, Sinisa Pajevicc, Olena Bukaloa, William C. Huffmana, Hiroaki Wakea, Peter J. Basserd, Shahriar SheikhBahaeie, Vanja Lazarevicf, Jeffrey C. Smithe, and R. Douglas Fieldsa,1 aSection on Nervous System Development and Plasticity, The Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892; bThe Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD 20817; cMathematical and Statistical Computing Laboratory, Office of Intramural Research, Center for Information