Mechanisms of Node of Ranvier Assembly
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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. -
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. -
Thenerveimpulse05.Pdf
The nerve impulse. INTRODUCTION Axons are responsible for the transmission of information between different points of the nervous system and their function is analogous to the wires that connect different points in an electric circuit. However, this analogy cannot be pushed very far. In an electrical circuit the wire maintains both ends at the same electrical potential when it is a perfect conductor or it allows the passage of an electron current when it has electrical resistance. As we will see in these lectures, the axon, as it is part of a cell, separates its internal medium from the external medium with the plasma membrane and the signal conducted along the axon is a transient potential difference1 that appears across this membrane. This potential difference, or membrane potential, is the result of ionic gradients due to ionic concentration differences across the membrane and it is modified by ionic flow that produces ionic currents perpendicular to the membrane. These ionic currents give rise in turn to longitudinal currents closing local ionic current circuits that allow the regeneration of the membrane potential changes in a different region of the axon. This process is a true propagation instead of the conduction phenomenon occurring in wires. To understand this propagation we will study the electrical properties of axons, which include a description of the electrical properties of the membrane and how this membrane works in the cylindrical geometry of the axon. Much of our understanding of the ionic mechanisms responsible for the initiation and propagation of the action potential (AP) comes from studies on the squid giant axon by A. -
Spatial Extent of Neurons: Dendrites and Axons
Spatial extent of neurons: dendrites and axons Morphological diversity of neurons Cortical pyramidal cell Purkinje cell Retinal ganglion cells Motoneurons Dendrites: spiny vs non-spiny Recording and simulating dendrites Axons - myelinated vs unmyelinated Axons - myelinated vs unmyelinated • Myelinated axons: – Long-range axonal projections (motoneurons, long-range cortico-cortical connections in white matter, etc) – Saltatory conduction; – Fast propagation (10s of m/s) • Unmyelinated axons: – Most local axonal projections – Continuous conduction – Slower propagation (a few m/s) Recording from axons Recording from axons Recording from axons - where is the spike generated? Modeling neuronal processes as electrical cables • Axial current flowing along a neuronal cable due to voltage gradient: V (x + ∆x; t) − V (x; t) = −Ilong(x; t)RL ∆x = −I (x; t) r long πa2 L where – RL: total resistance of a cable of length ∆x and radius a; – rL: specific intracellular resistivity • ∆x ! 0: πa2 @V Ilong(x; t) = − (x; t) rL @x The cable equation • Current balance in a cylinder of width ∆x and radius a • Axial currents leaving/flowing into the cylinder πa2 @V @V Ilong(x + ∆x; t) − Ilong(x; t) = − (x + ∆x; t) − (x; t) rL @x @x • Ionic current(s) flowing into/out of the cell 2πa∆xIion(x; t) • Capacitive current @V I (x; t) = 2πa∆xc cap M @t • Kirschoff law Ilong(x + ∆x; t) − Ilong(x; t) + 2πa∆xIion(x; t) + Icap(x; t) = 0 • In the ∆x ! 0 limit: @V a @2V cM = 2 − Iion @t 2rL @x Compartmental appoach Compartmental approach Modeling passive dendrites: Cable equation -
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. -
Structure and Function Relationship in Nerve Cells & Membrane Potential
Structure and Function Relationship in Nerve Cells & Membrane Potential Asist. Prof. Aslı AYKAÇ NEU Faculty of Medicine Biophysics Nervous System Cells • Glia – Not specialized for information transfer – Support neurons • Neurons (Nerve Cells) – Receive, process, and transmit information Neurons • Neuron Doctrine – The neuron is the functional unit of the nervous system • Specialized cell type – have very diverse in structure and function Neuron: Structure/Function • designed to receive, process, and transmit information – Dendrites: receive information from other neurons – Soma: “cell body,” contains necessary cellular machinery, signals integrated prior to axon hillock – Axon: transmits information to other cells (neurons, muscles, glands) • Information travels in one direction – Dendrite → soma → axon How do neurons work? • Function – Receive, process, and transmit information – Conduct unidirectional information transfer • Signals – Chemical – Electrical Membrane Potential Because of motion of positive and negative ions in the body, electric current generated by living tissues. What are these electrical signals? • receptor potentials • synaptic potentials • action potentials Why are these electrical signals important? These signals are all produced by temporary changes in the current flow into and out of cell that drives the electrical potential across the cell membrane away from its resting value. The resting membrane potential The electrical membrane potential across the membrane in the absence of signaling activity. Two type of ions channels in the membrane – Non gated channels: always open, important in maintaining the resting membrane potential – Gated channels: open/close (when the membrane is at rest, most gated channels are closed) Learning Objectives • How transient electrical signals are generated • Discuss how the nongated ion channels establish the resting potential. -
Myelin Biogenesis Is Associated with Pathological Ultrastructure That Is
bioRxiv preprint doi: https://doi.org/10.1101/2021.02.02.429485; this version posted February 4, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Myelin biogenesis is associated with pathological ultrastructure that 2 is resolved by microglia during development 3 4 5 Minou Djannatian1,2*, Ulrich Weikert3, Shima Safaiyan1,2, Christoph Wrede4, Cassandra 6 Deichsel1,2, Georg Kislinger1,2, Torben Ruhwedel3, Douglas S. Campbell5, Tjakko van Ham6, 7 Bettina Schmid2, Jan Hegermann4, Wiebke Möbius3, Martina Schifferer2,7, Mikael Simons1,2,7* 8 9 1Institute of Neuronal Cell Biology, Technical University Munich, 80802 Munich, Germany 10 2German Center for Neurodegenerative Diseases (DZNE), 81377 Munich, Germany 11 3Max-Planck Institute of Experimental Medicine, 37075 Göttingen, Germany 12 4Institute of Functional and Applied Anatomy, Research Core Unit Electron Microscopy, 13 Hannover Medical School, 30625, Hannover, Germany 14 5Department of Neuronal Remodeling, Graduate School of Pharmaceutical Sciences, Kyoto 15 University, Sakyo-ku, Kyoto 606-8501, Japan. 16 6Department of Clinical Genetics, Erasmus MC, University Medical Center Rotterdam, 3015 CN, 17 the Netherlands 18 7Munich Cluster of Systems Neurology (SyNergy), 81377 Munich, Germany 19 20 *Correspondence: [email protected] or [email protected] 21 Keywords 22 Myelination, degeneration, phagocytosis, microglia, oligodendrocytes, phosphatidylserine 23 24 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.02.02.429485; this version posted February 4, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. -
The Importance of Myelin
The importance of myelin Nerve cell Nerves carry messages between different parts of the body insulating outer coating of nerves (myelin sheath) Normal nerve Damaged nerve myelin myelin sheath is sheath is intact damaged or destroyed message moves quickly message moves slowly Nerve cells transmit impulses Nerve cells have a long, thin, flexible fibre that transmits impulses. These impulses are electrical signals that travel along the length of the nerve. Nerve fibres are long to enable impulses to travel between distant parts of the body, such as the spinal cord and leg muscles. Myelin speeds up impulses Most nerve fibres are surrounded by an insulating, fatty sheath called myelin, which acts to speed up impulses. The myelin sheath contains periodic breaks called nodes of Ranvier. By jumping from node to node, the impulse can travel much more quickly than if it had to travel along the entire length of the nerve fibre. Myelinated nerves can transmit a signal at speeds as high as 100 metres per second – as fast as a Formula One racing car. normal damaged nerve nerve Loss of myelin leads to a variety of symptoms If the myelin sheath surrounding nerve fibres is damaged or destroyed, transmission of nerve impulses is slowed or blocked. The impulse now has to flow continuously along the whole nerve fibre – a process that is much slower than jumping from node to node. Loss of myelin can also lead to ‘short-circuiting’ of nerve impulses. An area where myelin has been destroyed is called a lesion or plaque. This slowing and ‘short-circuiting’ of nerve impulses by lesions leads to a variety of symptoms related to nervous system activity. -
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]). -
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 -
The Myelin-Forming Cells of the Nervous System (Oligodendrocytes and Schwann Cells)
The Myelin-Forming Cells of the Nervous System (oligodendrocytes and Schwann cells) Oligodendrocyte Schwann Cell Oligodendrocyte function Saltatory (jumping) nerve conduction Oligodendroglia PMD PMD Saltatory (jumping) nerve conduction Investigating the Myelinogenic Potential of Individual Oligodendrocytes In Vivo Sparse Labeling of Oligodendrocytes CNPase-GFP Variegated expression under the MBP-enhancer Cerebral Cortex Corpus Callosum Cerebral Cortex Corpus Callosum Cerebral Cortex Caudate Putamen Corpus Callosum Cerebral Cortex Caudate Putamen Corpus Callosum Corpus Callosum Cerebral Cortex Caudate Putamen Corpus Callosum Ant Commissure Corpus Callosum Cerebral Cortex Caudate Putamen Piriform Cortex Corpus Callosum Ant Commissure Characterization of Oligodendrocyte Morphology Cerebral Cortex Corpus Callosum Caudate Putamen Cerebellum Brain Stem Spinal Cord Oligodendrocytes in disease: Cerebral Palsy ! CP major cause of chronic neurological morbidity and mortality in children ! CP incidence now about 3/1000 live births compared to 1/1000 in 1980 when we started intervening for ELBW ! Of all ELBW {gestation 6 mo, Wt. 0.5kg} , 10-15% develop CP ! Prematurely born children prone to white matter injury {WMI}, principle reason for the increase in incidence of CP ! ! 12 Cerebral Palsy Spectrum of white matter injury ! ! Macro Cystic Micro Cystic Gliotic Khwaja and Volpe 2009 13 Rationale for Repair/Remyelination in Multiple Sclerosis Oligodendrocyte specification oligodendrocytes specified from the pMN after MNs - a ventral source of oligodendrocytes