Neuronal Signaling Neuroscience Fundamentals > the Nerve Cell > the Nerve Cell
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Glossary - Cellbiology
1 Glossary - Cellbiology Blotting: (Blot Analysis) Widely used biochemical technique for detecting the presence of specific macromolecules (proteins, mRNAs, or DNA sequences) in a mixture. A sample first is separated on an agarose or polyacrylamide gel usually under denaturing conditions; the separated components are transferred (blotting) to a nitrocellulose sheet, which is exposed to a radiolabeled molecule that specifically binds to the macromolecule of interest, and then subjected to autoradiography. Northern B.: mRNAs are detected with a complementary DNA; Southern B.: DNA restriction fragments are detected with complementary nucleotide sequences; Western B.: Proteins are detected by specific antibodies. Cell: The fundamental unit of living organisms. Cells are bounded by a lipid-containing plasma membrane, containing the central nucleus, and the cytoplasm. Cells are generally capable of independent reproduction. More complex cells like Eukaryotes have various compartments (organelles) where special tasks essential for the survival of the cell take place. Cytoplasm: Viscous contents of a cell that are contained within the plasma membrane but, in eukaryotic cells, outside the nucleus. The part of the cytoplasm not contained in any organelle is called the Cytosol. Cytoskeleton: (Gk. ) Three dimensional network of fibrous elements, allowing precisely regulated movements of cell parts, transport organelles, and help to maintain a cell’s shape. • Actin filament: (Microfilaments) Ubiquitous eukaryotic cytoskeletal proteins (one end is attached to the cell-cortex) of two “twisted“ actin monomers; are important in the structural support and movement of cells. Each actin filament (F-actin) consists of two strands of globular subunits (G-Actin) wrapped around each other to form a polarized unit (high ionic cytoplasm lead to the formation of AF, whereas low ion-concentration disassembles AF). -
Biopsychology 2012 – Sec 003 (Dr
Biopsychology 2012 – sec 003 (Dr. Campeau) Study Guide for First Midterm What are some fun facts about the human brain? - there are approximately 100 billion neurons in the brain; - each neuron makes between 1000 to 10000 connections with other neurons; - speed of action potentials varies from less than 1 mph and up to 100 mph. What is a neuron? A very specialized cell type whose function is to receive, process, and send information; these cells are found in the central nervous system (CNS – brain, spinal cord, retina) and the peripheral nervous system (PNS – the rest of the body). What is a nerve? They are axons of individual neurons in bundles or strands of many axons. What are the major parts of a neuron? - cell membrane: “skin” of the neuron; - cytoplasm: everything inside the skin; - nucleus: contains chromosomes (DNA); - ribosomes: generate proteins from mRNA; - mitochondria: energy “generator” of cells (produce ATP); - mitochondria: moves “stuff” inside the neuron (like a tow rope); - soma: cell body, excluding dendrites and axons; - dendrites and spines: part of the neuron usually receiving information from other neurons; - axons: part of the neuron that transmits information to other neurons; - myelin sheath: surrounds axons and provides electrical “insulation”; - nodes of Ranvier: small area on axons devoid of myelin sheath; - presynaptic terminal: area of neuron where neurotransmitter is stored and released by action potentials. What are the different neuron types according to function? 1. Sensory neurons: neurons specialized to “receive” information about the environment. 2. Motor neurons: neurons specialized to produce movement (contraction of muscles). 3. Interneurons or Intrinsic neurons: neurons, usually with short axons, that handle local information. -
The Creation of Neuroscience
The Creation of Neuroscience The Society for Neuroscience and the Quest for Disciplinary Unity 1969-1995 Introduction rom the molecular biology of a single neuron to the breathtakingly complex circuitry of the entire human nervous system, our understanding of the brain and how it works has undergone radical F changes over the past century. These advances have brought us tantalizingly closer to genu- inely mechanistic and scientifically rigorous explanations of how the brain’s roughly 100 billion neurons, interacting through trillions of synaptic connections, function both as single units and as larger ensem- bles. The professional field of neuroscience, in keeping pace with these important scientific develop- ments, has dramatically reshaped the organization of biological sciences across the globe over the last 50 years. Much like physics during its dominant era in the 1950s and 1960s, neuroscience has become the leading scientific discipline with regard to funding, numbers of scientists, and numbers of trainees. Furthermore, neuroscience as fact, explanation, and myth has just as dramatically redrawn our cultural landscape and redefined how Western popular culture understands who we are as individuals. In the 1950s, especially in the United States, Freud and his successors stood at the center of all cultural expla- nations for psychological suffering. In the new millennium, we perceive such suffering as erupting no longer from a repressed unconscious but, instead, from a pathophysiology rooted in and caused by brain abnormalities and dysfunctions. Indeed, the normal as well as the pathological have become thoroughly neurobiological in the last several decades. In the process, entirely new vistas have opened up in fields ranging from neuroeconomics and neurophilosophy to consumer products, as exemplified by an entire line of soft drinks advertised as offering “neuro” benefits. -
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, -
Oligodendrocytes in Development, Myelin Generation and Beyond
cells Review Oligodendrocytes in Development, Myelin Generation and Beyond Sarah Kuhn y, Laura Gritti y, Daniel Crooks and Yvonne Dombrowski * Wellcome-Wolfson Institute for Experimental Medicine, Queen’s University Belfast, Belfast BT9 7BL, UK; [email protected] (S.K.); [email protected] (L.G.); [email protected] (D.C.) * Correspondence: [email protected]; Tel.: +0044-28-9097-6127 These authors contributed equally. y Received: 15 October 2019; Accepted: 7 November 2019; Published: 12 November 2019 Abstract: Oligodendrocytes are the myelinating cells of the central nervous system (CNS) that are generated from oligodendrocyte progenitor cells (OPC). OPC are distributed throughout the CNS and represent a pool of migratory and proliferative adult progenitor cells that can differentiate into oligodendrocytes. The central function of oligodendrocytes is to generate myelin, which is an extended membrane from the cell that wraps tightly around axons. Due to this energy consuming process and the associated high metabolic turnover oligodendrocytes are vulnerable to cytotoxic and excitotoxic factors. Oligodendrocyte pathology is therefore evident in a range of disorders including multiple sclerosis, schizophrenia and Alzheimer’s disease. Deceased oligodendrocytes can be replenished from the adult OPC pool and lost myelin can be regenerated during remyelination, which can prevent axonal degeneration and can restore function. Cell population studies have recently identified novel immunomodulatory functions of oligodendrocytes, the implications of which, e.g., for diseases with primary oligodendrocyte pathology, are not yet clear. Here, we review the journey of oligodendrocytes from the embryonic stage to their role in homeostasis and their fate in disease. We will also discuss the most common models used to study oligodendrocytes and describe newly discovered functions of oligodendrocytes. -
Nernst Potentials and Membrane Potential Changes
UNDERSTANDING MEMBRANE POTENTIAL CHANGES IN TERMS OF NERNST POTENTIALS: For seeing how a change in conductance to ions affects the membrane potential, follow these steps: 1. Make a graph with membrane potential on the vertical axis (-100 to +55) and time on the horizontal axis. 2. Draw dashed lines indicating the standard Nernst potential (equilibrium potential) for each ion: Na+ = +55 mV, K+ = -90mV, Cl- = -65 mV. 3. Draw lines below the horizontal axis showing the increased conductance to individual ions. 4. Start plotting the membrane potential on the left. Most graphs will start at resting potential (-70 mV) 5. When current injection (Stim) is present, move the membrane potential upward to Firing threshold. 6. For the time during which membrane conductance to a particular ion increases, move the membrane potential toward the Nernst potential for that ion. 7. During the time when conductance to a particular ion decreases, move the membrane potential away from the Nernst potential of that ion, toward a position which averages the conductances of the other ions. 8. When conductances return to their original value, membrane potential will go to its starting value. +55mV ACTION POTENTIAL SYNAPTIC POTENTIALS 0mV Membrane potential Firing threshold Firing threshold -65mV -90mV Time Time Na+ K+ Conductances Stim CHANGES IN MEMBRANE POTENTIAL ALLOW NEURONS TO COMMUNICATE The membrane potential of a neuron can be measured with an intracellular electrode. This 1 provides a measurement of the voltage difference between the inside of the cell and the outside. When there is no external input, the membrane potential will usually remain at a value called the resting potential. -
Neurotransmitter Actions
Central University of South Bihar Panchanpur, Gaya, India E-Learning Resources Department of Biotechnology NB: These materials are taken/borrowed/modified/compiled from various resources like research articles and freely available internet websites, and are meant to be used solely for the teaching purpose in a public university, and for serving the needs of specified educational programmes. Dr. Jawaid Ahsan Assistant Professor Department of Biotechnology Central University of South Bihar (CUSB) Course Code: MSBTN2003E04 Course Name: Neuroscience Neurotransmitter Actions • Excitatory Action: – A neurotransmitter that puts a neuron closer to an action potential (facilitation) or causes an action potential • Inhibitory Action: – A neurotransmitter that moves a neuron further away from an action potential • Response of neuron: – Responds according to the sum of all the neurotransmitters received at one time Neurotransmitters • Acetylcholine • Monoamines – modified amino acids • Amino acids • Neuropeptides- short chains of amino acids • Depression: – Caused by the imbalances of neurotransmitters • Many drugs imitate neurotransmitters – Ex: Prozac, zoloft, alcohol, drugs, tobacco Release of Neurotransmitters • When an action potential reaches the end of an axon, Ca+ channels in the neuron open • Causes Ca+ to rush in – Cause the synaptic vesicles to fuse with the cell membrane – Release the neurotransmitters into the synaptic cleft • After binding, neurotransmitters will either: – Be destroyed in the synaptic cleft OR – Taken back in to surrounding neurons (reuptake) Excitable cells: Definition: Refers to the ability of some cells to be electrically excited resulting in the generation of action potentials. Neurons, muscle cells (skeletal, cardiac, and smooth), and some endocrine cells (e.g., insulin- releasing pancreatic β cells) are excitable cells. -
Rapid and Efficient Generation of Oligodendrocytes from Human
Rapid and efficient generation of oligodendrocytes PNAS PLUS from human induced pluripotent stem cells using transcription factors Marc Ehrlicha,b, Sabah Mozafaric,d,e,f, Michael Glatzab, Laura Starosta,b, Sergiy Velychkob, Anna-Lena Hallmanna,b, Qiao-Ling Cuig, Axel Schambachh, Kee-Pyo Kimb, Corinne Bachelinc,d,e,f, Antoine Marteync,d,e,f, Gunnar Hargusa,b, Radia Marie Johnsoni, Jack Antelg, Jared Sterneckertj, Holm Zaehresb,k, Hans R. Schölerb,l, Anne Baron-Van Evercoorenc,d,e,f, and Tanja Kuhlmanna,1 aInstitute of Neuropathology, University Hospital Münster, 48149 Muenster, Germany; bDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, 48149 Muenster, Germany; cINSERM, U1127, F-75013 Paris, France; dCNRS, UMR 7225, F-75013 Paris, France; eSorbonne Universités, Université Pierre et Marie Curie Paris 06, UM-75, F-75005 Paris, France; fInstitut du Cerveau et de la Moelle epinière-Groupe Hospitalier Pitié-Salpêtrière, F-75013 Paris, France; gMontreal Neurological Institute, McGill University, Montreal, QC, Canada H3A 2B4; hInstitute of Experimental Hematology, Hannover Medical School, 30625 Hannover, Germany; iDepartment of Physiology, McGill University, Montreal, QC, Canada H3A 2B4; jDFG Research Center for Regenerative Therapies, Technische Universität Dresden, 01307 Dresden, Germany; kMedical Faculty, Department of Anatomy and Molecular Embryology, Ruhr-University Bochum, 44801 Bochum, Germany; and lMedicial Faculty, Westphalian Wilhelms-University of Muenster, 48149 Muenster, Germany Edited by Brigid L. M. Hogan, Duke University Medical Center, Durham, NC, and approved February 1, 2017 (received for review August 30, 2016) Rapid and efficient protocols to generate oligodendrocytes (OL) more, these protocols require long culture periods (70–150 d) to + from human induced pluripotent stem cells (iPSC) are currently obtain O4 OL and show limited efficiency (9–12). -
Neurotransmitter Release Is Blocked Intracellularly by Botulinum
Proc. Nati. Acad. Sci. USA Vol. 85, pp. 4090-4094, June 1988 Neurobiology Neurotransmitter release is blocked intracellularly by botulinum neurotoxin, and this requires uptake of both toxin polypeptides by a process mediated by the larger chain (cholinergic synapse/noncholinergic synapse/intraceliular in ection/quantal release/Aplysia cahifornica) B. POULAIN*, L. TAUC*, E. A. MAISEYt, J. D. F. WADSWORTHt, P. M. MOHANt, AND J. 0. DOLLYt *Laboratoire de Neurobiologie Cellulaire et Moldculaire, Centre National de la Recherche Scientifique, Gif-sur-Yvette, 91190 France; tDepartment of Biochemistry, Imperial College, London SW7 2AZ, United Kingdom; and tDepartment of Zoology, S.V. University, Tirupati, 515502, A.P. India Communicated by C. Ladd Prosser, February 17, 1988 ABSTRACT Botulinum neurotoxins (types A and B), lacking for a multistep process of intoxication (2, 9) and, in which are microbial proteins consisting of two disulfide-linked particular, for the inactivation by BoNT of an intracellular chains, inhibit specifically and with high potency the release of component that is involved in the release of AcCho and, acetylcholine from peripheral nerve terminals. As a prerequi- perhaps, all transmitters. Furthermore, the role of the HC site for a long-term development of effective treatments for and LC of BoNT in such a scheme for its neuroparalytic botulism, the internalization and inhibitory action of the toxin action remains to be established. Pertinent questions to be and its constituent chains were examined by electrophysiolog- answered include (i) whether the HC, by virtue of its ability ical methods at identified synapses inAplysia preparations that to recognize neural membrane receptors (8, 10), allows allow both intracellular and bath application of the neurotox- functional recognition ofcholinergic terminals and whether it ins. -
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. -
Absence of S100A4 in the Mouse Lens Induces an Aberrant Retina-Specific Differentiation Program and Cataract
www.nature.com/scientificreports OPEN Absence of S100A4 in the mouse lens induces an aberrant retina‑specifc diferentiation program and cataract Rupalatha Maddala1*, Junyuan Gao2, Richard T. Mathias2, Tylor R. Lewis1, Vadim Y. Arshavsky1,3, Adriana Levine4, Jonathan M. Backer4,5, Anne R. Bresnick4 & Ponugoti V. Rao1,3* S100A4, a member of the S100 family of multifunctional calcium‑binding proteins, participates in several physiological and pathological processes. In this study, we demonstrate that S100A4 expression is robustly induced in diferentiating fber cells of the ocular lens and that S100A4 (−/−) knockout mice develop late‑onset cortical cataracts. Transcriptome profling of lenses from S100A4 (−/−) mice revealed a robust increase in the expression of multiple photoreceptor‑ and Müller glia‑specifc genes, as well as the olfactory sensory neuron‑specifc gene, S100A5. This aberrant transcriptional profle is characterized by corresponding increases in the levels of proteins encoded by the aberrantly upregulated genes. Ingenuity pathway network and curated pathway analyses of diferentially expressed genes in S100A4 (−/−) lenses identifed Crx and Nrl transcription factors as the most signifcant upstream regulators, and revealed that many of the upregulated genes possess promoters containing a high‑density of CpG islands bearing trimethylation marks at histone H3K27 and/or H3K4, respectively. In support of this fnding, we further documented that S100A4 (−/−) knockout lenses have altered levels of trimethylated H3K27 and H3K4. Taken together, -
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