4-Nervous-System-Structure-PPT.Pdf
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
7.016 Introductory Biology Fall 2018
7.016: Fall 2018: MIT 7.016 Recitation 15 – Fall 2018 (Note: The recitation summary should NOT be regarded as the substitute for lectures) (This material is COPYRIGHT protected.) Summary of Lecture 22 (11/2): Neurons and action potentials: Ions can move across membranes through pumps and channels. Integral membrane proteins like these cross the membrane via transmembrane domains. Pumps are ATPases that set up the concentration gradients of ions across cell membranes, such that K+ is high inside cells and other ions (such as Cl–, Na+, and Ca2+) are high outside cells. A membrane potential is only set up by ions that move freely across the membrane through open channels, creating one side of the membrane that is more positive relative to the other side. This movement of ions does not dissipate the concentration gradient because the number of ions that move to generate a membrane potential is very small compared to the number of ions that need to be pumped to create a concentration gradient. Most cell membranes only contain open K+ channels and thus only K+ flows freely across membranes through channels; K+ is high inside, causing it to flow outside, giving the inside of cells a negative membrane potential. Ions can move across the membrane through open ion channels. Two forces act to dictate this movement – the concentration gradient and the electrical gradient. Ions move down their concentration gradient through channels, and ions move towards the side of the membrane that harbors the opposite charge. Neurons are the cells of your nervous system that make connections with each other to transmit impulse/ signals. -
Genetic Alteration of the Metal/Redox Modulation of Cav3.2 T-Type
Genetic alteration of the metal/redox modulation of Cav3.2 T-type calcium channel reveals its role in neuronal excitability Tiphaine Voisin, Emmanuel Bourinet, Philippe Lory To cite this version: Tiphaine Voisin, Emmanuel Bourinet, Philippe Lory. Genetic alteration of the metal/redox mod- ulation of Cav3.2 T-type calcium channel reveals its role in neuronal excitability. The Journal of Physiology, Wiley, 2016, 594 (13), pp.3561–74. 10.1113/JP271925. hal-01940961 HAL Id: hal-01940961 https://hal.archives-ouvertes.fr/hal-01940961 Submitted on 30 Nov 2018 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. J Physiol 594.13 (2016) pp 3561–3574 3561 Genetic alteration of the metal/redox modulation of Cav3.2 T-type calcium channel reveals its role in neuronal excitability Tiphaine Voisin1,2,3, Emmanuel Bourinet1,2,3 and Philippe Lory1,2,3 1Centre National pour la Recherche Scientifique UMR 5203, D´epartement de Physiologie, Institut de G´enomique Fonctionnelle, Universit´edeMontpellier, Montpellier, F-34094 France 2Institut National de la Sant´eetdelaRechercheM´edicale, U 1191, Montpellier, F-34094 France Neuroscience 3LabEx ‘Ion Channel Science and Therapeutics’, Montpellier, F-34094 France Key points r In this study, we describe a new knock-in (KI) mouse model that allows the study of the H191-dependent regulation of T-type Cav3.2 channels. -
Electrical Activity of the Heart: Action Potential, Automaticity, and Conduction 1 & 2 Clive M
Electrical Activity of the Heart: Action Potential, Automaticity, and Conduction 1 & 2 Clive M. Baumgarten, Ph.D. OBJECTIVES: 1. Describe the basic characteristics of cardiac electrical activity and the spread of the action potential through the heart 2. Compare the characteristics of action potentials in different parts of the heart 3. Describe how serum K modulates resting potential 4. Describe the ionic basis for the cardiac action potential and changes in ion currents during each phase of the action potential 5. Identify differences in electrical activity across the tissues of the heart 6. Describe the basis for normal automaticity 7. Describe the basis for excitability 8. Describe the basis for conduction of the cardiac action potential 9. Describe how the responsiveness relationship and the Na+ channel cycle modulate cardiac electrical activity I. BASIC ELECTROPHYSIOLOGIC CHARACTERISTICS OF CARDIAC MUSCLE A. Electrical activity is myogenic, i.e., it originates in the heart. The heart is an electrical syncitium (i.e., behaves as if one cell). The action potential spreads from cell-to-cell initiating contraction. Cardiac electrical activity is modulated by the autonomic nervous system. B. Cardiac cells are electrically coupled by low resistance conducting pathways gap junctions located at the intercalated disc, at the ends of cells, and at nexus, points of side-to-side contact. The low resistance pathways (wide channels) are formed by connexins. Connexins permit the flow of current and the spread of the action potential from cell-to-cell. C. Action potentials are much longer in duration in cardiac muscle (up to 400 msec) than in nerve or skeletal muscle (~5 msec). -
Electrolyte Disorders and Arrhythmogenesis
Cardiology Journal 2011, Vol. 18, No. 3, pp. 233–245 Copyright © 2011 Via Medica REVIEW ARTICLE ISSN 1897–5593 Electrolyte disorders and arrhythmogenesis Nabil El-Sherif1, Gioia Turitto2 1State University of NY, Downstate Medical Center and NY Harbor VA Healthcare System, Brooklyn, NY, USA 2Methodist University Hospital, Brooklyn, NY, USA Abstract Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mecha- nisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of elec- trolyte disorders. Potassium (K+) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most signifcant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and + non cardiac drugs are known to suppress the HERG K channel and hence the IK, and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricu- lar tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia de- pends on serum K+ level. At 5.5–7.0 mmol/L K+, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K+, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca++) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathy- roidism, results in shortening of both intervals. -
Two Components of the Cardiac Action Potential I
Two Components of the Cardiac Action Potential I. Voltage-time course and the effect of acet.flcholine on atrial and nodal cells of the rabbit heart ANTONIO PAES de CARVALHO, BRIAN FRANCIS HOFFMAN, and MARILENE de PAULA CARVALHO From the Instituto de Biofisica da Universidade Federal do Rio de Janeiro, Rio de Janeiro (GB), Brazil, and the Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York 10032 ABSTRACT Transmembrane potentials recorded from the rabbit heart in vitro were displayed as voltage against time (V, t display), and dV/dt against voltage (I?, V or phase-plane display). Acetylcholine was applied to the record- ing site by means of a hydraulic system. Results showed that (a) differences in time course of action potential upstroke can be explained in terms of the rela- tive magnitude of fast and slow phases of depolarization; (b) acetylcholine is capable of depressing the slow phase of depolarization as well as the plateau of the action potential; and (¢) action potentials from nodal (SA and AV) cells seem to lack the initial fast phase. These results were construed to support a two-component hypothesis for cardiac electrogenesis. The hypothesis states that cardiac action potentials are composed of two distinct and physiologically separable "components" which result from discrete mechanisms. An initial fast component is a sodium spike similar to that of squid nerve. The slow com- ponent, which accounts for both a slow depolarization during phase 0 and the plateau, probably is dependent on the properties of a slow inward current hav- ing a positive equilibrium potential, coupled to a decrease in the resting potas- sium conductance. -
V=Nx76xs 4FRE the Following Content Is Provided Under a Creative Commons License
MITOCW | watch?v=Nx76XS_4FRE The following content is provided under a Creative Commons license. Your support will help MIT OpenCourseWare continue to offer high quality educational resources for free. To make a donation or view additional materials from hundreds of MIT courses, visit MIT OpenCourseWare at ocw.mit.edu. HAZEL SIVE: Some good questions. Let's zip through quickly. Why can't an initial depolarization travel along the length of the axon? Last time, we went through in detail how a signal is transmitted from the outside to the inside of the cell by ion flux across the membrane, and then how that ion flux is transmitted down the neuron. Remember that the ions entering the cell are just ions. They'll diffuse away. And so the depolarization kind of dissipates. And it then needs to be regenerated. The action potential, each small depolarization or the whole signal, each small depolarization with a specific magnitude, the reversal of membrane potential going from about minus 60 millivolts, negative inside, to plus 55 or 60 millivolts, positive inside. Each of those is an action potential. And here is an interesting one. Why doesn't the membrane potential stop at zero when sodium rushes into the cell during an action potential, which is what you'd expect if sodium was just moving along its concentration radian? Because the potential's not only governed by sodium influx. There are chloride ions outside the cell and potassium ions inside over the duration of the potential. And as we'll discuss briefly in a moment, it's during the rectification process that you go back to zero, and then you reverse membrane potential again. -
Electrophysiological Foundations of Cardiac Arrhythmias Clinical Electrophysiology Mark E
Second Edition Electrophysiological Foundations Andrew L. Wit of Cardiac Arrhythmias Penelope A. Boyden A Bridge Between Basic Mechanisms and Electrophysiological Foundations of Cardiac Arrhythmias Electrophysiological Foundations of Cardiac Clinical Electrophysiology Mark E. Josephson Second Edition Hein J. Wellens Now in an abridged second edition, Electrophysiological Foundations of Cardiac Arrhythmias focuses on teaching the fundamental concepts of cardiac cellular • Boyden Josephson Wellens Wit electrophysiology with an emphasis on the relationship of basic mechanisms to clinical cardiac arrhythmias. Understanding this relationship and the electrophysiological mechanisms underlying arrhythmogenesis will be invaluable Electrophysiological to physicians entering the fields of cardiology and clinical electrophysiology, as well as those scientists and clinicians already working in these areas. These essential concepts of electrophysiology include discussion on action potentials, ion channels and currents, and mechanisms of arrhythmias, and Foundations of provide the working knowledge that will enable the reader to approach a board exam confidently. Additionally, the authors build a base of understanding that will prepare the reader for more advanced texts, such as Josephson’s Clinical Cardiac Electrophysiology: Techniques and Interpretations. Cardiac Arrhythmias About the Authors The authors, Andrew L. Wit, PhD, Penelope A. Boyden, PhD, Mark E. Josephson, A Bridge Between MD, and Hein J. Wellens, MD, PhD, have spent four lifetimes investigating and defining electrophysiological mechanisms of cardiac arrhythmias. But equally important, they have devoted their careers to teaching this subject to students of all levels, from medical Basic Mechanisms and students to more advanced cardiology and clinical electrophysiology fellows. Clinical Electrophysiology ISBN 978-1-942909-42-2 Second Edition 90000> This book includes access to a free digital edition for use by the first buyer. -
Topic 2 – Neuronal Physiology
Index Topic 2 – Neuronal Physiology - Resting membrane potential - The NA+-K+ pump - Channels - Graded potentials - Action potentials - Voltage-gated channels o Voltage-gated Na+ channel o Voltage-gated K+ channel § Repolarisation § Depolarisation - Propagation of action potentials Topic 3 – The Peripheral Nervous System - Efferent division o Somatic nervous system o Autonomic nervous system § Sympathetic nervous sysmte § Parasympathetic nervous system o Cholinergic neurons o Adrenergic neurons o Dominance o Rules about neurons o Neuromuscular junction o Comparison of a synapse and a neuromuscular junction Topic 4 – Skeletal Muscle - General points - Organisation of a muscle - Thick filaments - Thin filaments o Actin o Tropomyosin o Troponin - Transverse tubular system (t-tubules) - Sarcoplasmic reticulum - Contraction of a skeletal muscle fibre - Filament slide switch - Muscle twitches o Amount of fibres o Amount of force o Twitch response o Twitch summation o Tetanic contraction o ATP and skeletal muscle contraction o Direct phosphorylation o Oxidative phosphorylation o Glycolysis Topic 5 – Smooth Muscle - Similarities with skeletal muscle - Differences with skeletal muscle - Structure of smooth muscle - Dense bodies - Smooth muscle contraction ‘switch’ - Relaxation - Multi-unit smooth muscle - Single-unit smooth muscle o Pacemaker potentials o Slow-wave potentials Topic 6 – Gastrointestinal Physiology - Processes o Mobility o Secretion o Digestion o Absorption - Digestive system composition o List of organs o Importance of ‘separation’ -
Graded Potentials and Action Potentials
GRADED POTENTIALS AND ACTION POTENTIALS Near East University Faculty of Medicine Department of Biophysics Dr. Aslı AYKAÇ Nervous System Nervous system cells are comprised of glia and neurons. Neurons are responsible for receive, process, and transmit information in nervous system. • Glia – Not specialized for information transfer – Support neurons • Neurons (Nerve Cells) – Receive, process, and transmit information Information travels in one direction Dendrite → soma → axon Voltmetre (mV) 0 30 -30 50 -50 -70 outside ATP inside • All cells have electrical potential difference between inside and outside of the cell. • Transient changes in the membrane potential of its resting level produce electrical signals. – Such changes are the most important way that nerve cells process and transmit information. These signals occur in two forms: 1. graded potentials 2. action potentials Graded potentials are important in short distances. Action potentials are the long distance signals of nerve and muscle membranes. Nerve and muscle cells as well as some endocrine, immune, and reproductive cells have plasma membranes capable of producing action potentials. • These membranes – are called excitable membranes. – Their ability to generate action potentials is known as excitability. All cells are capable of conducting graded potentials, but excitable membranes can conduct action potentials. Changes in Membrane Potential depolarize The terms repolarize are used to describe hyperpolarize the direction of changes in the membrane potential relative to the resting potential. ) Membrane potential (mV potential Membrane Time The resting membrane potential (at -70 mV) is polarized. “Polarized” means that the outside and inside of a cell have a different net charge. • The membrane is said to be depolarized when its potential is less negative than the resting level. -
Lecture 7 Cell Signaling in the Nervous System All Body Cells Display a Membrane Potential, Which Is a Separation of Positive and Negative Charges Across the Membrane
Lecture 7 Cell signaling in the nervous system All body cells display a membrane potential, which is a separation of positive and negative charges across the membrane. This potential is related to the uneven distribution of Na, K, and large intracellular protein anions between the intracellular fluid (ICF) and extracellular fluid (ECF), and to the differential permeability of the plasma membrane to these ions. Membrane potential Types of changes in membrane potential are shown in Figure1: Figure 1 Types of changes in membrane potential. Electrical signals are produced by changes in ion movement across the plasma membrane Because the water-soluble ions responsible for carrying charge cannot penetrate the plasma membrane’s lipid bilayer, these charges can cross the membrane only through channels specific for them or by carrier-mediated transport. Membrane channels may be either leak channels or gated channels. As described in Chapter 3, leak channels, which are open all the time, permit unregulated leakage of their specific ion across the membrane through the channels .Gated channels, in contrast, have gates that can be open or closed, permitting ion passage through the channels when open and preventing ion passage through the channels when closed. Gate opening and closing results from a change in the conformation (shape) of the protein that forms the gated channel. There are four kinds of gated channels, depending on the factor that causes the change in channel conformation: (1) voltage-gated channels open or close in response to changes in membrane potential; (2) chemically gated channels change conformation in response to binding of a specific extracellular chemical messenger to a surface membrane receptor; (3) mechanically gated channels respond to stretching or other mechanical deformation; and (4) thermally gated channels respond to local changes in temperature (heat or cold). -
The Cells That Make Us Who We Are How Neurons Communicate With
Communication within the Nervous System The Cells that make us who we are How neurons communicate with one another Garrett: Brain & Behavior 4e 1 The Cells That Make Us Who We Are • How many are there? • Neurons: 100 billion • Make up 10% of brain volume • Glia: Many more! • Make up 90% of brain volume • Neurons: Jobs include • convey sensory information to the brain; • carry out operations involved in thought and feeling; • Send commands out to the body. • Dendrites • Cell body or soma Garrett: Brain & Behavior 4e • Axons insulated with myelin (secreted by glia), with end terminals that release neurotransmitters from vesicles into the synapse 2 The Cells That Make Us Who We Are Figure 2.3: Components of a Neuron Garrett: Brain & Behavior 4e 3 The Cells That Make Us Who We Are Figure 2.4 a,b : The Three Shapes of Neurons • Unipolar neurons (a) • Bipolar neurons (b) • Multipolar neurons • Figure 2 .3, previous slide Garrett: Brain & Behavior 4e 4 The Cells That Make Us Who We Are Table 2.1: The Three Types of Neurons Figure 2.4c: The Three Shapes of Neurons Type Shape Description Motor neuron Multipolar Output to muscles/organs Sensory neuron Unipolar or Bipolar Input from receptors Interneuron Multipolar Most within the CNS. Most common. Garrett: Brain & Behavior 4e 5 The Cells That Make Us Who We Are Figure 2.5: Composition of the Cell Membrane • Lipids • Heads attracted to water in and outside the cell, tails repelled by water • Creates a double-layer membrane • Proteins • Hold the cells together • Controls the environment in and around the cell Garrett: Brain & Behavior 4e 6 The Neural Membrane • The neuron has a selectively-permeable membrane. -
Resting Membrane Potential
Chapter 06 Lecture Outline See separate PowerPoint slides for all figures and tables pre- inserted into PowerPoint without notes. Copyright ©2017 McGraw-Hill Education. Permission required for reproduction or display. 1 Topics Section A Cells of the nervous Section C Synapses system 6.8 Functional anatomy of synapses 6.1 Structure and maintenance of 6.9 Mechanisms of neurotransmitter neurons release 6.2 Functional classes of neurons 6.10 Activation of the postsynaptic cell 6.3 Glial cells 6.11 Synaptic integration 6.4 Neural growth and regeneration 6.12 Synaptic strength Section B Membrane Potentials 6.13 Neurotransmitters and 6.5 Basic principles of electricity neuromodulators 6.6 The resting membrane potential 6.14 Neuroeffector communication 6.7 Graded potentials and action Section D Structure of the nervous potentials system 6.15 Central nervous system: Brain 6.16 Central nervous system: Spinal cord 6.17 Peripheral nervous system 6.18 Autonomic nervous system 6.19 Protective elements associated 2 with the brain The Nervous System • The Nervous System has two major divisions: – The Central Nervous System (CNS), which is composed of the brain and spinal cord. – The Peripheral Nervous System (PNS) is composed of the nerves that connect the brain or spinal cord with the body’s muscles, glands, and sense organs. • The neuron is the basic cell type of both systems. 3 Structure of a Neuron 4 Schwann Cells and Myelin • Schwann cells surround and form myelin sheaths around the larger nerve fibers. These are vital to regeneration and proper nerve signal conduction. 5 Myelination of Axons 6 Axonal Transport 7 Functional Classes of Neurons 8 Functional Classes of Neurons 9 10 Synapses Synapses can use both chemical and electrical stimuli to pass information.