11 Introduction to the Nervous System and Nervous Tissue
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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). -
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. -
Electrical Synapses Are Drivers of Neural Plasticity Through Passage of Small Molecules
Electrical Synapses are Drivers of Neural Plasticity Through Passage of Small Molecules Lisa Voelker A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Washington 2019 Reading Committee: Jihong Bai, Chair Linda Buck Cecilia Moens Program Authorized to Offer Degree: Molecular and Cellular Biology ©Copyright 2019 Lisa Voelker 2 University of Washington Abstract Electrical Synapses are Drivers of Neural Plasticity through Passage of Small Molecules Lisa Voelker Chair of the Supervisory Committee: Jihong Bai Department of Biochemistry In order to respond to changing environments and fluctuations in internal states, animals adjust their behavior through diverse neuromodulatory mechanisms. In this study we show that electrical synapses between the ASH primary quinine-detecting sensory neurons and the neighboring ASK neurons are required for modulating the aversive response to the bitter tastant quinine in C. elegans. Mutant worms that lack the electrical synapse proteins INX-18 and INX-19 become hypersensitive to dilute quinine. Cell-specific rescue experiments indicate that inx-18 operates in ASK while inx-19 is required in both ASK and ASH for proper quinine sensitivity. Imaging analyses find that INX-19 in ASK and ASH localizes to the same regions in the nerve ring, suggesting that both sides of ASK-ASH electrical synapses contain INX-19. While inx-18 and inx-19 mutant animals have a similar behavioral phenotype, several lines of evidence suggest the proteins encoded by these genes play different roles in modulating the aversive quinine response. First, INX-18 and INX-19 localize 3 to different regions of the nerve ring, indicating that they are not present in the same synapses. -
Neural Control of Movement: Motor Neuron Subtypes, Proprioception and Recurrent Inhibition
List of Papers This thesis is based on the following papers, which are referred to in the text by their Roman numerals. I Enjin A, Rabe N, Nakanishi ST, Vallstedt A, Gezelius H, Mem- ic F, Lind M, Hjalt T, Tourtellotte WG, Bruder C, Eichele G, Whelan PJ, Kullander K (2010) Identification of novel spinal cholinergic genetic subtypes disclose Chodl and Pitx2 as mark- ers for fast motor neurons and partition cells. J Comp Neurol 518:2284-2304. II Wootz H, Enjin A, Wallen-Mackenzie Å, Lindholm D, Kul- lander K (2010) Reduced VGLUT2 expression increases motor neuron viability in Sod1G93A mice. Neurobiol Dis 37:58-66 III Enjin A, Leao KE, Mikulovic S, Le Merre P, Tourtellotte WG, Kullander K. 5-ht1d marks gamma motor neurons and regulates development of sensorimotor connections Manuscript IV Enjin A, Leao KE, Eriksson A, Larhammar M, Gezelius H, Lamotte d’Incamps B, Nagaraja C, Kullander K. Development of spinal motor circuits in the absence of VIAAT-mediated Renshaw cell signaling Manuscript Reprints were made with permission from the respective publishers. Cover illustration Carousel by Sasha Svensson Contents Introduction.....................................................................................................9 Background...................................................................................................11 Neural control of movement.....................................................................11 The motor neuron.....................................................................................12 Organization -
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. -
Student Academic Learning Services Nervous System Quiz
Student Academic Learning Services Page 1 of 8 Nervous System Quiz 1. The term central nervous system refers to the: A) autonomic and peripheral nervous systems B) brain, spinal cord, and cranial nerves C) brain and cranial nerves D) spinal cord and spinal nerves E) brain and spinal cord 2. The peripheral nervous system consists of: A) spinal nerves only B) the brain only C) cranial nerves only D) the brain and spinal cord E) the spinal and cranial nerves 3. Which of these cells are not a type of neuroglia found in the CNS: A) astrocytes B) microglia C) Schwann cells D) ependymal cells E) oligodendrocytes 4. The Schwann cells form a myelin sheath around the: A) dendrites B) cell body C) nucleus D) axon E) nodes of Ranvier 5. The neuron processes that normally receives incoming stimuli are called: A) axons B) dendrites C) neurolemmas D) Schwann cells E) satellite cells www.durhamcollege.ca/sals Student Services Building (SSB), Room 204 905.721.2000 ext. 2491 This document last updated: 7/29/2011 Student Academic Learning Services Page 2 of 8 6. Collections of nerve cell bodies inside the PNS are called: A) ganglia B) tracts C) nerves D) nuclei E) tracts or ganglia 7. Which of the following best describes the waxy-appearing material called myelin: A) an outermembrane on a neuroglial cell B) a lipid-protein (lipoprotein) cell membrane on the outside of axons C) a mass of white lipid material that surrounds the cell body of a neuron D) a mass of white lipid material that insulates the axon of a neuron E) a mass of white lipid material that surrounds the dendrites of a neuron 8. -
Interplay Between Gating and Block of Ligand-Gated Ion Channels
brain sciences Review Interplay between Gating and Block of Ligand-Gated Ion Channels Matthew B. Phillips 1,2, Aparna Nigam 1 and Jon W. Johnson 1,2,* 1 Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA; [email protected] (M.B.P.); [email protected] (A.N.) 2 Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA * Correspondence: [email protected]; Tel.: +1-(412)-624-4295 Received: 27 October 2020; Accepted: 26 November 2020; Published: 1 December 2020 Abstract: Drugs that inhibit ion channel function by binding in the channel and preventing current flow, known as channel blockers, can be used as powerful tools for analysis of channel properties. Channel blockers are used to probe both the sophisticated structure and basic biophysical properties of ion channels. Gating, the mechanism that controls the opening and closing of ion channels, can be profoundly influenced by channel blocking drugs. Channel block and gating are reciprocally connected; gating controls access of channel blockers to their binding sites, and channel-blocking drugs can have profound and diverse effects on the rates of gating transitions and on the stability of channel open and closed states. This review synthesizes knowledge of the inherent intertwining of block and gating of excitatory ligand-gated ion channels, with a focus on the utility of channel blockers as analytic probes of ionotropic glutamate receptor channel function. Keywords: ligand-gated ion channel; channel block; channel gating; nicotinic acetylcholine receptor; ionotropic glutamate receptor; AMPA receptor; kainate receptor; NMDA receptor 1. Introduction Neuronal information processing depends on the distribution and properties of the ion channels found in neuronal membranes. -
Chapter 8 Nervous System
Chapter 8 Nervous System I. Functions A. Sensory Input – stimuli interpreted as touch, taste, temperature, smell, sound, blood pressure, and body position. B. Integration – CNS processes sensory input and initiates responses categorizing into immediate response, memory, or ignore C. Homeostasis – maintains through sensory input and integration by stimulating or inhibiting other systems D. Mental Activity – consciousness, memory, thinking E. Control of Muscles & Glands – controls skeletal muscle and helps control/regulate smooth muscle, cardiac muscle, and glands II. Divisions of the Nervous system – 2 anatomical/main divisions A. CNS (Central Nervous System) – consists of the brain and spinal cord B. PNS (Peripheral Nervous System) – consists of ganglia and nerves outside the brain and spinal cord – has 2 subdivisions 1. Sensory Division (Afferent) – conducts action potentials from PNS toward the CNS (by way of the sensory neurons) for evaluation 2. Motor Division (Efferent) – conducts action potentials from CNS toward the PNS (by way of the motor neurons) creating a response from an effector organ – has 2 subdivisions a. Somatic Motor System – controls skeletal muscle only b. Autonomic System – controls/effects smooth muscle, cardiac muscle, and glands – 2 branches • Sympathetic – accelerator “fight or flight” • Parasympathetic – brake “resting and digesting” * 4 Types of Effector Organs: skeletal muscle, smooth muscle, cardiac muscle, and glands. III. Cells of the Nervous System A. Neurons – receive stimuli and transmit action potentials -
Polyribosomes Associated with Synaptic Specializations on Axon Initial Segments: Localization of Protein-Synthetic Machinery at Inhibitory Synapses
The Journal of Neuroscience October 1986, 6(10): 3079-3085 Polyribosomes Associated with Synaptic Specializations on Axon Initial Segments: Localization of Protein-Synthetic Machinery at Inhibitory Synapses Oswald Steward* and Charles E. Ribak-f *Departments of Neurosurgery and Physiology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, and TDepartment of Anatomy and Neurobiology, University of California at Irvine, Irvine, California 92717 Previous studies have revealed a selective association between report that showed some axonal ribosomes grouped at points polyribosomes and axospinous synapses in a variety of brain of branching and beneath synaptic contacts (Jones and Powell, regions. The present study evaluates whether polyribosomes are 1969). Therefore, they were usually considered, only in passing, also associated with the symmetrical and presumably inhibitory as exceptions to the rule. Thus, it has come to be accepted as a synaptic connections found on the initial segment of axons of central tenet that essentially all of the protein constituents of some neurons in the CNS. The initial segments of pyramidal the neuron, including those required for synaptic specializations, neurons in the sensorimotor cortex of the monkey and of granule were synthesized in the cell body, and somehow selectively cells in the hippocampus of the rat were examined. The initial transported to the sites at which they would be assembled (for segments of these cell types are contacted by GABAergic ter- a review, see Grafstein and Forman, 1980). minals that form symmetrical synaptic connections. In the pres- Over the past few years, a series of observations has given ent study, these initial segments were found to contain polyri- rise to an hypothesis that challenges the prevailing view that bosomes that tended to be selectively localized beneath the virtually all neuronal proteins are produced in the cell body and synaptic specializations. -
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). -
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.