The Transformations of Sound Stimuli Into Electrical Signals
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Hearing Loss Epidemic the Hair Cell
Hearing loss epidemic One in ten (30 million) Americans has hearing loss FUTURE THERAPIES FOR INNER - Causes include heredity, aging, noise exposure, disease EAR REGENERATION - Number is expected to double by 2030 Hearing loss is the #1 birth defect in America Albert Edge - 1 in 1000 newborns is born profoundly deaf Harvard Medical School - 2-3/1000 will have partial/progressive hearing loss Massachusetts Eye and Ear Infirmary Hearing loss prevalence increases with age - 1 in 3 over 65 years has significant hearing loss - Among seniors, hearing loss is the 3rd most prevalent condition 2 The inner ear The hair cell Auditory Hair Bundle Nerve Middle Ear Sensory hairs vibrate, "tip-links"open ion channels into hair cell Ions flow into hair cell, Inner Ear changing its electrical potential Hair External Ear Cells 3 4 1 The nerve fiber Sensorineural hearing loss: Hair cells and nerve fibers Cochlear Implant can directly stimulate Electric potential causes chemical neurotransmitter release from synapse Sensory Cell Loss NeurotransmitterNeurotransmitter diffuses to nerve fiber and excites electrical activity in the form of action potentials Hair Cell Nerve Fiber Loss 5 6 Regeneration of hair cells in chick inner ear Can stem cell-derived inner ear progenitors replace lost hair cells in vivo (and restore hearing)? Normal Hair Cells Damaged Hair Cells Regenerated Hair Cell Bundles Li et al., TMM (2004) 2 Approaches to regenerating inner ear cells Gene therapy I. Generation of inner ear cells by gene therapy • New hair cells: transfer Atoh1 gene II. -
Action Potential and Synapses
SENSORY RECEPTORS RECEPTORS GATEWAY TO THE PERCEPTION AND SENSATION Registering of inputs, coding, integration and adequate response PROPERTIES OF THE SENSORY SYSTEM According the type of the stimulus: According to function: MECHANORECEPTORS Telereceptors CHEMORECEPTORS Exteroreceptors THERMORECEPTORS Proprioreceptors PHOTORECEPTORS interoreceptors NOCICEPTORS STIMULUS Reception Receptor – modified nerve or epithelial cell responsive to changes in external or internal environment with the ability to code these changes as electrical potentials Adequate stimulus – stimulus to which the receptor has lowest threshold – maximum sensitivity Transduction – transformation of the stimulus to membrane potential – to generator potential– to action potential Transmission – stimulus energies are transported to CNS in the form of action potentials Integration – sensory information is transported to CNS as frequency code (quantity of the stimulus, quantity of environmental changes) •Sensation is the awareness of changes in the internal and external environment •Perception is the conscious interpretation of those stimuli CLASSIFICATION OF RECEPTORS - adaptation NONADAPTING RECEPTORS WITH CONSTANT FIRING BY CONSTANT STIMULUS NONADAPTING – PAIN TONIC – SLOWLY ADAPTING With decrease of firing (AP frequency) by constant stimulus PHASIC– RAPIDLY ADAPTING With rapid decrease of firing (AP frequency) by constant stimulus ACCOMODATION – ADAPTATION CHARACTERISTICS OF PHASIC RECEPTORS ALTERATIONS OF THE MEMBRANE POTENTIAL ACTION POTENTIAL TRANSMEMBRANE POTENTIAL -
Pain-Enhancing Mechanism Through Interaction Between TRPV1 and Anoctamin 1 in Sensory Neurons
Pain-enhancing mechanism through interaction between TRPV1 and anoctamin 1 in sensory neurons Yasunori Takayamaa, Daisuke Utab, Hidemasa Furuec,d, and Makoto Tominagaa,d,1 aDivision of Cell Signaling, Okazaki Institute for Integrative Bioscience, Okazaki 444-8787, Japan; bDepartment of Applied Pharmacology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan; cDivision of Neural Signaling, National Institute for Physiological Sciences, Okazaki 444-8787, Japan; and dDepartment of Physiological Sciences, Graduate University for Advanced Studies, Okazaki 444-8787, Japan Edited by David Julius, University of California, San Francisco, CA, and approved March 20, 2015 (received for review November 11, 2014) The capsaicin receptor transient receptor potential cation channel channels. Mammalian TRPV1 is activated by noxious heat, acid, and vanilloid 1 (TRPV1) is activated by various noxious stimuli, and the many chemical compounds including capsaicin (16–18). The calcium stimuli are converted into electrical signals in primary sensory permeability of TRPV1 is more than 10 times that of sodium, neurons. It is believed that cation influx through TRPV1 causes suggesting that TRPV1 could activate anoctamins readily, leading depolarization, leading to the activation of voltage-gated sodium to further depolarization. ANO1 plays an important role in noci- channels, followed by the generation of action potential. Here we ception in primary sensory neurons (19), and bradykinin-induced report that the capsaicin-evoked action potential could be induced and neuropathic pain-related behaviors were reduced in ANO1 by two components: a cation influx-mediated depolarization caused conditional-knockout mice (20, 21), suggesting that interaction be- by TRPV1 activation and a subsequent anion efflux-mediated de- tween the two proteins could strongly enhance nociceptive signals. -
Cells of Adult Brain Germinal Zone Have Properties Akin to Hair Cells and Can Be Used to Replace Inner Ear Sensory Cells After Damage
Cells of adult brain germinal zone have properties akin to hair cells and can be used to replace inner ear sensory cells after damage Dongguang Weia,1, Snezana Levica, Liping Niea, Wei-qiang Gaob, Christine Petitc, Edward G. Jonesa, and Ebenezer N. Yamoaha,1 aDepartment of Anesthesiology and Pain Medicine, Center for Neuroscience, Program in Communication and Sensory Science, University of California, 1544 Newton Court, Davis, CA 95618; bDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA 94080; and cUnite´deGe´ne´ tique et Physiologie de l’Audition, Unite´Mixte de Recherche S587, Institut National de la Sante´et de la Recherche Me´dicale-Universite´Paris VI, Colle`ge de France, Institut Pasteur, 25 Rue du Dr Roux, 75724 Paris, Cedex 15, France Edited by David Julius, University of California, San Francisco, CA, and approved October 27, 2008 (received for review August 15, 2008) Auditory hair cell defect is a major cause of hearing impairment, often and have an actin-filled process as in the HCs. Thus, we surmise that leading to spiral ganglia neuron (SGN) degeneration. The cell loss that cells of the adult forebrain germinal zone might be potential follows is irreversible in mammals, because inner ear hair cells (HCs) candidate cells to be used autologously for the replacement of have a limited capacity to regenerate. Here, we report that in the nonrenewable HCs and SGNs. adult brain of both rodents and humans, the ependymal layer of the Ependymal cells adjacent to the spinal canal proliferate exten- lateral ventricle contains cells with proliferative potential, which sively upon spinal cord injuries (16, 17). -
Smelling Better with Chloride COMMENTARY Stephan Fringsa,1
COMMENTARY Smelling better with chloride COMMENTARY Stephan Fringsa,1 The sense of smell and its astonishing performance coding is the solution to the problem of low-selectivity pose biologists with ever new riddles. How can the receptors (2). system smell almost anything that gets into the nose, However, the necessity to operate OSNs with fuzzy distinguish it from countless other odors, memorize odorant receptors creates another problem, as it limits it forever, and trigger reliably adequate behavior? the efficacy of the transduction process. OSNs trans- Among the senses, the olfactory system always duce chemical signals through a metabotropic path- seems to do things differently. The olfactory sensory way (Fig. 1A). Such pathways translate external stimuli neurons (OSNs) in the nose were suggested to use an into cellular responses by G-protein–coupled recep- unusual way of signal amplification to help them in tors. Their efficacy depends on the duration of recep- responding to weak stimuli. This chloride-based tor activity: the longer the receptor is switched on, the mechanism is somewhat enigmatic and controversial. more G protein can be activated. This is well studied in A team of sensory physiologists from The Johns photoreceptors, where the rhodopsin molecule may Hopkins University School of Medicine has now de- stay active for more than a second after absorbing a veloped a method to study this process in detail. photon. Within this time, it can activate hundreds of G Li et al. (1) demonstrate how OSNs amplify their proteins, one after the other, thus eliciting a robust electrical response to odor stimulation using chlo- cellular response to a single photon. -
Review of Hair Cell Synapse Defects in Sensorineural Hearing Impairment
Otology & Neurotology 34:995Y1004 Ó 2013, Otology & Neurotology, Inc. Review of Hair Cell Synapse Defects in Sensorineural Hearing Impairment *†‡Tobias Moser, *Friederike Predoehl, and §Arnold Starr *InnerEarLab, Department of Otolaryngology, University of Go¨ttingen Medical School; ÞSensory Research Center SFB 889, þBernstein Center for Computational Neuroscience, University of Go¨ttingen, Go¨ttingen, Germany; and §Department of Neurology, University of California, Irvine, California, U.S.A. Objective: To review new insights into the pathophysiology of are similar to those accompanying auditory neuropathy, a group sensorineural hearing impairment. Specifically, we address defects of genetic and acquired disorders of spiral ganglion neurons. of the ribbon synapses between inner hair cells and spiral ganglion Genetic auditory synaptopathies include alterations of glutamate neurons that cause auditory synaptopathy. loading of synaptic vesicles, synaptic Ca2+ influx or synaptic Data Sources and Study Selection: Here, we review original vesicle turnover. Acquired synaptopathies include noise-induced publications on the genetics, animal models, and molecular hearing loss because of excitotoxic synaptic damage and subse- mechanisms of hair cell ribbon synapses and their dysfunction. quent gradual neural degeneration. Alterations of ribbon synapses Conclusion: Hair cell ribbon synapses are highly specialized to likely also contribute to age-related hearing loss. Key Words: enable indefatigable sound encoding with utmost temporal precision. GeneticsVIon -
Purinergic Signaling in Cochlear Supporting Cells Reduces Hair
RESEARCH ARTICLE Purinergic signaling in cochlear supporting cells reduces hair cell excitability by increasing the extracellular space Travis A Babola1, Calvin J Kersbergen1, Han Chin Wang1†, Dwight E Bergles1,2,3* 1The Solomon Snyder Department of Neuroscience, Johns Hopkins University, Baltimore, United States; 2Department of Otolaryngology Head and Neck Surgery, Johns Hopkins University, Baltimore, United States; 3Kavli Neuroscience Discovery Institute, Johns Hopkins University, Baltimore, United States Abstract Neurons in developing sensory pathways exhibit spontaneous bursts of electrical activity that are critical for survival, maturation and circuit refinement. In the auditory system, intrinsically generated activity arises within the cochlea, but the molecular mechanisms that initiate this activity remain poorly understood. We show that burst firing of mouse inner hair cells prior to hearing onset requires P2RY1 autoreceptors expressed by inner supporting cells. P2RY1 activation triggers K+ efflux and depolarization of hair cells, as well as osmotic shrinkage of supporting cells that dramatically increased the extracellular space and speed of K+ redistribution. Pharmacological inhibition or genetic disruption of P2RY1 suppressed neuronal burst firing by reducing K+ release, but unexpectedly enhanced their tonic firing, as water resorption by supporting cells reduced the extracellular space, leading to K+ accumulation. These studies indicate that purinergic signaling in *For correspondence: supporting cells regulates hair cell -
Nomina Histologica Veterinaria, First Edition
NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria. -
Plan of the Lecture Afferent Innervation Outer Hair Cell 'Electromotility'
Plan of the lecture Afferent innervation Outer hair cell ‘electromotility’ Efferent inhibitory feedback from the brain 1 Will describe results obtained by intracellular voltage-clamp recording from afferent dendrites at point of contact with IHCs. The peculiar advantages of this experiment provide new insights into ribbon function, and perhaps by extension, into mechanisms of transmitter release more generally. 2 Low frequency tones produce ‘phase-locked’ activity in afferent fibers (turtle). 3 Type I afferents contact single inner hair cells and make up 95% of the VIIIth nerve. The main (only?) source of acoustic information to the brain. Type II afferent contact many outer hair cells. Not known what information they carry to the brain, although it is suspected they may only be activated during very loud sound. 4 5 6 This is what the mammalian cochlea (2-3 week old rat) really looks like. These are otic capsules, the bony chamber within the temporal bone of the skull that encloses the inner ear. On the right is the intact capsule. On the left the surgeon (Dr. E. Wersinger, PhD) has dissected away the surrounding bone to reveal the soft tissues of the cochlear spiral. 7 Postsynaptic recordings to study transmitter release. 8 Seen at higher temporal resolution, the majority of synaptic events have classic ‘alpha’ shape with a rapid rise and slower fall. At room temperature these in a fraction of a ms, and fall with a time constant of 1 ms. 9 10 The synaptic currents reverse in sign near 0 mV, so flow through non-selective cation channels. -
The Basic Hypothesis for Mechanotransduction in Sensory Receptors
Trakia Journal of Sciences, Vol. 17, Suppl. 2, pp 22-26, 2019 Copyright © 2019 Trakia University Available online at: http://www.uni-sz.bg ISSN 1313-3551 (online) doi:10.15547/tjs.2019.s.02.006 THE BASIC HYPOTHESIS FOR MECHANOTRANSDUCTION IN SENSORY RECEPTORS Ch. Chouchkov, Iv. Maslarski* Department of Anatomy, Histology, Pathology and Forensic Medicine, Faculty of Medicine, SU “St. Kliment Ohridski”, Sofia, Bulgaria ABSTRACT One of the most involving problem in the nerve tissue organization is the process of information transduction in the sеnsory receptors and the associated with them sensory cells. The aim of the present report is to review and discuss the data during the latter twenty years about the localization of molecules recently localized in different structural elements of sensory corpuscles and their possible role in the process of mechanotransduction. The most important obligatory parts in the process of mechanotransduction of all sensory receptors are their non-myelinated parts and their bulbous ends or so called nerve endings, like Pacinian and Meissner corpuscles, Krauses bulb, Golgi-Mazzoni corpuscle and Merkel disk. In conclusion, it is still a matter of elucidation in the future to precisely localize the proteins making up the mechanosensitive ion channels. There also exist difficulties regarding the correlation of the physiological with morphological data due to the fact that the receptor axolemma is surrounded by complex cellular structures whose isolation is hard to perform. Key words: Merkel disk, Pacinian corpuscle, Schwann inner core complex, neurotransmission INTRODUCTION mechanotransduction. The sensory receptors, One of the most intriguing problem in the responsible for the process of nerve tissue organization is the process of mechanotransduction are designed as information transduction in the sеnsory mechanoreceptors. -
Pejvakin, a Candidate Stereociliary Rootlet Protein, Regulates Hair Cell Function in a Cell-Autonomous Manner
The Journal of Neuroscience, March 29, 2017 • 37(13):3447–3464 • 3447 Neurobiology of Disease Pejvakin, a Candidate Stereociliary Rootlet Protein, Regulates Hair Cell Function in a Cell-Autonomous Manner X Marcin Kazmierczak,1* Piotr Kazmierczak,2* XAnthony W. Peng,3,4 Suzan L. Harris,1 Prahar Shah,1 Jean-Luc Puel,2 Marc Lenoir,2 XSantos J. Franco,5 and Martin Schwander1 1Department of Cell Biology and Neuroscience, Rutgers the State University of New Jersey, Piscataway, New Jersey 08854, 2Inserm U1051, Institute for Neurosciences of Montpellier, 34091, Montpellier cedex 5, France, 3Department of Otolaryngology, Head and Neck Surgery, Stanford University, Stanford, California 94305, 4Department of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, Colorado 80045, and 5Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado 80045 Mutations in the Pejvakin (PJVK) gene are thought to cause auditory neuropathy and hearing loss of cochlear origin by affecting noise-inducedperoxisomeproliferationinauditoryhaircellsandneurons.Herewedemonstratethatlossofpejvakininhaircells,butnot in neurons, causes profound hearing loss and outer hair cell degeneration in mice. Pejvakin binds to and colocalizes with the rootlet component TRIOBP at the base of stereocilia in injectoporated hair cells, a pattern that is disrupted by deafness-associated PJVK mutations. Hair cells of pejvakin-deficient mice develop normal rootlets, but hair bundle morphology and mechanotransduction are affected before the onset of hearing. Some mechanotransducing shorter row stereocilia are missing, whereas the remaining ones exhibit overextended tips and a greater variability in height and width. Unlike previous studies of Pjvk alleles with neuronal dysfunction, our findings reveal a cell-autonomous role of pejvakin in maintaining stereocilia architecture that is critical for hair cell function. -
YAP Mediates Hair Cell Regeneration in Balance Organs of Chickens, but LATS Kinases Suppress Its Activity in Mice
The Journal of Neuroscience, May 13, 2020 • 40(20):3915–3932 • 3915 Development/Plasticity/Repair YAP Mediates Hair Cell Regeneration in Balance Organs of Chickens, But LATS Kinases Suppress Its Activity in Mice Mark A. Rudolf,1 Anna Andreeva,2 Mikolaj M. Kozlowski,1 Christina E. Kim,1 Bailey A. Moskowitz,1 Alejandro Anaya-Rocha,3 Matthew W. Kelley,3 and Jeffrey T. Corwin1,4 1Department of Neuroscience, University of Virginia School of Medicine, Charlottesville, Virginia 22908, 2School of Sciences and Humanities, Nazarbayev University, Nursultan 010000, Republic of Kazakhstan, 3Laboratory of Cochlear Development, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892, and 4Department of Cell Biology, University of Virginia School of Medicine, Charlottesville, Virginia 22908 Loss of sensory hair cells causes permanent hearing and balance deficits in humans and other mammals, but for nonmam- mals such deficits are temporary. Nonmammals recover hearing and balance sensitivity after supporting cells proliferate and differentiate into replacement hair cells. Evidence of mechanical differences between those sensory epithelia and their sup- porting cells prompted us to investigate whether the capacity to activate YAP, an effector in the mechanosensitive Hippo pathway, correlates with regenerative capacity in acceleration-sensing utricles of chickens and mice of both sexes. After hair cell ablation, YAP accumulated in supporting cell nuclei in chicken utricles and promoted regenerative proliferation, but YAP remained cytoplasmic and little proliferation occurred in mouse utricles. YAP localization in supporting cells was also more sensitive to shape change and inhibition of MST1/2 in chicken utricles than in mouse utricles. Genetic manipulations showed that in vivo expression of the YAP-S127A variant caused robust proliferation of neonatal mouse supporting cells, which pro- duced progeny that expressed hair cell markers, but proliferative responses declined postnatally.