BookVickram Ramkumar, Leonard P. Rybak, editors.
Summary: The primary goal of this project is to describe our current understanding of the oxidant hypothesis of noise and drug-induced hearing loss and show how this process translates into cochlear inflammation. Basic cellular mechanisms underlying the contribution of oxidant stress to hearing loss will be explained and molecular pathways leading to inflammatory processes will be outlined. Several different aspects of the cochlear inflammatory process will be discussed in detail. These include the sources of inflammatory cells, chemokines, inflammatory cytokines and the roles of cochlear resident immune cells in mediating hearing loss. In addition, evidence for a robust cochlear-based steroid axis which is activated by cochlear stress and serves a protective system. The role of the strial vasculature networks which aid in maintenance of the blood-labyrinth barrier and control the entry of circulating immune cells into the cochlea will be described. Molecular pathways leading to activation of the local inflammatory process will be highlighted and otoprotective treatment options will be discussed. The relevance of certain clinically used anti-inflammatory interventions, such as trans-tympanic steroids and other drugs will also be discussed. Furthermore, we will examine recent patents focusing on the use of anti-inflammatory agents for the treatment of drug and noise-induced hearing loss. It is our hope that this book would provide a better understanding of the interaction of oxidative stress and inflammation in hearing loss. This book should provide basic information to scientists in the field of auditory research and to enlighten clinicians who treat patients with potentially ototoxic drugs.
Contents:
Intro; Preface; Contents; Contributors;
Chapter 1: The Cochlea; 1 Fluid Spaces intheCochlea; 2 Cochlear Duct; 3 Tectorial Membrane; 4 Basilar Membrane; 5 The Lateral Wall oftheCochlea; 6 The Spiral Ligament; 7 Stria Vascularis; Basal Cells; 8 Endocochlear Potential; 9 Organ ofCorti; 10 Mechano-transduction; 11 Hair Cell Synapses; References;
Chapter 2: Oxidative Stress andHearing Loss; 1 Introduction; 2 Oxidative Stress; Free Radicals; Oxidative Stress andCytotoxicity; 3 Cochlear Targets ofOxidative Stress; Sensory Epithelium; Lateral Wall; Modiolus. 2 Bounds Related toCurrent Perspectives ofNoise-Induced Damage andFunctional Loss: Cellular Elements ofCochleaTemporary Threshold Shifts (TTS) andAssociated Cellular Elements atRisk forDamage; Previously Described Protective Mechanisms Against NIHL; 3 Elements ofCorticotropin Releasing Factor (Hormone) Signaling Systems, andTheir Expression intheMammalian Inner Ear; A Novel Theory ofLocal Cochlear Signaling Systems Protective AgainstCellular Damage andAssociated NIHL; 4 Inflammatory/Immune Responses intheCochlea Are Driven byAcoustic Over-Exposure. 4 Oxidative Stress inAcquired Hearing LossEnvironmental Exposures; Therapeutic Drugs andAgents; Aging; 5 Interventional Approaches andChallenges; Biomarkers ofOxidative Stress; Otoprotection by Targeting Oxidative Stress; Potential Interference withCell Signaling andDrug Activity; References;
Chapter 3: Corticotropin Releasing Factor Signaling intheMammalian Cochlea: AnIntegrative Niche forCochlear Homeostatic Balance Against Noise; 1 Introduction; The Evolution ofHypotheses ConcerningNoise-Induced Hearing Loss. CRF Signaling Is Involved withtheInflammatory Process5 Local (Cochlear) CRF Signaling VersusSystemic HPA Axis: ATale ofTiming, Balance ofMechanistic Actions, andDirect VersusIndirect Signaling; The Indirect CRF Signaling System; The Direct CRF Signaling System, andIts Potential Role inCochlear Function andProtection fromNoise-Induced Damage; 6 Of Glucocorticoids, Clocks, Entrainment, andaPotential Interaction BetweenSystemic andPeripheral CRF Signaling Systems Important forInflammatory Responses intheCochlea; Glucocorticoid Function; Glucocorticoid Receptors. Physiological OscillationsThe Master Clock oftheSuprachiasmatic Nucleus; Peripheral Clocks; 7 A Confluence ofBiological Disciplines That Includes Circadian Biology, Immunology, andCochlear Molecular Neurobiology Converge toSuggest aRole forCochlear CRF Signaling inModulating Inflammatory Responses intheCochlea; A Theory ofCochlear Inflammatory Response toTraumatic Noise Would Include theFollowing Aspects ofSignaling; 8 Conclusions; References;
Chapter 4: Cochlear Vascular Pathology andHearing Loss; 1 Introduction; 2 Blood Supply totheLateral Wall.