Nonclassical Ion Channels in the Nervous System.
Series Methods in Signal Transduction SerEditor: Milton : Taylor & Francis Group, 2021Fecha de copyright: ©2021Descripción: 1 online resource (429 pages)Tipo de contenido:- text
- computer
- online resource
- 9781000403749
| Imagen de cubierta | Tipo de ítem | Biblioteca actual | Biblioteca de origen | Colección | Ubicación en estantería | Signatura topográfica | Materiales especificados | Info Vol | URL | Copia número | Estado | Notas | Fecha de vencimiento | Código de barras | Reserva de ítems | Prioridad de la cola de reserva de ejemplar | Reservas para cursos | |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Libro electrónico | Biblioteca Encarnación Valdés Acceso en línea | Disponible | EBC6691015 |
Descripciones mejoradas de Syndetics:
Ion channels generate bioelectricity. Recent findings have documented the biophysical properties, the structure, assembly and regulation, and function and dysfunction of nonclassical nervous system ion channels. This book reviews nonclassical ion channel research, ranging from the basic biology, structure, regulations to their functions not only in normal physiology but also neurological disorders, using a variety of cutting-edge techniques and novel animal models.
Intro -- Half Title -- Series Page -- Title Page -- Copyright Page -- Contents -- Preface -- Editors -- Contributors -- 1. Endogenous Activation and Neurophysiological Functions of Acid-Sensing Ion Channels -- 1.1 Introduction -- 1.2 Endogenous Conditions That May Activate ASICs -- 1.2.1 Metabolic Production of Protons -- 1.2.1.1 Carbon Dioxide -- 1.2.1.2 Lactate -- 1.2.2 Acidification Niche and Proton Generators -- 1.2.2.1 Na+/H+ Exchangers (NHEs) -- 1.2.2.2 Hydrogen Voltage-Gated Channel 1 (Hv1) -- 1.2.2.3 Carbonic Anhydrases (CAs) -- 1.3 ASICs and Neurophysiological Functions -- 1.3.1 Synaptic Development -- 1.3.2 Synaptic Plasticity -- 1.3.3 Regional Specific Functions of ASICs -- 1.3.3.1 Amygdala -- 1.3.3.2 Retina -- 1.3.3.3 Dorsal Root Ganglia (DRG) -- 1.4 Summary and Outlook -- Acknowledgements -- References -- 2. Acid-Sensing Ion Channels and Synaptic Plasticity: A Revisit -- 2.1 Introduction -- 2.2 Protons and ASICs in Synaptic Transmission -- 2.2.1 Protons Act as a Neurotransmitter in Synaptic Signaling -- 2.2.2 Modulation of Synaptic Transmission by ASICs -- 2.3 ASIC1a in Synaptic Plasticity -- 2.3.1 ASIC1a in LTP -- 2.3.1.1 Hippocampus -- 2.3.1.2 Amygdala -- 2.3.1.3 ACC -- 2.3.2 ASIC1a in LTD -- 2.3.2.1 Hippocampus -- 2.3.2.2 Insular Cortex -- 2.4 ASICs in Synaptic Remodeling -- 2.5 Summary and Future Perspectives -- Acknowledgements -- References -- 3. Trimeric Scaffold Ligand-Gated Ion Channels -- 3.1 An Introduction of Trimeric Scaffold of Ligand-Gated Ion Channels (TS-LGICs) -- 3.2 Subunit Stoichiometry and Single Subunit Architecture of P2X Receptors and ASIC Channels -- 3.3 Ion Permeation Pathway of P2X Receptors and ASIC Channels -- 3.4 Ligand Recognitions of P2X Receptors and ASIC Channels -- 3.5 Coordinated Allostery During Channel Activation of P2X Receptors and ASIC Channels.
3.6 Ionic Selectivity of P2X Receptors and ASIC Channels -- 3.7 Architecture and Function of the Intracellular Domain of P2X Receptors and ASIC Channels -- 3.8 Other Endogenous or Exogenous Agonists of P2X Receptors and ASIC Channels -- 3.9 Perspectives -- Acknowledgments -- References -- 4. Eukaryotic Mechanosensitive Ion Channels -- 4.1 Introduction -- 4.1.1 MS and Novel MA Ion Channels-Concepts and Physiology -- 4.1.1.1 ASICs -- 4.1.1.2 TRP Channels -- 4.1.1.3 TMEM150C -- 4.1.1.4 TMEM63 (OSCA) -- 4.1.1.5 TMEM120A (TACAN) -- 4.1.1.6 TMEM87A (Elkin1) -- 4.1.2 Piezo Channels-Physiology and Activation Insights -- 4.1.2.1 Piezo Channels Are Bona fide Mechanically Activated Ion Channels -- 4.1.2.2 Structures and Activation Mechanisms of Piezo Channels -- 4.1.2.3 Physiology of Piezo Channels -- 4.2 Conclusion and Future Directions -- References -- 5. Ion Channels in Human Pluripotent Stem Cells and Their Neural Derivatives -- 5.1 Introduction -- 5.1.1 Derivation of Neurons and Glia from hPSCs -- 5.1.2 Models to Study Ion Channel Properties of hPSC Derived Neurons and Glia -- 5.2 Ion Channels in hPSCs -- 5.3 Ion Channels in hPSC Neural Derivativesin Vitro and in Vivo -- 5.3.1 Human PSC-Derived Multipotent Neural Progenitor Cells (NPCs) -- 5.3.2 Human PSC-Derived Excitatory Cortical Neurons -- 5.3.3 Human PSC-Derived GABAergic Interneurons -- 5.3.4 Human PSC-Derived Dopaminergic Neurons -- 5.3.5 Human PSC-Derived Motor Neurons -- 5.3.6 Human PSC-Derived Sensory Neurons -- 5.3.7 Human PSC-Derived Serotonin Neurons -- 5.3.8 Human PSC-Derived Glial Cells -- 5.3.9 Human PSC-Derived Cells in Transplantation Models -- 5.3.10 Two-Dimensional Human Cell Culture and Cell Transplantation as Models to Study Channelopathy -- 5.4 Ion Channels in hPSC-Derived Brain Organoids -- 5.4.1 Ion Channels in Brain Organoids.
5.4.2 Ion Channels in Sensory Organ-Specific Organoids -- 5.4.3 Organoids as a Model to Study Channelopathies -- 5.5 Concluding Remarks -- References -- 6. Exocytosis of Nonclassical Neurotransmitters -- 6.1 Introduction -- 6.2 Ca2+ Triggering of Classical Neurotransmitter (Glutamate and γ-Aminobutyric Acid, GABA) Vesicle Exocytosis at Synapses -- 6.3 Synaptotagmins as Ca2+ Sensors for Exocytosis -- 6.4 Three Modes of Synaptic Release and Their Respective Calcium Sensor(s) -- 6.4.1 Synchronous Release -- 6.4.2 Asynchronous Release -- 6.4.3 Spontaneous Release -- 6.5 Nonclassical Neurotransmitters and Neuropeptide Release -- 6.6 Monoamine Neurotransmitters -- 6.6.1 Dopamine -- 6.6.2 Norepinephrine -- 6.6.3 Serotonin -- 6.7 Neuropeptide Exocytosis -- 6.7.1 Oxytocin -- 6.7.2 Neuropeptide Y (NPY) -- 6.8 Neuro-endocrine Exocytosis -- 6.9 Summary and Outlook -- References -- 7. Nonclassical Ion Channels in Learning and Memory -- 7.1 Introduction -- 7.2 Main Text -- 7.2.1 Distribution and Activation of ASICs -- 7.2.2 ASIC1a in Spatial Learning and Memory -- 7.2.3 ASIC1a in Fear Learning and Memory -- 7.2.4 ASIC1a in Extinction Learning and Memory -- 7.2.5 ASIC1a in Appetitive Learning and Memory -- 7.2.6 ASIC1a in Procedural Learning and Memory -- 7.3 Summary -- Acknowledgments -- References -- 8. Neuropeptide Regulation of Ion Channels and Food Intake -- 8.1 Central Neuropeptide-Producing Neurons in the Control of Food -- 8.1.1 Neurons That Synthesize AgRP and POMC in the ArcuateNucleus of the Hypothalamus -- 8.1.2 Oxytocin Neurons in the Paraventricular Nucleus of the Hypothalamus -- 8.1.3 Neurons That Synthesize Melanin-Concentrating Hormone and Orexin in Lateral Hypothalamus -- 8.1.4 Neuropeptide-Producing Neurons in the Nucleus of the Solitary Tract -- 8.2 Ion Channels in the Neuropeptide Modulation of Neuronal Activity and Neurotransmitter Release.
8.2.1 G-protein Coupled Receptors -- 8.2.2 Inwardly Rectifying Potassium Channels -- 8.2.3 ATP-Sensitive Potassium Channels -- 8.2.4 Non-Selective Cation Channels -- 8.2.5 Voltage-Gated Calcium Channel and Neurotransmitter Release -- 8.3 Neuropeptide Receptors and Ion Channels in Developing Pharmacotherapy in Obesity -- 8.3.1 Dysfunctional Neuropeptide Signaling in Obesity -- 8.3.2 Dysfunctional Neuropeptide Modulation of Ion Channels in Obesity -- 8.3.3 Drugs Target Neuropeptide Receptors and Ion Channels for the Treatment of Obesity -- References -- 9. Prefrontal Inhibitory Signaling in the Control of Social Behaviors -- 9.1 Introduction -- 9.2 The Function of the mPFC in Social Interaction Behavior -- 9.2.1 Correlation Between the mPFC and Social Interaction -- 9.2.2 Causal Role of the mPFC in Social Interaction -- 9.3 Prefrontal Inhibition Is Crucial for Social Interaction -- 9.3.1 Evidence from Human Clinical Studies -- 9.3.2 Evidence from Animal Models of Diseases -- 9.3.3 Restoration of Prefrontal Cortical Inhibition Rescues Social Impairments -- 9.4 IN Subtype-Differential Modulation on Social Behavior -- 9.4.1 A Comparison Between PV INs and SST INs -- 9.4.2 PV INs in the mPFC Are Necessary for the Control of Sociability -- 9.4.3 SST INs in the mPFC Are Required for Emotion Discrimination -- 9.5 Perspectives -- Acknowledgments -- References -- 10. Studying Brain Function Using Non-human Primate Models -- 10.1 Studying High-level Visual Processing Research Using Non-human Primate Models -- 10.1.1 Object and Face Recognition in NHPs -- 10.1.2 Visual-Guide Motion in NHPs -- 10.2 Studying Vocal Communication and Auditory Function Using the Marmoset Monkey -- 10.2.1 Marmosets' Vocal Communication -- 10.2.2 Marmosets' Auditory System -- 10.3 Studying Prosocial Behavior Using the Marmoset Monkey -- 10.3.1 Prosocial Behaviors in Marmoset.
10.3.2 The Role of Hormones in Prosocial Behavior -- 10.4 Studying Self-awareness Using the Non-human Primate Model -- 10.4.1 The History of MSR in Non-human Primates -- 10.4.2 The Secret of MSR: Multisensory Integration -- 10.5 Transgenic Research in the Non-human Primate Model -- 10.5.1 Transgenic NHPs History -- 10.5.2 The Application of Transgenic NHPs -- 10.6 Conclusion -- References -- 11. Application of In Vivo Ca2+ Imaging in the Pathological Study of Autism Spectrum Disorders -- 11.1 The Biology of Ca2+ -- 11.2 Genetically Encoded Ca2+ Indicators (GECIs) -- 11.3 Two-Photon Ca2+ Imaging -- 11.4 Miniature Single-Photon Fluorescence Microscope -- 11.5 The Application of Miniature Single-Photon Fluorescence Microscopes in Neuroscience Research -- References -- 12. Nonclassical Ion Channels in Depression -- 12.1 Introduction -- 12.2 Neuroplasticity for Depression -- 12.3 HCN Channels in Depression -- 12.4 ASICs in Depression -- 12.5 P2XRs in Depression -- 12.6 TRP Channels in Depression -- 12.7 TREK1 in Depression -- 12.8 Implications -- References -- 13. Ion Channels of Reward Pathway in Drug Abuse -- 13.1 Transient Receptor Potential Channels -- 13.2 Acid-Sensing Ion Channels -- 13.3 Hyperpolarization-Activated Cyclic Nucleotide--Gated (HCN) Channels -- 13.4 P2X Receptors -- 13.5 γ-Aminobutyric Acid Type A (GABAA) Receptors -- Acknowledgment -- References -- 14. Ion Channel Conformational Coupling in Ischemic Neuronal Death -- 14.1 Introduction -- 14.2 Ion Conduction-Independent Functions of Ion Channels -- 14.3 Conformational Changes of ASIC1a Mediate Ischemic Neuronal Necroptosis -- 14.3.1 ASIC1a-Mediated Acidic Neuronal Death Is Independent from Ca2+ Signaling -- 14.3.2 Exposure of CP-1 Cytotoxic Motif Is Essential for ASIC1a-Mediated Neuronal Death -- 14.3.3 RIPK-1 Plays a Key Role in ASIC1a-Mediated Acidotoxicity.
14.3.4 ASIC1a Mediates Neuronal Necroptosis in Ischemic Brain.
Description based on publisher supplied metadata and other sources.
Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, 2021. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries.
ALA COVID Relief Fund
Notas de autor provistas por Syndetics
Tian-Le Xu, PhD, Principal Investigator and Professor
Collaborative Innovation Center for Brain Science, Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai
Dr. Tian-Le Xu obtained PhD of Neurobiology from Fourth Military Medical University. He did his postdoc training at Kyushu University and then joined University of Science and Technology of China as Professor. He was a principal investigator at Institute of Neuroscience, Chinese Academy of Sciences. Currently, he is Professor at Department of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine. Dr. Xu's research focuses on neuronal signaling and related neural disorders including chronic pain and ischemic stroke, with an emphasis on the role of acid-sensing ion channels (ASICs) in these processes. The research from Dr. Xu's lab has unveiled rich and new knowledge on the regulation and diverse functions of ASICs in health and disease.
Long-Jun Wu, PhD, Professor and Consultant
Department of Neurology, Mayo Clinic
Dr. Long-Jun Wu received PhD of Neurobiology from University of Science and Technology of China. After postdoc trainings at University of Toronto and Harvard Medical School, Dr. Wu was Instructor at Harvard Medical School and then Assistant Professor at Rutgers University. Currently, he is Professor and Consultant at Department of Neurology, Mayo Clinic. Dr. Wu's recent research primarily focuses on the neuroimmune interaction, particularly the function of microglial ion channels and receptors, in normal and diseased brain. By understanding and manipulating microglial functions, Dr. Wu's research aim to develop potential therapeutics targeting microglia in the treatment of various neurological disorders, such as epilepsy, chronic pain, stroke, neurodegeneration and autoimmune neurology.