Note: 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.