Reviews of Physiology, Biochemistry and Pharmacology 186

Acknowledgements
Contents
Patch Clamp: The First Four Decades of a Technique That Revolutionized Electrophysiology and Beyond
1 The Scenario
2 The Emergence of the Concept of the Ion-Permeable Channel
3 The Consolidation of the Channel Concept
4 A New Approach to the Membrane Surface
5 The Preliminary Steps
6 The Patch Clamp Enters Adulthood
7 The Dissemination
8 Strengths and Liabilities
9 Variations on the Basic Theme
9.1 The Loose Patch
9.2 The Whole Cell and Its Potential
9.3 The Perforated Patch
9.4 Intracellular Perfusion
9.5 Capacitance Measurements and Vesicular Release
9.6 Patching Subcellular Organelles
9.7 The Patch Pipette as a Bridge Between Molecular Biology and Channel Biophysics
9.8 Patch Clamp and Calcium Imaging
9.9 Patching Slices from the Central Nervous System
10 In Vivo Patch Clamp
11 Two Different Approaches to Automated Patch Clamp
12 A Few Final Considerations
References
Roles of Intramolecular Interactions in the Regulation of TRP Channels
1 Introduction
2 Intramolecular Interactions in TRP Channels
2.1 Shared Intramolecular Interactions Mediated by Conserved Residues Across TRP Members and Species
2.2 Subfamily- or Member-Specific Intramolecular Interactions
2.2.1 Interactions Within Extracellular/Luminal Domains
2.2.2 Transmembrane Domains
2.2.3 Intracellular Domains
3 Regulation of TRP Intramolecular Interactions by Chemical Ligands
3.1 PIP2
3.2 Cannabinoids (CBD)
3.3 2-ABP
3.4 Specific Ligands
4 Implications in TRP Causing Human Diseases
5 Discussions and Perspectives
References
The Emerging Pro-Algesic Profile of Transient Receptor Potential Vanilloid Type 4
1 Introduction
2 Cell Mechanisms of TRPV4-Mediated Pain
2.1 TRPV4 and Protein-Protein Interactions
2.2 TRPV4 and Calcium Signalling
2.3 Modulation of TRPV4 Activity by Intracellular and Extracellular Enzymes
2.4 Post-Ca2+ Influx Events in TRPV4 Pain Pathways
2.5 Overview
3 Physical Pressure/Stress-Induced Mechanical Hyperalgesia
3.1 Discrete Pressure/Stretch at the Cell Membrane (Extracellular Hypotonicity)
3.2 Pressure Applied to, or Within, the Body
4 Inflammation-Induced Hyperalgesia
4.1 Role of Inflammatory Mediators
4.2 Neurogenic Inflammation
4.3 Inflammation-Induced Responses Mediated by TRPV4
4.4 Formalin- and CFA-Induced Pain
4.5 Pain from Osteoarthritis and Gout
4.5.1 Osteoarthritic Pain
4.5.2 Gout Pain
4.6 Visceral Pain
4.6.1 Irritable Bowel Syndrome
4.6.2 Inflammatory Bowel Disease
4.6.3 Pancreatitis
4.6.4 Cystitis
5 Peripheral Neuropathic Pain
5.1 Chemotherapeutic-Induced Peripheral Neuropathy
5.1.1 Paclitaxel-Induced Neuropathy
5.1.2 Thalidomide-Induced Neuropathy
5.2 Cancer-Induced Peripheral Neuropathy
5.3 Diabetic Peripheral Neuropathy
6 Headache and Temporomandibular Joint Dysfunction
7 Conclusion
References
Role of Oxytocin in Different Neuropsychiatric, Neurodegenerative, and Neurodevelopmental Disorders
1 Introduction
1.1 Neurobiology of the OT System in the Brain
1.2 Pharmacological Regulation of OTR Binding and G Protein Coupling
1.3 Intracellular OTR Effectors
1.3.1 The MAP Kinase Cascade
1.3.2 Nitric Oxide (NO) Production
1.3.3 Eukaryotic Elongation Factor 2 (eEF2) Phosphorylation/Dephosphorylation
1.3.4 GABA Transporters and the Developmentally Regulated GABA Switch
1.4 The Intranasal Route of Administration
2 Effect of OT in Brain Disorders
2.1 Epilepsy
2.2 Schizophrenia (SCZ)
2.3 Parkinson´s Disease (PD)
2.4 Attention Deficit and Hyperactivity Disorder (ADHD)
2.5 Migraine
2.6 Depression
2.7 Autism Spectrum Disorder (ASD)
3 Effect of OT During the COVID-19 Pandemic
4 Conclusion
References
Role of Distinct Fat Depots in Metabolic Regulation and Pathological Implications
1 Introduction
2 Heterogeneity of Fat Depots: Morphology, Molecular Variability, and Differentiation
2.1 Not All White Adipose Tissue (WAT)s Are Physiologically Identical
2.2 Brown Adipose Tissue (BAT): House of Futile Mitochondria
2.3 Beige Fat: A Recent Discovery
3 BAT as a Coordinating Center of Metabolism
3.1 Amino Acids as Substrate
3.2 BAT as a Sugar Sink
3.3 Lipid Clearance by BAT
4 WAT: More Than an Inert Fat Storage Site
4.1 Fat Remobilization
4.2 Vascularization of WAT
4.3 Browning of WAT
4.4 Pathological Changes in WAT Distribution
5 Altered WAT Function in Diabetic Pathogenesis
5.1 Insulin Signaling Is a Major Determiner of WAT
5.2 Signals Opposing Insulin Action Are Equally Important
5.3 Metabolites May Have a More Critical Role in WAT Regulation
5.4 Altered Chemokines and Adipomyokines in Diabetes
6 Why Does Exercise Improve WAT Metabolism?
6.1 Exercise-Induced Myokines
6.2 Exercise-Induced Chemokines from Other Organs
7 Outlook and Future Direction
References
Autocrine, Paracrine, and Endocrine Signals That Can Alter Alveolar Macrophages Function
1 Introduction
2 Autocrine Signals of Alveolar Macrophages
2.1 Interferons
2.2 Interleukins
2.3 Tumor Necrosis Factor
2.4 Transforming Growth Factor-β1
2.5 Other AM-Derived Signals
3 Paracrine Signals of Alveolar Macrophages
3.1 Alveolar Epithelial Cells
3.2 T Cells
3.3 Paracrine Signaling from Other Cells
4 Endocrine Signals of Alveolar Macrophages
5 Therapeutic Manipulation of Alveolar Macrophages
6 Perspectives
References