Trace Amines and Neurological Disorders

Potential Mechanisms and Risk Factors
 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 12. Juli 2016
  • |
  • 432 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
E-Book | PDF mit Adobe DRM | Systemvoraussetzungen
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
978-0-12-803616-7 (ISBN)
 

Trace Amines and Neurological Disorders: Potential Mechanisms and Risk Factors explores trace amines which, under normal conditions, are present in the mammalian brain and peripheral nervous tissues at very low (nanomolar) concentrations. However, in a diverse array of human pathologies ranging from substance abuse, depression, attention deficit hyperactivity disorder, eating disorders, schizophrenia, and other neurological and neuropsychiatric diseases, the levels of trace amines are unusually high with an imbalance in their functions. Furthermore, the rapid turnover of trace amines is evidenced by their dramatic increases following treatment with monoamine oxidase inhibitors (MAOI) or deletion of the MAO genes. This suggests that the concentration of trace amines may be considerably higher at neuronal synapses than predicted by steady-state measures, implicating some pathophysiological role. Therefore, understanding molecular mechanisms and developing selective agonists and antagonists for trace amine-associated receptors (TAARs) has become a good approach for treating these diseases. Although the effects of trace amines at low physiological concentrations in mammalian species have been difficult to demonstrate, they may serve to maintain the neuronal activity of other monoamine neurotransmitters by possessing postsynaptic modulatory effects, particularly dopamine and serotonin, within defined physiological limits. Such an effect of trace amines makes them ideal candidates for the development of novel therapeutics for a wide range of human disorders. This book presents up-to-date, cutting-edge, and comprehensive information on the link between trace amines and neurological disorders.


  • Focuses on recent findings on trace amines, providing insights into the functional significance, molecular mechanisms, and biological relevance of TAARS in neurological disorders
  • Edited work with chapters authored by leaders in the field from around the globe, the broadest, most expert coverage available
  • Provides cutting-edge research on trace amines-mediated signaling in vertebrate model systems
  • Englisch
  • San Diego
  • |
  • USA
Elsevier Science
  • 11,68 MB
978-0-12-803616-7 (9780128036167)
0128036168 (0128036168)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Trace Amines and Neurological Disorders
  • Copyright Page
  • Dedication
  • Contents
  • List of Contributors
  • Foreword by J.J. Canales
  • Foreword by D.K. Grandy
  • Preface
  • Acknowledgments
  • I. Introduction and Description of Trace Amines and Trace Amine-Associated Receptors
  • 1 Trace Amines: An Overview
  • Introduction
  • Trace Amine-Associated Receptors
  • TAs in Invertebrates
  • Conclusion
  • References
  • 2 Methods of Trace Amine Analysis in Mammalian Brain
  • Introduction
  • Methods of Trace Amine Analysis
  • Gas Chromatography
  • Gas Chromatography-Mass Spectrometry
  • High-Performance Liquid Chromatography
  • Thin-Layer Chromatography
  • Radioenzymatic Methods
  • Protocols for Trace Amine Analysis in Brain
  • Determination of p-TA in Rat Brain
  • Determination of PEA, m-TA, and p-TA in Rat Brain
  • Determination of T in Rat Brain
  • Determination of PEOH, m-OA, and p-OA in Rat Brain
  • Conclusion
  • Acknowledgments
  • References
  • 3 Synthesis and Neurochemistry of Trace Amines
  • Introduction
  • Vertebrate Trace Amines
  • Trace Amine Synthesis
  • AADC Tissue Distribution
  • AADC Regulation
  • Trace Amine Degradation
  • Trace Amine Storage and Release
  • Vertebrate Trace Amine Receptors
  • Invertebrate Trace Amines
  • Trace Amines as Invertebrate Neurotransmitters
  • Invertebrate Trace Amine Receptors
  • p-Octopamine Receptors
  • p-Tyramine Receptors
  • Trace Amine Synthesis by Prokaryotes
  • Concluding Statements
  • References
  • 4 The Origin and Evolution of the Trace Amine-Associated Receptor Family in Vertebrates
  • Introduction
  • The Evolutionary Origin of TAARs
  • TAAR Genes in Various Vertebrate Species
  • TAARs Originated From the Common Ancestor of Jawless and Jawed Vertebrates
  • 5-HT-4 Receptors Are the Most Closely Related GPCRs to TAARs
  • Evolution of TAAR Gene Family
  • Subfamilies of Vertebrate TAARs
  • Expansion of Subfamily I TAAR Genes in Teleost Fishes
  • Degeneration of TAAR Genes in Amphibian, Reptiles, and Birds
  • A Slight Increase of Mammalian TAAR Genes
  • Summary: The Evolutionary History of TAAR Gene Family
  • Adaptive Evolution of TAARs
  • Teleost Fishes
  • Mammals
  • Conclusion and Perspectives
  • References
  • 5 Differential Modulation of Adrenergic Receptor Signaling by Octopamine, Tyramine, Phenylethylamine, and 3-Iodothyronamine
  • Introduction
  • Aminergic Receptors with Partially Overlapping Ligand-Binding Profiles
  • Indications for Binding and Action of the Trace Amines OA, PEA, and TYR at Adrenergic Receptors
  • Signaling Modification at ADRB1 and ADRB2 by OA, TYR, and PEA
  • 3-T1AM Is a Multi-GPCR Target Ligand
  • Thyronamines-A Peculiar Subclass of Thyroid Hormone-Derived Trace Amines
  • 3-T1AM Mediates Selective Signaling at ADRA2A and TAAR1/ADRA2A Hetero-Oligomerization Modifies ADRA2A Signaling
  • 3-T1AM Interacts with ß-Adrenergic Receptor 2
  • 3-T1AM Is an Inverse Agonist at Human TAAR5
  • An Axis Between Thyronamines, TRP Channel-Mediated Ca2+ Flux, and ß-Adrenergic Receptors
  • Conclusion
  • Acknowledgments
  • References
  • 6 Effects of Trace Amines on the Dopaminergic Mesencephalic System
  • Introduction
  • The DAergic Mesencephalic System
  • DAergic Transmission
  • Trace Amines
  • Trace Amines-Associated Receptors
  • Role of TAs in the Modulation of DAergic Mesencephalic System
  • TAs-Induced DA Release
  • Direct Interaction of TAs with DAT
  • TAAR1-Mediated DA Release
  • TAAR1-Induced Modulation of DAergic Neuron Firing Activity
  • TAs-Induced Modulation of D2 Receptors
  • TAs-Induced Modulation of Glutamatergic and GABAergic Transmission on DAergic Mesencephalic Neurons
  • TAs Involvement in Brain Disorders Associated With DAergic Dysfunction
  • Conclusion
  • References
  • 7 Trace Amine-Associated Receptors in the Cellular Immune System
  • Introduction
  • RNA Expression of TAAR in Blood Leukocytes
  • Protein Expression of TAAR in Blood Leukocytes
  • Signal Transduction of TAAR in Blood Leukocytes
  • Biogenic Amine-Induced and TAAR-Mediated Cellular Functions in Isolated Blood Leukocytes
  • Concluding Remarks
  • References
  • 8 Trace Amines and Their Receptors in the Control of Cellular Homeostasis
  • Introduction
  • Trace Amine-Associated Receptor 1
  • TAAR1 Role in Dopaminergic Transmission
  • TAAR1 Regulation of Other Neurotransmitters
  • Functional Relevance
  • TAAR1 in Schizophrenia
  • TAAR1 in Drug Abuse
  • Peripheral TAAR1
  • Trace Amines and Olfaction
  • Concluding Statements
  • References
  • 9 Trace Amine-Associated Receptor 1 Modulation of Dopamine System
  • Introduction
  • Expression
  • Cellular Signaling
  • TAAR1 Regulation of Dopamine System
  • TAAR1 and its Ligands
  • TAAR1 and Psychiatric Disorders
  • TAAR1 and Addiction
  • TAAR1 and Parkinson's Disease
  • Conclusion
  • References
  • 10 Trace Amines as Intrinsic Monoaminergic Modulators of Spinal Cord Functional Systems
  • Introduction
  • The Trace Amines and Their Receptors
  • Relating a Putative Intrinsic Spinal Cord TA-ergic System to Modulation of Intrinsic Spinal Locomotor Activity
  • Possible Physiological Relevance of the TAs
  • TAs as Effectors of Dietary and Metabolic Status
  • The Role of an Exquisitely Regulated Trace Aminergic System in Metamodulation
  • Future Considerations
  • Conclusion
  • Acknowledgments
  • References
  • 11 Trace Amine-Associated Receptors: Ligands and Putative Role in the Central Nervous System
  • Introduction
  • Trace Amine-Associated Receptors and Their Distribution
  • TAAR Ligands: Trace Amines
  • TAAR Ligands: Thyronamines
  • Pharmacological Agents as TAAR1 Ligands
  • Odorous Amines as TAAR Ligands
  • Lessons From Transgenic Mouse Models
  • Conclusion
  • References
  • 12 ß-Phenylethylamine Requires the Dopamine Transporter to Release Dopamine in Caenorhabditis elegans
  • Introduction
  • ßPEA Causes Behavioral Changes in Caenorhabditis elegans
  • ßPEA Activates the Ligand-Gated Chloride Channel LGC-55 to Generate Behavioral Effects in C. elegans
  • ßPEA Requires the Dopamine Transporter to Increase the Extracellular Levels of Dopamine in C. elegans
  • In C. elegans ßPEA Does Not Require the Vesicular Monoamine Transporter to Generate Dopamine Efflux
  • Conclusion
  • References
  • II. Trace Amines and Olfaction
  • 13 Trace Amine-Mediated Olfactory Learning and Memory in Mammals and Insects: A Brief Comparative Review
  • Introduction
  • Trace Amines: As Neurotransmitter, Neuromodulator, and Neurohormone
  • Trace Amine-Mediated Neuromodulatory Actions in Vertebrates
  • Trace Amine-Mediated Neuromodulatory Actions in Invertebrates
  • Chemosensory Receptors in Mammal and Insect Olfactory Systems
  • Trace Amine-Associated Receptors and Olfaction in Vertebrates
  • Trace Amine-Associated Receptors and Olfaction in Invertebrates
  • Conclusion
  • References
  • 14 Octopaminergic and Tyraminergic Signaling in the Honeybee (Apis mellifera) Brain: Behavioral, Pharmacological, an ...
  • Introduction
  • Biosynthesis of Tyramine and Octopamine
  • Distribution of Tyramine and Octopamine in the Brain of Adult Honeybees
  • Molecular and Pharmacological Properties of Honeybee Tyramine and Octopamine Receptors
  • The AmTyr1 Receptor
  • The AmTyr2 Receptor
  • The AmOcta1 Receptor
  • The AmOctß Receptors
  • Physiological and Behavioral Aspects of Octopamine and Tyramine Signaling
  • Locomotor Activity
  • Visual Sensitivity and Phototaxis
  • Gustatory and Olfactory Sensitivity
  • Nonassociative Learning
  • Associative Learning
  • Division of Labor
  • Conclusion
  • References
  • 15 Octopamine and Tyramine Signaling in Locusts: Relevance to Olfactory Decision-Making
  • Introduction
  • Olfactory Decision-Making in Locusta
  • Decision-Making in Animals
  • Locust Phase Polyphenism
  • Olfactory Decision-Making in the Phase Change of Locusta
  • Tyrosine Metabolism in Gregarious and Solitary Locusts
  • Octopamine and Tyramine Signaling
  • Octopamine and Tyramine Signaling in Insects
  • Distribution of Octopamine in the Locust Central Nervous System
  • Distribution of Tyramine in the Locust Central Nervous System
  • Distribution of Octopamine and Tyramine Receptors in the Central Nervous System
  • Convergence and Divergence in Distribution of Octopamine and Tyramine Signaling in the Central Nervous System
  • Distribution of Octopamine and Tyramine Signaling Suggests Their Relevance to Olfactory Sensation
  • Octopamine and Tyramine Signaling Mediate Olfactory Decision-Making in Locusta
  • Potential Mechanism by Which Octopamine-Oara and Tyramine-TAR Signaling Mediate Individual Olfactory Decision in Locusta
  • Octopamine-OARa and Tyramine-TAR Signaling in the Brain Mediate Individual Olfactory Decision-Making at the Neurochemical L ...
  • Octopamine-OARa and Tyramine-TAR Signaling in the Central Nervous System Mediate Olfactory Decision-Making at the Neurogene ...
  • Octopamine-OARa and Tyramine-TAR Signaling May Mediate Olfactory Decision-Making in a Seesaw Manner
  • Conclusion
  • Acknowledgments
  • References
  • III. Trace Amines and Neurological Disorders
  • 16 Neurochemical Aspects of Neurological Disorders
  • Introduction
  • Neurotraumatic Diseases
  • Molecular Aspects of Stroke
  • Molecular Aspects of SCI
  • Molecular Aspects of TBI
  • Neurodegenerative Diseases
  • Molecular Aspects of AD
  • Molecular Aspects of PD
  • Molecular Aspects of HD
  • Molecular Aspects of ALS
  • Molecular Aspects of Prion Diseases
  • Neuropsychiatric Diseases
  • Molecular Aspects of Depression
  • Molecular Aspects of Autism
  • Conclusion
  • References
  • 17 Trace Amines and Their Relevance to Neurological Disorders: A Commentary
  • Introduction
  • Association Between Trace Amines and Neurological Disorders
  • Conclusion
  • References
  • 18 Trace Amines in Neuropsychiatric Disorders
  • Introduction
  • Discovery of Trace Amines
  • Distribution of Trace Amines
  • Genetics and Location of TAAR1
  • Monoamines and Their Effect
  • Mechanism of Action of TAAR1
  • Pharmacogenetic Perspective
  • Trace Amines in Neuropsychiatric Disorders
  • Schizophrenia
  • Migraine Headaches
  • Depression
  • Attention Deficit Hyperactivity Disorder
  • Conclusion
  • References
  • 19 ß-Phenylethylamine-Class Trace Amines in Neuropsychiatric Disorders: A Brief Historical Perspective
  • Introduction
  • Trace Amines and Schizophrenia
  • Trace Amines and Affective Disorders
  • Trace Amines and Extrapyramidal Disorders
  • Trace Amines and Migraine
  • Trace Amines and Attention Deficit Hyperactivity Disorders
  • Novel Monosubstituted PEA Derivatives: Could These Trace Amines Lead to New Pharmacological Treatments?
  • Conclusion
  • Acknowledgments
  • References
  • 20 Involvement of So-Called D-Neuron (Trace Amine Neuron) in the Pathogenesis of Schizophrenia: D-Cell Hypothesis
  • Introduction
  • So-Called D-Neuron (Trace Amine (TA) Neuron)
  • Definition of "D-Neuron"
  • Anatomy and Species Differences
  • Lack of D-Neurons in Striatum and Nucleus Accumbens of Schizophrenia
  • Trace Amine-Associated Receptor, Type 1 (TAAR1)
  • Functions
  • Acts of TAAR1 on Ventral Tegmental Area (VTA) Dopamine (DA) Neuron
  • A New "D-Cell Hypothesis" of SchIzophrenia
  • Critical Theory for the Molecular Basis of Mesolimbic Dopamine Hyperactivity
  • D-Cell Hypothesis Explains Disease Progression of Schizophrenia, Leading to Establish Novel Therapeutic Strategies
  • Some Evidences Supporting the D-Cell Hypothesis of Schizophrenia
  • D-Cell Hypothesis: Link of NSC Dysfunction Hypothesis and Dopamine Hypothesis of Schizophrenia
  • Conclusion
  • Acknowledgments
  • References
  • 21 3-Iodothyronamine, a New Chapter in Thyroid Story: Implications in Learning Processes
  • Introduction
  • T1AM has some but not all the Features of a Trace Amine
  • Pharmacological Features of T1AM and of its Oxidative Metabolite in Rodents
  • T1AM and TA1 Behave as Neuromodulators of the Histaminergic System
  • T1AM and TA1 also Revert Scopolamine- and Diazepam-Induced Amnesia
  • The Histamine-Thyroid Axes as a Novel Potential Target for Diagnosis or Therapy of Neurodegenerative Disorders
  • Conclusion
  • References
  • 22 Trace Amine Receptors and Mood Disorders: Focusing on Depression
  • Introduction
  • TAs and Depression
  • Colocalization of TAs and Traditional Neurotransmitters
  • Alteration of TAs in Depressive Disorder
  • Modulation Effects of TAs on Neurotransmitters
  • TAs and Antidepressants
  • Trace Amine-Associated Receptors
  • Conclusion
  • Acknowledgments
  • References
  • 23 Trace Amine-Associated Receptor 1: Implications for Treating Stimulant Drug Addiction
  • Introduction
  • Effects of Stimulant Drugs
  • Treatment of Addiction and Animal Models
  • Addiction-Related Studies Using Genetically Altered Mice
  • Addiction-Related Studies Using TAAR1 Agonists
  • Conclusions From the Drug Studies
  • Implications and Issues
  • Conclusion
  • References
  • 24 Trace Amines and Their Potential Role in Primary Headaches: An Overview
  • Introduction
  • Pathophysiology of Cluster and Migraine Headaches
  • Genetics of Primary Headaches
  • Genetics of Cluster Headache
  • Genetics of Migraine Headache
  • Pharmacology of Primary Headaches
  • Neuropeptides in Primary Headaches
  • Catecholamines in Primary Headaches
  • Trace Amines in Primary Headaches
  • Molecular Mechanisms Underlying Primary Headaches
  • Conclusion
  • References
  • IV. Perspective
  • 25 Perspective and Directions for Future Research on Trace Amines and Neurological Disorders
  • Introduction
  • Neurological Disorders
  • TAARs and Their Relevance to Neurological Disorders
  • GPCRs Signaling
  • TAAR-Mediated Signaling
  • Conclusion
  • References
  • Index
  • Back Cover

Dateiformat: EPUB
Kopierschutz: Adobe-DRM (Digital Rights Management)

Systemvoraussetzungen:

Computer (Windows; MacOS X; Linux): Installieren Sie bereits vor dem Download die kostenlose Software Adobe Digital Editions (siehe E-Book Hilfe).

Tablet/Smartphone (Android; iOS): Installieren Sie bereits vor dem Download die kostenlose App Adobe Digital Editions (siehe E-Book Hilfe).

E-Book-Reader: Bookeen, Kobo, Pocketbook, Sony, Tolino u.v.a.m. (nicht Kindle)

Das Dateiformat EPUB ist sehr gut für Romane und Sachbücher geeignet - also für "fließenden" Text ohne komplexes Layout. Bei E-Readern oder Smartphones passt sich der Zeilen- und Seitenumbruch automatisch den kleinen Displays an. Mit Adobe-DRM wird hier ein "harter" Kopierschutz verwendet. Wenn die notwendigen Voraussetzungen nicht vorliegen, können Sie das E-Book leider nicht öffnen. Daher müssen Sie bereits vor dem Download Ihre Lese-Hardware vorbereiten.

Weitere Informationen finden Sie in unserer E-Book Hilfe.


Dateiformat: PDF
Kopierschutz: Adobe-DRM (Digital Rights Management)

Systemvoraussetzungen:

Computer (Windows; MacOS X; Linux): Installieren Sie bereits vor dem Download die kostenlose Software Adobe Digital Editions (siehe E-Book Hilfe).

Tablet/Smartphone (Android; iOS): Installieren Sie bereits vor dem Download die kostenlose App Adobe Digital Editions (siehe E-Book Hilfe).

E-Book-Reader: Bookeen, Kobo, Pocketbook, Sony, Tolino u.v.a.m. (nicht Kindle)

Das Dateiformat PDF zeigt auf jeder Hardware eine Buchseite stets identisch an. Daher ist eine PDF auch für ein komplexes Layout geeignet, wie es bei Lehr- und Fachbüchern verwendet wird (Bilder, Tabellen, Spalten, Fußnoten). Bei kleinen Displays von E-Readern oder Smartphones sind PDF leider eher nervig, weil zu viel Scrollen notwendig ist. Mit Adobe-DRM wird hier ein "harter" Kopierschutz verwendet. Wenn die notwendigen Voraussetzungen nicht vorliegen, können Sie das E-Book leider nicht öffnen. Daher müssen Sie bereits vor dem Download Ihre Lese-Hardware vorbereiten.

Weitere Informationen finden Sie in unserer E-Book Hilfe.


Download (sofort verfügbar)

128,52 €
inkl. 19% MwSt.
Download / Einzel-Lizenz
ePUB mit Adobe DRM
siehe Systemvoraussetzungen
PDF mit Adobe DRM
siehe Systemvoraussetzungen
Hinweis: Die Auswahl des von Ihnen gewünschten Dateiformats und des Kopierschutzes erfolgt erst im System des E-Book Anbieters
E-Book bestellen

Unsere Web-Seiten verwenden Cookies. Mit der Nutzung dieser Web-Seiten erklären Sie sich damit einverstanden. Mehr Informationen finden Sie in unserem Datenschutzhinweis. Ok