Catecholamines I by H. BönischCatecholamines I by H. Bönisch

Catecholamines I

byH. Bönisch, J.P.M. Finberg, W.W. Fleming

Paperback | March 8, 2012

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Catecholamines are important transmitter substances in the autonomic and central nervous systems. These two volumes provide a comprehensive presentation of the state-of-the-art of catecholamine research and development in the past 15 years. The volumes present in-depth reviews of topical areas of catecholamine research in which substantial progress has been made and which are of current interest to various theoretical and clinical disciplines. Each topic has been dealt with by an established expert. Clinical subjects of relevant importance are included. Catecholamines are of interest in pharmacology, physiology, biochemistry, as well as in neurology, psychiatry, internal medicine (cardiology, hypertension, asthma), ophthalmology and anesthesiology.
Title:Catecholamines IFormat:PaperbackDimensions:571 pages, 24.4 × 17 × 0.01 inPublished:March 8, 2012Publisher:Springer-Verlag/Sci-Tech/TradeLanguage:English

The following ISBNs are associated with this title:

ISBN - 10:3642466273

ISBN - 13:9783642466274

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Table of Contents

1 Transport and Storage of Catecholamines in Vesicles.- A. Introduction.- B. Biogenesis.- I. Formation and Types of Vesicles.- II. Biogenesis of Proteins, Mucopolysaccharides and Phospholipids.- III. Biogenesis of Catecholamines.- IV. Biogenesis of ATP.- C. Uptake.- I. Uptake of Catecholamines.- 1. Dependence on Temperature: Nucleotide and Ionic Requirements.- 2. Specificity of the Uptake of Catecholamines: Structure-Uptake Relationship.- 3. Stereospecificity of the Uptake of Catecholamines.- 4. Uptake of Catecholamines into Different Synaptic Vesicles of the Brain.- 5. Effects of Drugs on the Uptake of Catecholamines.- a. Inhibition by Drugs which Deplete Catecholamines.- b Inhibition by Monoamines.- 6. Ontogenesis of the Uptake of Catecholamines into Synaptic Vesicles.- II. Uptake of Nucleotides.- III. Uptake of Ascorbate.- IV. Enzymes Involved in the Uptake of Catecholamines, Nucleotides and Ascorbate.- 1. ATPase.- 2. Phosphoryl Group-Transferring Enzymes.- 3. Electron-Transferring Enzymes.- V. Uptake of Calcium.- VI. Utilization of Energy Required for Uptake.- 1. pH of Chromaffin Granules.- 2. Ion Movements Across the Chromaffin Granule Membrane.- a. Ion Permeability of the Membrane.- b. Generation of an Electrochemical Gradient Across the Membrane.- 3. Bioenergetic Aspects of the Uptake of Catecholamines and ATP.- D. Stroage.- I. Storage in Chromaffin Granules.- II. Storage in Synaptic Vesicles.- E. References.- 2 Occurrence and Mechanism of Exocytosis in Adrenal Medulla and Sympathetic Nerve.- A. Introduction.- B. Evidence for Exocytosis.- I. Adrenal Medulla.- 1. Biochemical Evidence for Exocytosis.- a. Secretion of Soluble Proteins from Chromaffin Granules.- b. Secretion of Other Soluble Constituents of Chromaffin Granules.- c. Retention of Membrane Constituents During Secretion..- d. Exposure of Membrane Antigens of Chromaffin Granules on Cell Surface During Secretion.- 2. Morphological Evidence for Exocytosis.- 3. Exocytosis: An All or None Release Process.- 4. The Fate of the Granule Membrane After Exocytosis.- 5. Conclusions.- II. Sympathetic Nerve.- 1. Biochemical Evidence for Exocytosis.- a. Secretion of Chromogranin A, Dopamin ß-Hydroxylase and Enkephalin.- b. Secretion of Other Constituents from Noradrenaline Storage Vesicles.- c. Conclusions.- 2. Morphological Evidence for Exocytosis.- 3. Immunohistochemical Evidence for Exocytosis.- 4. Electrophysiological Evidence for Exocytosis.- 5. The Contribution of Large and Small Dense Core Vesicles to Exocytosis and Their Possible Relationship.- 6. Conclusions.- C. Mechanism of Exocytosis.- I. Molecular Organization of Membranes Involved in Exocytosis.- II. Additional Factors Necessary for Exocytosis.- 1. Metabolic Energy.- 2. Calcium.- 3. Cyclic Nucleotides.- 4. Protein Kinase C, Polyphosphoinositide Metabolism and Contents GTP-Binding Proteins.- 5. Metalloendoprotease.- III. The Mechanism of Membrane Attachment.- 1. The Role of Contractile Proteins.- 2. The Role of Changes in the Charge of Granule Membranes.- a. Phosphorylation of Phosphatidylinositol.- b. Phosphorylation of Proteins of Granule Membranes.- c. Methylation of Granule Membrane Components.- 3. The Role of Calcium and Specific Proteins.- 4. Conclusions.- IV. Mechanism of Fusion.- 1. The Behaviour of Membrane Proteins During Fusion.- 2. The Role of Lipids in Fusion.- 3. Relationship of Fusion and Mg2+-ATP Release Reaction..- V. Experimental Models for Elucidating the Mechanism of Exocytosis in Adrenal Medulla.- VI. General Conclusions.- D. References.- 3 Monamine Oxidase.- A. Introduction.- B. Classification.- C. Distribution and Localization.- D. Properties of the Enzyme.- I. Molecular Weight.- II. Cofactors.- 1. Flavin.- 2. Metal Ions.- III. The Active Site.- E. Kinetics of the Reaction.- F. Reaction Mechanism.- G. Specificity.- H. The Influence of Membrane Environment.- J. Multiple Forms.- I. Electrophoretic Studies.- II. Selective Inhibitors.- III. Substrate Specificities.- IV. Other Evidence for Multiple Forms.- V. The Nature of the Two Forms.- VI. Evidence for an Association of Type A Activity with Neurones.- K. Multiple Forms as an In Vivo Reality and Their Function.- I. Evidence from Animal Studies.- II. Evidence from Human Studies.- L. Inhibitors.- I. Classification and Mechanism of Action.- 1. Hydrazines.- 2. Cyclopropylamines.- 3. Propargylamines.- 4. Reversible Inhibitors.- II. Selectivity of MAO Inhibition - Acute vs. Chronic Studies.- III. Pharmacological Actions of MAO Inhibitors.- 1. Interaction with Centrally-Acting Drugs.- 2. Potentiation of Peripheral Effects of Sympathomimetic Amines.- a. Effects of Inhibition of Extraneuronal MAO on the Actions of Indirect Sympathomimetic Amines.- b. Effects of Inhibition of Neuronal MAO on the Actions of Indirect Sympathomimetic Amines.- 3. Effects on Blood Pressure.- 4. Other Pharmacological Effects of MAO Inhibitors.- M. Physiological Role and Functional Activity of MAO; Biochemical and Behavioural Correlates.- N. Psychiatric and Neurological Disorders: MAO Activity and MAO Inhibitors as Drugs.- I. Depressive Illness.- II. Parkinson's Disease.- O. Future Perspectives.- P. Addendum.- Q. References.- 4 The Transport of Amines Across the Axonal Membranes of Noradrenergic and Dopaminergic Neurones.- A. Introduction.- B. Neuronal Uptake.- I. Terminology and Methodology.- 1. Definition of Terms.- 2. Methodological Considerations.- II. Characteristics of Neuronal Uptake.- 1. Basic Properties.- 2. Structural Requirements.- 3. Temperature-Dependence and Metabolic Requirements.- 4. Ionic Requirements.- III. Inhibitors of Neuronal Uptake.- 1. Cocaine.- 2. Tricyclic Antidepressants and Related Compounds..- 3. Irreversible Uptake Inhibitors.- 4. Monovalent Cations.- 5. Binding Studies with Inhibitors of Neuronal Uptake.- C. Neuronal Amine Metabolism.- I. Formation of Metabolites Through MAO Activity.- II. Is There any Intraneuronal Formation of O-Methylated Metabolites?.- D. Neuronal Efflux.- I. Terminology and Methodology.- II. Spontaneous Neuronal Efflux.- III. Carrier-Mediated Neuronal Efflux.- 1. Efflux Induced by Phenylethylamines.- 2. Efflux Induced by Changes in Transmembrane Ion Gradients.- E. Proposed Mechanism of Neuronal Uptake: A Summing up.- I. General Considerations.- II. Models Accounting for the Ion-Dependence.- F. References.- 5 The Mechanism of Action of Indirectly Acting Sympathomimetic Amines.- A. Introduction.- B. The Adrenergic Nerve Ending.- I. Inward Transport by Uptake1.- II. The Outward Transport of Noradrenaline.- III. The Effect of Reserpine-like Drugs.- C. The Experimental Models.- I. Adrenergic Nerve Endings After Inhibition of Vesicular Uptake and of MAO.- II. Adrenergic Nerve Endings After Inhibition of MAO..- III. Intact Adrenergic Nerve Endings.- D. Carrier-Mediated Uptake of (+)-Amphetamine.- E. The Release of 3H-Noradrenaline After Inhibition of MAO and of Vesicular Uptake.- F. Factors Involved in the Release of Axoplasmic 3H-Noradrenaline.- I. Facilitated Exchange Diffusion.- H. The Co-transport of Sodium.- III. The Co-transport of Chloride.- IV. Inhibition of Neuronal Re-uptake.- G. The Release of 3H-Noradrenaline from Adrenergic Nerve Endings with Intact Storage Vesicles and Intact MAO (COMT Inhibited).- H. The Effects of Indirectly Acting Amines in the Presence of a Reserpine-like Compound.- J. Factors Which Influence the 3H-Noradrenaline-Releasing Effect of Indirectly Acting Amines.- I. Neuronal Uptake.- II Inhibition of Neuronal MAO.- III. The Existence of a Reserpine-like Effect for the Indirectly Acting Amine.- IV. Mobilization of Vesicular 3H-Noradrenaline.- V. Exocytotic Release in the Absence of Extracellular Calcium.- VI. The Axoplasmic Compartment(s).- K. The Release by Indirectly Acting Amines of Dopamine from Dopaminergic Nerve Endings.- L. Conclusions.- M. References.- 6 The Extraneuronal Uptake and Metabolism of Catecholamines.- A. Introduction.- I. The Extraneuronal System.- II. Other Non-neuronal Systems.- B. Uptake2.- I. Inward Transport.- 1. Definition and Occurrence of Uptake2.- 2. The Stereoselectivity of Uptake2.- 3. The Substrate Spectrum of Uptake2.- 4. The Distribution of 3H-Catecholamines in the Rat Heart.- 5. The "Lipophilic Entry" of Agents into Extraneuronal Cells.- II. Outward Transport.- 1. The Susceptibility of the Efflux of Catecholamines to Inhibition of Uptake2.- 2. The Interaction Between Different Substrates of Uptake2.- III. The Effects of Various Ions on Uptake2.- C. The Extraneuronal Metabolizing Systems.- I. The Extraneuronal O-Methylating System.- 1. The Kinetic Constants.- 2. The Revised Mathematical Model.- 3. The Functional Characteristics.- 4. The Intracellular Enzyme.- 5. The Increase of Sinside Induced by Inhibition of the Intracellular Enzyme.- 6. The Importance of "Lipophilic Entry" of Catecholamines.- II. The Extraneuronal Deaminating System.- III. The Co-existence of the Two Extraneuronal Enzymes.- D. Supersensitivity to Catecholamines After Inhibition of the Extraneuronal O-Methylating System.- E. The Interaction Between the Neuronal and the Extraneuronal Sites of Loss.- F. Conclusions: A Comparison of Uptake2 with Uptake1.- G. References.- 7 Catecholamines Receptors.- A. Introduction.- B. Relationship of Catecholamine Receptors to Effector Systems.- I. Cyclic AMP Formation.- II. Calcium Flux and Phosphatidylinositol Breakdown.- III. Other Effects of Catecholamines.- C. In Vitro Binding Assays.- I. Assay of ?-Adrenoceptors.- II. Assay of ?-Adrenoceptors.- III. Assay of Dopamine Receptors.- D. In Vitro Properties of Adrenoceptors.- I. Effects of Guanine Nucleotides.- 1. Effects of Guanine Nucleotides on ?-Adrenoceptors.- 2. Effects of Guanine Nucleotides on ?-Adrenoceptors.- 3. Effects of Guanine Nucleotides on Dopamine Receptors.- II. Effects of Ions.- 1. Effects of Ions on ?-Adrenoceptors.- 2. Effects of Ions on ?-Adrenoceptors.- 3. Effects of Ions on Dopamine Receptors.- III. Energetics of the Interactions of Agonists and Antagonists with Catecholamine Receptors.- 1. Energetics of Interactions with ?-Adrenoceptors.- 2. Energetics of Interactions with Dopamine Receptors.- IV. Effects of Membrane Altering Agents.- 1. Effects on ?-Adrenoceptors.- 2. Effects on Dopamine Receptors.- E. Localization of Catecholamine Receptors.- F. Multiplicity of Catecholamine Receptor Subtypes.- I. ?-Adrenoceptor Subtypes.- II. ?-Adrenoceptor Subtypes.- III. Dopamine Receptor Subtypes.- IV. Assay of Receptor Subtypes.- G. Regulation of the Sensitivity of Catecholamine Receptor Systems.- I. Effects of Decreased Stimulation.- II. Effects of Increased Stimulation.- III. Specific Alterations in Receptor Subtypes Caused by Changes in the Availability of Neurotransmitters.- IV. Regulation of Responsiveness Not Mediated by Changes in the Density of Receptors.- V. Effects of Hormones on Catecholamine Receptors and Responsiveness.- H. Agonist-Induced Desensitization.- J. Ontogeny of Catecholamine Receptors in the Central Nervous System.- K. Solubilization, Purification, and Reconstitution of Catecholamine Receptor/Effector Systems.- L. Molecular Cloning of Catecholamine Receptors.- M. Conclusion.- N. References.- 8 Presynaptic Receptors on Catecholamine Neurones.- A. Introduction and Definition of Terms.- B. The Dopamine Autoreceptor.- I. Basic Functions of the Dopamine Autoreceptor.- 1. Modulation of Depolarization-Evoked Dopamine Release.- a. The Origins of the Hypothesis that Dopamine Autoreceptors Modulate Dopamine Release.- b. Seven Years of Controversy.- c. The Dopamine Autoreceptor Modulating 3H-Dopamine Release Rediscovered.- d. A Physiological Role for the Dopamine Autoreceptor?.- e. The Mechanism of Action of the Dopamine Autoreceptor Modulating Depolarization-Evoked Release of 3H-Dopamine.- f. Are Autoreceptors Located on Dopaminergic Terminals or is There a Trans-synaptic Second Messenger?.- g. Autoreceptor Modulation of 3H-Dopamine Release from Synaptosomes.- h. Conclusions.- 2. Synthesis of Dopamine, In Vitro and In Vivo.- a. The Origins of the Hypothesis that Dopamine Autoreceptors Modulate the Synthesis of Dopamine.- b. The Localization of Synthesis-Modulating Dopamine Autoreceptors to Dopaminergic Terminals.- c. The Case Against Dopamine Autoreceptors Modulating the Synthesis of Dopamine.- d. Conclusions.- 3. Electrical Activity of Dopaminergic Neurones.- a. The Origins of the Hypothesis that Dopamine Autoreceptors Modulate the Firing of Dopaminergic Neurones.- b. The Debate over the Polysynaptic Feedback Loop vs. an Autoreceptor Mechanism for the Actions of Amphetamine.- c. Autoreceptor Mechanism for the Effects of Apomorphine and Dopamine on the Firing of Dopaminergic Neurones.- d. Pharmacological Aspects of the Dopamine Autoreceptor Modulating the Firing of Dopaminergic Neurones.- e. Electrophysiological Aspects of the Function of the Dopamine Autoreceptor.- f. Conclusions.- g. Questions for Future Electrophysiological Studies of Dopamine Autoreceptors.- II. Studies on the Functions of the Dopamine Autoreceptor.- 1. Locomotor Sedation.- a. The Origin of Behavioural Models for Dopamine Autoreceptor Function.- b. Criticisms of the Autoreceptor Hypothesis as the Mechanism of Locomotor Sedation Induced by Low Doses of Dopamine Receptor Agonists.- 2. "Turnover" of Dopamine.- a. Release of Newly Synthesized and Endogenous Dopamine.- b. Disappearance of Dopamine After a-Methyl-tyrosine Administration.- c. The ?-Butyrolactone Model.- d. Measurement of Dopamine Metabolites.- ?. The Involvement of Autoreceptors vs. the Long-Loop Feed-back.- ?. Effects of Chronic Administration of Neuroleptics on Dopamine Metabolite Levels.- III. Receptor Binding Identification of the Dopamine Autoreceptor.- 1. Successes and Failures in Detecting Dopamine Autoreceptors with Receptor Binding Techniques.- 2. The Proliferation of Dopamine Receptor Binding Sub-sites and Their Questionable Relationship to Functional Dopamine Receptors.- 3. D3:A Binding Site in Search of a Function.- 4. Conclusions.- IV. Dopamine Neurones Without Autoreceptors.- 1. The Frontal Cortex.- 2. The Median Eminence.- V. The Role of Somatodendritic Dopamine Autoreceptors...- VI. The Pharmacological Characteristics of the Dopamine Autoreceptor.- 1. In Vitro Pharmacological Characterization of Dopamine Autoreceptors.- 2. In Vivo Pharmacological Characterization of Dopamine Autoreceptors.- VII. Potential Clinical Relevance of Dopamine Autoreceptors..- 1. A Model for the Pre- and Postsynaptic Actions of Neuroleptics.- 2. The Therapeutic Mechanism of Action of Neuroleptics..- 3. A Role of the Dopamine Autoreceptor in the Therapeutic Action of Neuroleptics?.- 4. Agonists Acting at the Dopamine Autoreceptor: Potential as Therapeutic Agents.- C. Presynaptic Heteroreceptors Modulating Dopamine Function..- I. Cholinoceptors Modulating Dopamine Function.- II. Opiate Receptors Modulating Dopamine Function.- III. Excitatory Amino Acid Receptors Modulating Dopamine Function.- IV. GABA Receptors Modulating Dopamine Function.- V. Other Presynaptic Heteroreceptors Modulating Dopamine Function.- VI. The Physiological Relevance of Presynaptic Heteroreceptors..- D. Autoadrenoceptors.- I. Functions_of ?2 -Autoadrenoceptors.- 1. Modulation of Noradrenaline Release.- 2. Modulation of the Electrical Activity of Noradrenergic Neurones.- a. The Superior Cervical Ganglion.- b. The Locus Coeruleus.- II. Comparisons Between ?2-Autoadrenoceptors and the Dopamine Autoreceptor.- III. Presynaptic ?-Autoadrenoceptors on Peripheral Noradrenergic Neurones.- E. Presynaptic Dopamine Receptors Modulating Noradrenaline Release.- F. Conclusions.- G. References.- 9 Adaptive Supersensitivity.- A. Introduction.- B. The Induction of Adaptive Supersensitivity.- I. Experimental Procedures Which Have Been Used to Produce Supers ensitivity.- II. Effector Cell Activity (Use-Disuse) Versus Trophic Substances as Factors Regulating Sensitivity.- 1. Skeletal Muscle.- 2. Smooth Muscle.- C. Characteristics of Adaptive Supersensitivity.- I. Temporal Aspects.- II. Agonist Specificity.- D. Possible Mechanisms for Changes in Sensitivity of Effector Cells and Evidence Supporting or Opposing these Mechanisms.- I. Changes in Receptors.- 1. Skeletal Muscle and Application of Receptor Theory.- 2. Salivary Glands.- 3. Smooth Muscle.- 4. Cardiac Muscle.- 5. Pineal Gland.- 6. Peripheral and Central Nervous System.- II. Changes in Electrophysiologic Characteristics.- 1. Skeletal Muscle.- 2. Smooth Muscle.- 3. Cardiac Muscle.- 4. Central Nervous System.- III. The Role of "Second Messengers" in Supersensitivity.- 1. Calcium.- a. Skeletal Muscle.- b. Cardiac Muscle.- c. Smooth Muscle.- d. Central Nervous System.- 2. Cyclic Nucleotides.- 3. Phosphoinositides.- IV. Cell-to-Cell Coupling.- E. Summary and Conclusions.- I. Skeletal Muscle.- II. Smooth Muscle.- III. Cardiac Muscle.- IV. Exocrine Glands.- V. Pineal Gland.- VI. Central Nervous System.- F. References.