Autonomic and Enteric Ganglia

I. History and Anatomical Bases of Ganglionic and Enteric Transmission.- 1. Historical Development of Concepts of Ganglionic Transmission.- I. Anatomical and Morphological Aspects of Past Ganglionic Research.- II. Neurotransmitters.- III. Neuropharmacology and Neurophysiology.- IV. Unanswered Questions.- References.- 2. Anatomy, Histology, and Electron Microscopy of Sympathetic, Parasympathetic, and Enteric Neurons.- I. Introduction.- II. Parasympathetic and Sympathetic Ganglia.- A. Gross Anatomical Considerations.- B. Convergence and Divergence.- C. Origin of Fibers That Form Postganglionic Nerves from Superior Cervical Ganglia.- D. Innervation of the Gallbladder.- E. Innervation of the Urinary Bladder.- F. Ultrastructural Considerations of Principal Sympathetic Ganglion Cells.- III. Chromaffin Cells, Small Intensely Fluorescent Cells, Small Granule-Containing Cells, Interneurons, Paraneurons, and Paraganglia.- IV. Enteric Nervous System.- A. Extrinsic Nerves.- B. Intrinsic Nerves.- C. Glial Cells.- V. Peptides in Other Autonomic Ganglia.- References.- II. Transmission and Modulation in Sympathetic Ganglia and Their Neuropharmacology.- 3. General Concepts of Ganglionic Transmission and Modulation.- I. Introduction.- A. Historical Remarks.- B. Scope of This Chapter.- II. Synaptic Transmission, Its Modulation, and Its Components.- A. Synaptic and Modulatory Events in Sympathetic Ganglia.- B. Neural Elements, Transmitters, and Modulators.- III. Interactions and Reflex Functions.- IV. Conclusions: Sympathetic Ganglia as “Little Brains”.- References.- 4. Electrophysiological Properties of Sympathetic Neurons.- I. Membrane Characteristics at Rest.- A. Resting Potential.- B. Electric Constants.- C. Voltage-Current Relationship.- II. Active Membrane Characteristics.- A. Action Potentials.- B. Afterpotentials.- III. Effects of Ions and Drugs.- A. Effects of Lithium.- B. Effects of Some Divalent Cations.- C. Effects of Catecholamines on Ca2+-Dependent Potentials.- D. Hyperpolarization Caused by the Activity of an Electrogenic Sodium Pump.- E. Rhythmic Hyperpolarizations in Caffeine-Treated Neurons.- IV. Conclusions.- References.- 5. General Characteristics and Mechanisms of Nicotinic Transmission in Sympathetic Ganglia.- I. Physiological Significance.- II. General Characteristics.- A. Amphibian Ganglia.- B. Mammalian Ganglia.- III. Reversal Potential and Ionic Mechanism of the Fast Excitatory Postsynaptic Potential.- A. Reversal Potential.- B. Effect of Ion Substitution.- IV. Relationship between the Synaptic Current and Potential.- A. Time-Course of the Synaptic Current.- B. Current-Voltage Relationship.- C. Reconstruction of the Fast Excitatory Postsynaptic Potential from the Fast Excitatory Postsynaptic Current.- D. Effects of Anticholinesterases.- E. Effects of Low Temperature.- V. Characteristics of the Ion-Channel Gating.- A. Physiological Significance of the Decay Phase of the Fast Excitatory Postsynaptic Current.- B. Noise Analysis.- C. Two Different Types of Ion Channels or a Single Type of Ion Channel Having a Complexed Pattern of Gating.- D. Comparison with Other Ion Channels Gated by the Nicotinic Action of Acetylcholine.- E. Acetylcholine-Activated Ion Channel in the Cultured Bullfrog Sympathetic Ganglion Cell.- VI. Mode of Acetylcholine Action on the Nicotinic Receptor.- A. Dose-Response Curve of Acetylcholine Action.- B. Pharmacological Characteristics of the Nicotinic Receptor.- VII. Regulatory Role of Ca2+ in the Gating Mechanism of the Nicotinic Receptor-Ion Channel Complex.- A. Bimodal Actions of Ca2+.- B. Changes in the Kinetic Parameters.- C. Possible Intracellular Action of Ca2+.- D. Ca2+ Binding at the Subsynaptic Membrane.- VIII. Plastic Modulation of the Nicotinic Receptor-Ion Channel Complex by Ca2+-Dependent Action Potentials.- IX. Desensitization of the Nicotinic Receptor.- X. Conclusions.- References.- 6. Nicotinic Receptors: Activation and Block.- I. General Characteristics.- II. Recognition Component.- A. Mechanisms of Acetylcholine Binding.- B. Specific Pharmacological Properties of Ganglionic Acetylcholine Receptors.- III. Ionic Channel.- A. Ionic Permeability.- B. Single-Channel Lifetime and Conductance.- IV. Blocking Mechanisms.- A. Mechanisms of the Blockade of Ganglionic Acetylcholine Receptors.- B. Chemical Structure of the Binding Site for Blocking Substances.- V. Conclusions.- References.- 7. Muscarinic Transmission.- I. Introduction.- II. Nature of the Slow Excitatory Postsynaptic Potential.- A. Conductance Change during the Slow Excitatory Postsynaptic Potential.- B. Effect of the Membrane Potential.- C. Ionic Environment and the Slow Excitatory Postsynaptic Potential.- III. Ionic Mechanism of the Slow Excitatory Postsynaptic Potential.- A. GK Inactivation Hypothesis.- B. Combined Mechanism of the GK Inactivation and the GNa and Gca Activations.- IV. Some Characteristic Features of the Slow Excitatory Postsynaptic Potential.- A. Time-Course and Synaptic Delay of the Slow Excitatory Postsynaptic Potential.- B. Characteristics of Conductance Change.- C. Role of Metabolism of Postganglionic Neurons.- V. Conclusions and Comment.- References.- 8. Peptidergic Transmission.- I. Noncholinergic Excitatory Synaptic Transmission in Sympathetic Ganglia.- II. Involvement of Peptides in Excitatory Synaptic Transmission in Sympathetic Ganglia.- A. Peptide Candidates for a Neurotransmitter Role in the Ganglia.- B. Electrophysiological Characteristics of Noncholinergic Excitatory Postsynaptic Potentials and Peptide-Induced Depolarization.- III. Modulation of Noncholinergic Excitatory Transmission and Peptide-Induced Excitation by Catecholamines and Cyclic Nucleotides.- IV. Summary.- References.- 9. Inhibitory Transmission: Slow Inhibitory Postsynaptic Potential.- I. Introduction.- II. Recording of the Slow Inhibitory Postsynaptic Potential.- III. Synaptic Mediation of the Slow Inhibitory Postsynaptic Potential.- A. Disynaptic Mediation.- B. Monosynaptic Mediation.- IV. Unusual Slow Inhibitory Postsynaptic Potentials and Related Responses.- A. Unusual Acetylcholine Responses.- B. Synaptically Induced K+-Activated Hyperpolarization.- V. Nature of the Slow Inhibitory Postsynaptic Potential.- A. Effect of Ouabain.- B. Effect of K+.- C. Membrane Conductance Changes.- D. Effects of the Membrane Potential Level on the Slow Inhibitory Postsynaptic Potential.- E. Ionic Mechanism of the Slow Inhibitory Postsynaptic Potential.- VI. Second Messengers.- VII. Conclusions.- References.- 10. Presynaptic Modulation: The Mechanism and Regulation of Transmitter Liberation in Sympathetic Ganglia.- I. Introduction.- II. Synthesis, Storage, and Turnover of Acetylcholine.- III. Quantal Release of Acetylcholine.- A. Spontaneous Release.- B. Evoked Release.- C. Regulation of Transmitter Liberation.- IV. Conclusions.- References.- 11. Presynaptic Modulation: Endogenous Substances with Ganglionic Depressant Actions.- I. Presynaptic Modulation.- II. Endogenous Substances with Presynaptic Depressant Actions.- A. Catecholamines.- B. Acetylcholine.- C. ?-Aminobutyric Acid.- D. Prostaglandin E1.- E. Enkephalins.- F. Serotonin (5-Hydroxytryptamine).- G. Histamine.- III. Conclusions.- References.- 12. Postsynaptic Modulation.- I. Introduction.- II. Modulation of the Resting Potential.- A. Catecholamines.- B. 5-Hydroxytryptamine.- C. Adenosine Triphosphate.- D. ?-Aminobutyric Acid.- III. Modulation of the Action Potential.- A. Acetylcholine.- B. Epinephrine.- C. Adenosine Triphosphate.- D. Polypeptides.- IV. Modulation of Receptor Sensitivity.- A. Catecholamines.- B. 5-Hydroxytryptamine.- C. Histamine.- D. Polypeptides.- E. Adenosine Triphosphate.- F. Cyclic Adenosine 3?,5?-Monophosphate.- V. Conclusions.- References.- 13. Pharmacology of Synaptic Ganglionic Transmission and Second Messengers.- I. Introduction.- II. Pharmacological Effects of Compounds That Are Present in the Ganglion.- A. ?-Aminobutyric Acid.- B. Serotonin (5-Hydroxytryptamine).- C. Histamine.- D. Peptides.- III. Small Intensely Fluorescent Cells and Ganglionic Transmission.- A. Location and Morphology.- B. Catecholamines and Cyclic Nucleotides, Small Intensely Fluorescent Cells, and Ganglionic Transmission.- C. Phosphatidate Metabolism.- IV. Effects of Anticholinesterases on the Ganglia.- V. Ganglionic Stimulating and Blocking Agents.- VI. Muscarinic Drugs.- VII. Toxins.- VIII. General Anesthetics and Barbiturates.- IX. Comments and Conclusions.- References.- III. Parasympathetic and Enteric Ganglia and Their Neuropharmacology.- 14. Excitatory Transmission in Parasympathetic Ganglia.- I. Introduction.- II. Extracellular Studies.- III. Intracellular Studies.- IV. Types of Excitatory Transmission in Parasympathetic Ganglia.- A. Excitatory Nicotinic Cholinergic Transmission.- B. Electrical Transmission.- C. Slow Excitatory Muscarinic Transmission.- V. Spontaneous Firing.- VI. Facilitation of Transmission.- VII. Conclusions.- References.- 15. Inhibition in Parasympathetic Ganglia.- I. Introduction.- II. Extracellular Studies.- A. In Vivo Investigations.- B. In Vitro Investigations.- III. Intracellular Studies.- A. Presynaptic Inhibition.- B. Postsynaptic Inhibition.- IV. Conclusions.- References.- 16. Transmission in Enteric Ganglia.- I. Introduction.- II. Electrophysiological Classifications of Neurons.- A. Extracellular Recording.- B. Intracellular Recording.- III. Myenteric Plexus Neurons.- A. Electrical Properties.- B. Fast Excitatory Postsynaptic Potentials.- C. Slow Excitatory Postsynaptic Potentials.- D. Slow Hyperpolarizing Inhibitory Postsynaptic Potentials.- E. Slow Depolarizing Inhibitory Postsynaptic Potentials.- F. Biphasic Synaptic Potentials.- G. Spontaneous Activity.- IV. Submucous Plexus Neurons.- V. Interconnections among Enteric Neurons in Relation to Movements of the Gut.- A. Ascending Excitation.- B. Descending Inhibition.- C. Descending Excitation.- D. Circumferential Excitation and Inhibition.- VI. Conclusions.- References.- IV. Spinal and Reflex Activities of the Ganglia.- 17. The Pharmacology of Sympathetic Preganglionic Neurons.- I. Introduction.- II. Approaches.- III. Pharmacology.- A. Serotonin.- B. Norepinephrine.- C. Acetylcholine.- D. Amino Acids.- IV. Conclusions.- References.- 18. Spontaneous and Reflex Activities: General Characteristics.- I. General Characteristics.- A. Origins.- B. Preganglionic Neurons.- C. Efferent Neurons of Autonomic Ganglia.- D. Afferent Neurons of Autonomic Ganglia.- II. Neuronal and Chemical Mechanisms of Natural Activity.- III. Conclusions.- References.- 19. Chemosensitivity of Visceral Primary Afferent Neurons: Nodose Ganglia.- I. Introduction.- A. Electrical Properties of Nodose Ganglion Cells.- II. Chemosensitivity of Nodose Ganglion Cells.- A. 5-Hydroxytryptamine.- B. Acetylcholine.- C. Bradykinin.- D. Histamine.- E. ?-Aminobutyric Acid.- F. Endogenous Opiatelike Substances.- G. Other Substances.- III. Interactions between Algesic and Analgesic Substances and Their Mechanisms.- IV. Summary.- References.- V. Clinical and CNS-Related Aspects of Ganglionic Transmission.- 20. Autonomic Disease and Clinical Applications of Ganglionic Agents.- I. Introduction.- II. Autonomic Disease.- A. Introduction.- B. Familial Dysautonomia.- C. Congenital Megacolon (Hirschsprung’s Disease).- D. Ocular Disorders.- E. Metabolic, Idiopathic, and Postinfectious, Long-Course Neuropathies.- F. Acute Autonomic Neuropathy.- G. Old-Age Dysautonomia.- H. Drug-Induced Autonomic Neuropathies.- I. Hypertension.- III. Mental Disease and the Autonomic Nervous System.- IV. Clinical Use of Ganglionic Drugs.- A. General and Past Uses of Ganglionic Drugs.- B. Use of Ganglionic Blockers in Essential or Chronic Hypertension.- V. Conclusions.- References.- 21. Ganglionic Transmission as a Model for CNS Function.- I. Introduction.- II. Muscarinic (Slow) and Nicotinic (Fast) Excitatory Potentials.- III. Inhibitory Response.- IV. Ganglionic Responses to Transmitters Other than Acetylcholine and Their Interactions.- A. Responses to Noncholinergic Neurotransmitters.- B. Neurotransmitter Interactions.- C. A Special Instance of Interactions: Rat Pelvic Ganglia.- V. Speculations on Special Relevance of Autonomic Ganglionic Phenomena to Higher CNS Function.- VI. Conclusions.- References.