Neuronal Acetylcholine Receptors

Ganglion-Blocking Activity.- 4.1.1. Mono-Quaternary Ammonium Compounds.- 4.1.2. Tertiary and Secondary Amines.- 4.1.3. Bis-Quaternary Ammonium Compounds.- 4.2. Classification of Ganglion-Blocking Agents according to Classical Characteristics of Their Blocking Effects.- 4.3. Pharmacological Specificity of Neuronal Nicotinic Acetylcholine Receptors.- 4.3.1. Neurons of Autonomic Ganglia.- 4.3.2. Molluscan Neurons.- 4.4. Conclusions.- 5. Molecular Mechanisms Underlying the Effects of Ganglion-Blocking Agents.- 5.1. Open-Channel Block.- 5.1.1. Effect of Ganglion-Blocking Agents on Integrated Activity of Nicotinic Acetylcholine-Sensitive Channels Recorded from the Whole Cell.- 5.1.2. Effect of Ganglion-Blocking Agents on the Acetylcholine-Induced Current in Strongly Depolarized Membrane.- 5.1.3. Effect of Ganglion-Blocking Agents on the Activity of a Single Acetylcholine-Sensitive Channel.- 5.2. Blocking of Recognition Center.- 5.3. Blocking of Closed Ionic Channel.- 5.4. The Mechanism for a Block by Tubocurarine.- 5.5. The Mechanism for a Block by Neurotoxins.- 5.5.1. Variability of the Effects Produced by ?-Toxins in Neuronal Nicotinic Acetylcholine Receptors.- 5.5.2. Binding of Neurotoxins to Neuronal Nicotinic Acetylcholine Receptors without Causing Their Blocking.- 5.5.3. Effects Produced on Neuronal Nicotinic Acetylcholine Receptors by Snake Venom Components Ineffective in Other Acetylcholine Receptors.- 5.5.4. Possible Functional Significance of the Sites That Bind Neurotoxins without Affecting Synaptic Transmission.- 5.5.5. The Effects of a Neurotoxin Obtained from Mollusc.- 5.6. Conclusions.- 6. Localization and Possible Functional Significance of the Sites in the Neuronal Nicotinic Acetylcholine Receptor Interacting with Blocking Agents.- 6.1. Localization of the Sites Interacting with Blocking Agents in the Receptor Molecule.- 6.2. Possible Functional Significance of Sites in the Ionic Channel of the Nicotinic Acetylcholine Receptor That Bind Blocking Agents.- 6.3. Conclusions.- 7. The Relation of Nicotinic Receptor Open-Channel Blockade to Blockade of Synaptic Transmission.- 7.1. Theoretical Predictions of Synaptic Transmission Blockade as Caused by Blockade of the Open Channel in Postsynaptic Receptors.- 7.2. Mechanisms Underlying Selectivity in Drug-Induced Blockade of Synaptic Transmission.- 7.3. Selectivity of Open-Channel Blockade in Postsynaptic Receptors Other Than Nicotinic Receptors in Autonomic Ganglia.- 7.4. Conclusions.- 8. Recognition Center of Muscarinic Acetylcholine Receptor.- 8.1. Stoichiometry of Interactions of Agonists and Antagonists with the Muscarinic Acetylcholine Receptor.- 8.2. Functional Organization and Chemical Structure of the Muscarinic Acetylcholine Receptor Recognition Center.- 8.2.1. Molecular Properties of the Muscarinic Acetylcholine Receptor.- 8.2.2. General Pharmacological Properties of Neuronal Muscarinic Acetylcholine Receptors.- 8.2.3. Peculiarities of the Muscarinic Acetylcholine Receptor Recognition Center.- 8.2.4. Heterogeneity of Muscarinic Acetylcholine Receptors.- 8.2.5. Chemical Nature of the Recognition Center.- 8.3. Conclusions.- 9. Mechanisms Underlying Muscarinic Postsynaptic Response.- 9.1. General Properties of Muscarinic Response.- 9.1.1. Muscarinic Responses in Various Types of Neurons.- 9.1.2. Factors Determining the Time Course of Muscarinic Response.- 9.2. Ionic Mechanisms Underlying Muscarinic Depolarization.- 9.2.1. General Characteristics.- 9.2.2. Decrease in Membrane Potassium Conductance.- 9.2.3. Increase in Membrane Conductance.- 9.2.4. Depolarization without Changes in Membrane Conductance.- 9.2.5. Ionic Mechanisms of Muscarinic Depolarization in Other Types of Cells.- 9.3. Mechanisms Underlying Muscarinic Hyperpolarization.- 9.3.1. Cellular Mechanisms Underlying Muscarinic Hyperpolarization in Mammalian Sympathetic Ganglion.- 9.3.2. General Characteristics of Ionic Mechanisms.- 9.3.3. Increase in Membrane Potassium Conductance.- 9.3.4. Decrease in Membrane Sodium Conductance.- 9.3.5. Activation of Electrogenic Na+ Pump.- 9.3.6. Decrease in Membrane Chloride Conductance.- 9.3.7. Unusual Membrane Hyperpolarization Caused by Acetylcholine.- 9.3.8. Ionic Mechanisms Underlying Muscarinic Hyperpolarization in Other Types of Cells.- 9.4. Ionic Mechanisms Underlying Activities of Muscarinic Acetylcholine Receptors of Various Subtypes.- 9.5. Coupling of Muscarinic Acetylcholine Receptors with Ionic Channels Involved in the Generation of Postysynaptic Response.- 9.5.1. Cyclic GMP.- 9.5.2. Ca2+Ions.- 9.5.3. Other Substances.- 9.6. Conclusions.- 10. Mechanisms of Muscarinic Regulation of Neuronal Electrical Activity.- 10.1. Regulation of Action Potential Characteristics.- 10.2. Effect of Muscarinic Postsynaptic Response on Neuronal Electrical Activity.- 10.3. Conclusions.- 11. Effects of Noncholinergic Transmitters on Neuronal Acetylcholine Receptors.- 11.1. Effects on Nicotinic Acetylcholine Receptors.- 11.2. Effects on Muscarinic Acetylcholine Receptors.- 11.3. Conclusions.- References.