Contents -- Preface -- List of Symbols -- Acronyms -- Introduction -- 1 Overview of Enteric Neurobiology -- 1.1 TheRoleof theGut -- 1.2 Regional Function in the Human Gut -- 1.3 The Intrinsic Innervation of the Gut -- 1.4 Gastrointestinal Smooth Muscle -- 1.5 Extrinsic Innervation -- 1.6 The Effect of Food on the Gut -- 1.7 Clinical Pharmacology -- 2 Myoelectrical Activity of the Smooth Muscle -- 2.1 Myoelectrical and Mechanical Activity -- 2.1.1 Biological Background -- 2.1.2 Mathematical Model -- 2.1.3 Numerical Algorithm -- 2.1.4 Physiological Response -- 2.1.5 Effect of Increase in gCLa -- 2.1.6 Effect of Increase in ˜gCa-K and ˜g T Ca -- 2.1.7 Effect of Cyclic Changes in ˜g T Ca -- 2.1.8 Effect of Increase in g L and g T -- 2.1.9 Effect of Increase in ˜gCa-K and Decrease in ˜g T Ca -- 2.1.10 Remarks -- 2.2 Effects of Ion Channel Modulators -- 2.2.1 Biological Background -- 2.2.2 Effect of Forskolin -- 2.2.3 Effect of Lemakalim -- 2.2.4 Effect of High Concentration of External K+ -- 2.2.5 Effect of Phencyclidine -- 2.2.6 Effects of Selective K+-Channel Agonists/ Antagonists -- 2.2.7 Remarks -- 3 Pharmacology of Myoelectrical Activity -- 3.1 Effects of Specific Inhibitors of the Ca2+-ATPase and the Ryanodine-Sensitive Ca2+ Channels of the Sarcoplasmic Reticulum -- 3.1.1 Effects of Cyclopiazonic Acid -- 3.1.2 Effects of Cyclopiazonic Acid and Ryanodine -- 3.1.3 Effects of Cyclopiazonic Acid and Non-Selective Ca2+ Channel Antagonists -- 3.1.4 Effects of Cyclopiazonic Acid and Selective Ca2+ Channel Antagonists -- 3.1.5 Effects of Thapsigargin, Non-Selective and Selective Ca2+ Channel Antagonists, and Ryanodine -- 3.1.6 Effects of Thapsigargin and High [Ca2+]0 -- 3.1.7 Effects of Thapsigargin, High [Ca2+]0, [K+]0 and Selective Ca2+ Channel Antagonists -- 3.2 Effects of 1,4-dihydropyridine Enantiomers (-)-(S)-Bay K 8644 and (+)-(R)-Bay K 8644.

3.2.1 Effects of (-)-(S)-Bay K 8644 -- 3.2.2 Effects of (-)-(S)-Bay K 8644 and High [K+]0 -- 3.2.3 Effects of (+)-(R)-Bay K 8644 -- 3.3 Effects of Motilides -- 3.3.1 Effects of Motilin and Erythromycin -- 3.3.2 Effects of Motilides and Ryanodine -- 3.3.3 Effects of Motilides, a Non-Selective Ca2+ Channel Blocker and Thapsigargin -- 3.4 Effects of Benzodiazepines -- 3.4.1 Effects of Benzodiazepines Alone -- 3.4.2 Reverse of the Effects of Benzodiazepines -- 3.5 Remarks -- 4 Physicochemical Basis of Synaptic Transmission -- 4.1 Introduction -- 4.2 Cholinergic Neurotransmission -- 4.2.1 Biological Background -- 4.2.2 Mathematical Model -- 4.2.3 Numerical Algorithm -- 4.2.4 Physiological Neurotransmission -- 4.2.5 Remarks -- 4.3 Inhibition of Cholinergic Neurotransmission -- 4.3.1 Introduction -- 4.3.2 Biological Background -- 4.3.3 Mathematical Model -- 4.3.4 Effect of Chloride Salts of Divalent Cations -- 4.3.5 Effect of β-Bungarotoxin -- 4.3.6 Effect of Botulinum Toxin -- 4.3.7 Change in the Concentration of Extracellular Ca2+ -- 4.3.8 Effect of Cholinergic Antagonists -- 4.4 Facilitation of Cholinergic Neurotransmission -- 4.4.1 Biological Background -- 4.4.2 Mathematical Model -- 4.4.3 Effect of Cholinergic Agonists -- 4.4.4 Effect of TTX -- 4.4.5 Effect of Repetitive Stimulation -- 4.4.6 Remarks -- 4.5 Adrenergic Neurotransmission -- 4.5.1 Biological Background -- 4.5.2 Mathematical Model -- 4.5.3 Physiological Adrenergic Transmission -- 4.5.4 Remarks -- 4.6 Altered Adrenergic Neurotransmission -- 4.6.1 Effects of Extracellular Ca2+ Removal and Application of TTX -- 4.6.2 Inhibition of Neuronal Uptake-1 Mechanism -- 4.6.3 Inhibition of Catechol-O-Methyltransferase -- 4.6.4 Mathematical Model -- 4.6.5 Effect of α1-Adrenoceptor Antagonists -- 4.6.6 Mathematical Model -- 4.6.7 Effect of the Repetitive Stimulation -- 4.6.8 Remarks -- REFERENCE.

5 Neuronal Assemblies -- 5.1 Planar Neuronal Network -- 5.1.1 Introduction -- 5.1.2 Biological Background -- 5.2 Inhibitory Neural Circuit -- 5.2.1 Axo-Axonal Interaction -- 5.2.2 Effect of COMT Inhibitors -- 5.2.3 Effect of α1-AdrenoceptorBlockers -- 5.3 AModelof theSensoryPathway -- 5.3.1 Introduction -- 5.3.2 Biological Background -- 5.3.3 Mathematical Model -- 5.3.4 Responses to Deformation -- 5.3.5 Effect of Iberiotoxin and CHTX -- 5.3.6 Effect of ω-CgTX -- 5.3.7 Effect of TTX -- 5.3.8 Effect of Purinoceptor Agonists -- 5.3.9 Effect of Protein Kinase C Activator -- 5.3.10 Effect of DPDPE -- 5.3.11 Remarks -- 5.4 Enteral Sympathetic Communication -- 5.4.1 Introduction -- 5.4.2 Mathematical Model -- 5.4.3 Effect of a Single Deformation -- 5.4.4 Effect of a Periodic Deformation -- 5.4.5 Effect of Intermittent Deformation -- 5.4.6 Remarks -- 5.5 A Planar Neuronal Network -- 5.5.1 Effect of Cholinergic and Adrenergic Agonists and Antagonists -- 5.5.2 Effect of Cholinesterase Inhibitors -- 5.5.3 Effect of Cholinergic Antagonists -- 5.5.4 Remarks -- 6 Multiple Neurotransmission -- 6.1 Co-transmission by Acetylcholine and Serotonin -- 6.1.1 Introduction -- 6.1.2 Biological Background -- 6.1.3 Mathematical Model -- 6.1.4 Electrical Activity of Mechanoreceptors -- 6.1.4.1 Physiological Response -- 6.1.4.2 Effect of 5-HT3Receptors -- 6.1.4.3 Effect of 5-HT3-Receptor Antagonists -- 6.1.5 Electrical Activity of the Primary Neuron -- 6.1.5.1 Stimulation of Mechanoreceptors -- 6.1.5.2 Effect of 5-HT3Receptors -- 6.1.5.3 Effect of 5-HT3-Receptor Antagonists -- 6.1.5.4 Effect of 5-HT4Receptors -- 6.1.5.5 Effect of Co-activation of 5-HT3 and 5-HT4 Receptors -- 6.1.5.6 Effect of Cisapride -- 6.1.6 Electrical Activity of the Motor Neuron -- 6.1.6.1 Effect of nACh Receptors -- 6.1.6.2 Effect of 5-HT3 and 5-HT4Receptors.

6.1.6.3 Effect of Co-activation of 5-HT3 and nACh Receptors -- 6.1.6.4 Effect of Co-activation of 5-HT4 and nACh Receptors -- 6.1.6.5 Effect of 5-HT3/5-HT4-Receptor Agonists andCo-activationofnAChReceptors -- 6.1.6.6 Effects of 5-HT3-Receptor Antagonist and Co-activationofnAChReceptors -- 6.1.7 Electrical Activity of Smooth Muscle -- 6.1.7.1 Effect of µAChReceptors -- 6.1.7.2 Effect of 5-HT4Receptors -- 6.1.7.3 Effect of Co-activation of 5-HT4 and µAChReceptors -- 6.1.7.4 Effect of 5-HT4 Receptor Antagonists and Co-activation of 5-HT3 and µAChReceptors -- 6.1.8 Remarks -- 6.2 Co-transmission by ACh and Excitatory Amino Acids -- 6.2.1 Biological Background -- 6.2.2 Electrical Activity of the Primary Neuron -- 6.2.2.1 Effect of Mechanical Stimulation -- 6.2.2.2 Effect of AMPA Receptors -- 6.2.2.3 Effect of NMDA Receptors -- 6.2.2.4 Effect of Co-activation of NMDA andAMPAReceptors -- 6.2.3 Electrical Activity of the Motor Neuron -- 6.2.3.1 Effect of nACh Receptors -- 6.2.3.2 Effect of NMDA Receptors -- 6.2.3.3 Effect of Co-activation of nACh and NMDA Receptors -- 6.2.3.4 Effect of Co-activation of nACh and AMPA Receptors -- 6.2.3.5 Effect of Co-activation of AMPA, NMDA and nACh Receptors -- 6.2.4 Smooth Muscle-Neuronal Chain Preparation -- 6.2.4.1 Effect of nACh Receptors -- 6.2.4.2 Effect of Co-activation of AMPA and nACh Receptors -- 6.2.4.3 Effect of Co-activation of nACh, AMPA and NMDA Receptors -- 6.2.5 Remarks -- 6.3 Co-transmission by ACh and Substance P -- 6.3.1 Introduction -- 6.3.2 Biological Background -- 6.3.3 Mathematical Model -- 6.3.4 Effect of Randomly Applied High FrequencyStimuli -- 6.3.5 Effect of Low Frequency Stimulation -- 6.3.6 Remarks -- 7 Functional Unit -- 7.1 Introduction -- 7.2 Biological Background -- 7.3 Mathematical Model -- 7.4 Numerical Algorithm -- 7.5 ElectromechanicalWave Phenomenon.

7.6 Effect of Lidocaine N-ethyl Bromide Quartery Salt QX-314 -- 7.7 Effect of Changes in Extracellular Ca2+ -- 7.8 Effect of Cholinergic Antagonists -- 7.9 Remarks -- 8 Dynamics of Intestinal Propulsion -- 8.1 Model Formulation -- 8.2 Numerical Algorithm -- 8.3 Pendular Movements -- 8.4 Segmental Contractions -- 8.5 Peristaltic Reflex -- 8.6 Effect of Multiple Neurotransmission and Drugs on Pellet Propulsion -- 8.6.1 Introduction -- 8.6.2 Effect of Co-Activation of 5-HT3, nACh and µAChReceptors -- 8.6.3 Effects of Alosetron -- 8.6.4 Effects of Selective 5-HT4 Receptor Agonists -- 8.6.5 Effects of Selective 5-HT4 Receptor Antagonists -- 8.6.6 Effect of Cisapride -- 8.7 Remarks -- References -- Index.