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Autonomic Nerves
Autonomic Nerves
Autonomic Nerves
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Autonomic Nerves

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Authored by the same team that created Cranial Nerves, this book provides an easy-to-follow overview of autonomic nerves. The first part describes their structure and function. The second part addresses autonomic control of individual organ systems in a problem-based learning format. Throughout, Autonomic Nerves describes afferent pathways, integrating structures and mechanisms, efferent pathways, and the autonomic effectors. Principles of autonomic neurotransmission are also discussed.

LanguageEnglish
Release dateDec 28, 2016
ISBN9781607959564
Autonomic Nerves

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    Autonomic Nerves - Linda Wilson-Pauwels, A.O.C.A., B.Sc.AAM, M.Ed., E.D.

    AUTONOMIC

    NERVES

    BASIC SCIENCE • CLINICAL ASPECTS • CASE STUDIES

    LINDA WILSON-PAUWELS, A.O.C.A., B.Sc.AAM, M.Ed., E.D.

    Associate Professor and Chair

    Biomedical Communications, Department of Surgery

    Faculty of Medicine

    University of Toronto

    Toronto, Ontario, Canada

    PATRICIA A. STEWART, B.Sc., M.Sc., Ph.D.

    Professor

    Department of Anatomy and Cell Biology

    Faculty of Medicine

    University of Toronto

    Toronto, Ontario, Canada

    ELIZABETH J. AKESSON, B.A., M.Sc.

    Assistant Professor

    Department of Anatomy

    Faculty of Medicine

    University of British Columbia

    Vancouver, British Columbia, Canada

    1997

    PMPHUSA, Ltd ~ Raleigh ~ North Carolina

    PMPH USA, Ltd.

    5711 Six Forks Road, Suite 210

    Raleigh, North Carolina 27609

    Tel: 919-502-4220

    Fax: 919-502-7673

    E-mail: info@pmph-usa.com

    © 1997 Linda Wilson-Pauwels, Patricia Stewart, Elizabeth Akesson

    Originally published by B.C. Decker, Hamilton, Ontario, Canada in 1997; ISBN 1-55009-030-5.

    All rights reserved. Without limiting the rights under copyright reserved above, no part of this publication may be reproduced, stored in or introduced into a retrieval system, or transmitted, in any form or by any means (electronic, mechanical, photocopying, recording, or otherwise), without the prior written permission of the publisher.

    17 18 19 20/KING/9 8 7 6 5 4

    ISBN-13    978-1-60795-289-3

    ISBN-10    1-60795-289-0

    eISBN-13    978-1-60795-956-4

    Printed in the United States of America by King Printing.

    Notice: The authors and publisher have made every effort to ensure that the patient care recommended herein, including choice of drugs and drug dosages, is in accord with the accepted standard and practice at the time of publication. However, since research and regulation constantly change clinical standards, the reader is urged to check the product information sheet included in the package of each drug, which includes recommended doses, warnings, and contraindications. This is particularly important with new or infrequently used drugs. Any treatment regimen, particularly one involving medication, involves inherent risk that must be weighed on a case-by-case basis against the benefits anticipated. The reader is cautioned that the purpose of this book is to inform and enlighten; the information contained herein is not intended as, and should not be employed as, a substitute for individual diagnosis and treatment.

    Preface

    The autonomic nervous system is complex, both structurally and functionally, and research in the field is changing our understanding of autonomic function at a rapid pace. This book is designed to make learning about the autonomic nervous system easier for teachers, students, and practitioners in medicine and the allied health professions. To facilitate learning, we make extensive use of conceptual illustrations: neural pathways, transmitters, and receptors are color coded, and arrows are used to show the direction of impulses. Considerable care is taken to integrate the written and visual components of each chapter. We attempt to simplify our representation and discussion of autonomic pathways and functional mechanisms without over-simplifying important concepts. We emphasize the major principles of autonomic function and resist the temptation to include a wealth of detail that might overwhelm the reader. For those who wish to delve deeper, we include a bibliography that lists several excellent publications that describe the autonomic nervous system in considerable detail.

    This book is divided into two parts. The first part describes the structure and function of the autonomic nerves, and the second part addresses autonomic control of individual organ systems in a problem-based learning format.

    In many other text books, the autonomic nervous system is narrowly defined as a motor system organized into two divisions: sympathetic and parasympathetic, whose effects are frequently antagonistic and whose balance of activities produces homeostasis. While this definition is simple and facilitates description of the autonomic nervous system, it ignores the important roles of sensory input, central integrating mechanisms, and the enteric nervous system. In this book, we define the autonomic nervous system much more broadly as the neurologic substrate that acts to maintain homeostasis in the body. We describe afferent (sensory) pathways, integrating structures and mechanisms, efferent (motor) pathways, and the autonomic effectors (smooth muscle cells, cardiac muscle cells, and exocrine secretory cells). We address the principles of autonomic neurotransmission with respect to the specialized morphology of the nerve endings and the variety of neurotransmitters and receptors that act in autonomic nerves and effector cells.

    The second part of the book consists of eight case studies. Each depicts a different aspect of the autonomic control of the organ systems, and each includes a history, a list of guiding questions, and a case discussion in which each of the learning objectives is addressed. The case studies are designed to be complete when isolated from the rest of the book.

    We are grateful to our colleagues, both in our home institutions and abroad, who were kind enough to answer burning questions, critique text and illustrations, and supply us with radiologic and photographic images. Their expertise was invaluable, and very much appreciated. They are:

    U. Ackerman, Ph.D., Department of Physiology, University of Toronto, Canada.

    C.E. Bayliss, M.D., M.Ed., F.R.C.S.(C), Departments of Physiology and Surgery, University of Toronto, Canada.

    G. Burnstock, D.Sc., F.A.A., M.R.C.P.(Hon), F.R.S., Department of Anatomy and Developmental Biology, University College, London, U.K.

    M. Costa, F.A.A., Department of Human Physiology, Flinders University, South Australia.

    J. Church, M.D., Ch.B., Ph.D., Department of Anatomy, University of British Columbia, Canada.

    W.G. Dail, Ph.D., Department of Anatomy, University New Mexico, U.S.A.

    D. Dixon, M.D., F.R.C.P.(C), Ophthalmologist, Brampton, Ontario, Canada.

    J. O. Dostrovsky, Ph.D., Department of Physiology, University of Toronto, Canada.

    G. Downey, M.D., F.R.C.P.(C), Department of Medicine, University of Toronto, Canada.

    D. Harrison, M.D., F.R.C.P.(C), BC Cancer Agency, Vancouver Centre, Vancouver, BC, Canada.

    K. Hayakawa, Technician, Department of Anatomy, University of Toronto, Canada.

    S. Kraft, M.D., F.R.C.S.(C), Department of Ophthalmology, University of Toronto, Canada.

    D. Mazierski, B.Sc.AAM, Biomedical Communications, Department of Surgery, University of Toronto, Canada.

    J. Mitchell, Ph.D., Department of Pharmacology, University of Toronto, Canada.

    M. Opas, Ph.D., Department of Anatomy and Cell Biology, University of Toronto, Canada.

    V. Palaty, Ph.D., Department of Anatomy, University of British Columbia, Canada.

    J.A. Pearson, Ph.D., Department of Anatomy, University of British Columbia, Canada.

    J. Saint-Cyr, Ph.D., Department of Anatomy and Cell Biology, University of Toronto, Canada.

    F. Silver, M.D., F.R.C.P.(C), Department of Medicine (Neurology), University of Toronto, Canada.

    E. L. Shorter, Ph.D., Departments of Medicine and History of Medicine, University of Toronto, Canada.

    S. Spacey, M.B.B.S., Neurology Resident, University of British Columbia, Vancouver Hospital, Canada.

    D.A. Stringer, B.Sc, M.B.B.S., F.R.C.R., F.R.C.P.(C), Section of Ultrasound and General Radiology, Department of Radiology, BC Children's Hospital, Vancouver, Canada.

    I.M. Taylor, M.D., Department of Anatomy and Cell Biology, University of Toronto, Canada.

    C. Thompson, B.Sc., Department of Anatomy and Cell Biology, University of Toronto, Canada.

    D. Van der Kooy, Ph.D., Department of Anatomy and Cell Biology, University of Toronto, Canada.

    A.W. Vogl, Ph.D., Department of Anatomy, University of British Columbia, Canada.

    M. J. Wiley, Ph.D., Department of Anatomy and Cell Biology, University of Toronto, Canada.

    H. Wolburg, Professor, Institut fur Pathology der Universitat Tubingen, Germany.

    N. Wooolridge, B.F.A., B.Sc. AAM, M.Sc., Biomedical Communications, University of Toronto, Canada.

    Linda Wilson-Pauwels

    Patricia Anne Stewart

    Betty Akesson

    Table of Contents

    Cover

    Title page

    Copyright

    Preface

    I Introduction

    II DEVELOPMENT OF THE AUTONOMIC NERVOUS SYSTEM

    III AUTONOMIC SENSORY COMPONENTS

    IV AUTONOMIC INTEGRATING COMPONENTS

    V AUTONOMIC MOTOR COMPONENTS

    VI AUTONOMIC NEUROTRANSMITTERS, RECEPTORS, AND EFFECTORS

    Case Study 1

    Case Study 2

    Case Study 3

    Case Study 4

    Case Study 5

    Case Study 6

    Case Study 7

    Case Study 8

    Bibliography

    Index

    Introduction

    I INTRODUCTION

    The nervous system can be divided into two semi-independent systems:

    1. The somatic nervous system allows us to act on the external environment, and can be defined as the neurologic substrate that allows the individual to respond voluntarily to consciously perceived sensory signals.

    2. The autonomic nervous system allows us to act on the body’s internal environment, and can be defined as the neurologic substrate that acts to maintain homeostasis (a steady state) in the body. For the most part, we are not aware of the workings of the autonomic nervous system in the same way as we are aware of other neurologic activities, such as seeing, feeling, or moving. Most autonomic sensory signals are not perceived consciously, and most autonomic motor activities are not under voluntary control. The name autonomic (self-governing) reflects the independent nature of this part of the nervous system.

    fig1-1

    Figure 1-1 The somatic (A) and autonomic (B and C) nervous systems are organized in a similar way in that signals from the periphery of the body and from higher levels of the nervous system drive or modify motor activities.

    SOMATIC AND AUTONOMIC NERVOUS SYSTEMS

    ARE ORGANIZED IN A SIMILAR WAY

    Both somatic and autonomic nervous systems include sensory neurons that carry signals to integrative neurons within the brain and spinal cord that construct an appropriate response, and motor neurons that carry the response back to the effector cells (Figure 1-1).

    Over short time spans, the nervous system can only respond to sensory input in two ways: it can cause a muscle, or group of muscles, to contract, or it can cause glands to secrete. Our entire behavioral repertoire can be reduced to combinations of these two actions: the somatic nervous system causes voluntary muscles to contract, whereas the autonomic nervous system causes or modifies involuntary muscle contraction and glandular secretion.

    B. C.

    THE SOMATIC AND AUTONOMIC NERVOUS SYSTEMS DIFFER MOST IN THEIR MOTOR COMPONENTS

    Somatic effectors (skeletal muscle fibers) are innervated by a single source: lower motor neurons in the brain stem or spinal cord. In contrast, most autonomic effectors (smooth muscle, cardiac muscle, secretory cells) are innervated by two autonomic sources: sympathetic and parasympathetic motor neurons (Figure 1-2).

    fig1-2

    Figure 1-2 (A) Somatic effector cells, i.e., skeletal muscle fibers receive their motor innervation from lower motor neurons only, whereas (B) Autonomic effector cells, e.g., cardiac pacemakers, receive their motor innervation from both sympathetic and parasympathetic postganglionic motor neurons.

    Somatic motor neurons, whose cell bodies reside in the motor nuclei of the brain stem and in the anterior horn of the spinal cord, project directly to their target cells, whereas autonomic motor neurons form two-neuron chains: preganglionic motor neurons, whose cell bodies reside in the central nervous system (brain stem or spinal cord), and postganglionic motor neurons, whose cell bodies reside in autonomic ganglia.

    This two-neuron arrangement has several advantages as follows:

    Firstly, a single preganglionic neuron synapses on large numbers of postganglionic neurons, thereby allowing for a small number of central neurons to influence large areas of the body. This is the principle of divergence of stimuli (Figure 1-3);

    Secondly, since sensory (afferent) axons course through the ganglia, a certain amount of sensory-motor integration can take place at the ganglionic level, thereby giving the autonomic nervous system a degree of autonomy from the central nervous system; and

    Thirdly, a single preganglionic neuron can synapse on both excitatory and inhibitory postganglionic neurons, thereby allowing for excitation and inhibition of various target cells to produce a high degree of functional coordination.

    fig1-3

    Figure 1-3 The principle of divergence of stimuli is illustrated in the sympathetic nervous system. Preganglionic motor neurons in the spinal cord project to numerous postganglionic motor neurons in the coeliac ganglion. In humans, the ratio of pre- to postganglionic neurons averages 1:120. It is higher in sympathetic than in parasympathetic pathways.

    Somatic motor neurons activate skeletal muscle fibers only, whereas autonomic motor neurons have a variety of targets including smooth muscle, endothelial cells, cardiac muscle, secretory cells, and chromaffin cells in the adrenal medulla.

    Somatic motor neuron terminals release their neurotransmitter at discrete sites close to the target muscle fibers, whereas postganglionic autonomic motor neuron terminals release their transmitter much more diffusely and at a distance from the effector cells (Figure 1-4).

    Somatic motor neurons secrete acetylcholine as their neurotransmitter, whereas autonomic neurons secrete mainly either acetylcholine or noradrenaline, plus one or more co-transmitters that modify and/or elicit a component of the response (see Fig. 1-4).

    fig1-4

    Figure 1-4

    (A) A terminal bouton of a somatic motor neuron releasing acetylcholine to activate somatic muscle cells (e.g., striated muscle);

    (B) A postganglionic motor neuron releasing acetylcholine (or noradrenaline) plus co-transmitters to activate smooth muscle cells.

    SOMATIC AND AUTONOMIC NERVOUS SYSTEM COMPONENTS INTERACT WITH EACH OTHER

    Some somatic sensory signals, such as those elicited by temperature changes in the skin, or food odors, give rise to autonomic responses, such as a change in blood circulation to the skin, or an increase in gastrointestinal activity. Conversely, some autonomic sensory signals give rise to motor events that involve both somatic and autonomic nerves. Often the somatic component of these activities proceeds in an unconscious, automatic way. These somatic events are fixed action patterns generated by central motor programs. They may be considered to be complex reflexes elicited by a single stimulus involving a chain of events proceeding in a predictable sequence, although the sequence is not absolutely fixed. The major combined somatic and autonomic functions are listed and discussed below. They are described in more detail in the appropriate chapters.

    Swallowing, Vomiting, and Defecating

    Gut movement is controlled almost entirely by the autonomic nervous system; however, activity at the oral and anal ends is controlled by the somatic nervous system. Swallowing, a voluntary thrusting of a bolus into the pharynx, elicits complex involuntary activity of the pharyngeal muscles which are controlled by the somatic nervous system. Contraction of the pharyngeal muscles propels the bolus into the upper end of the esophagus. Once the bolus enters the esophagus, the enteric component of the autonomic nervous system takes over and peristalsis propels the bolus along the gut.

    Vomiting begins with a prolonged burst of autonomic activity in the intestine distal to the stomach, followed by retching movements as the somatic motor system stimulates the diaphragm, intercostal muscles, and abdominal muscles to contract rhythmically. This process is coordinated by a vomiting, or emetic, center in the brain stem (Figure 1-5) (see also Case Study 3: Victoria and the Vicious Hot Dog: Emesis).

    During defecation, a fecal mass in the lower rectum stimulates anorectal stretch receptors. These, in turn, elicit relaxation of the internal anal sphincter via the autonomic nervous system and contraction of the diaphragm and abdominal wall muscles via the somatic nervous system. The resulting increase in intra-abdominal pressure causes the fecal mass to begin to move.

    fig1-5

    Figure 1-5 Autonomic and somatic events during vomiting. Autonomic neurons stimulate the smooth muscle of the small intestine, causing retrograde peristalsis that moves intestinal contents back into the stomach. Somatic neurons activate the diaphragm and body wall muscles to propel stomach contents into the esophagus and out of the mouth. Other somatic neurons activate the tongue and pharyngeal muscles to close the entrance to

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