Section I-Peripheral Nerve.- 1 Peripheral Nerve Structure.- 1. Introduction.- 2. Histology and Development.- 3. The Axon.- 3.1. Filaments and Microtubules.- 3.2. Other Organelles and the Axolemma.- 4. Sheaths of Axons.- 4.1. Schwann Cells.- 4.2. Myelin.- 4.3. Function of Schwann Cells and Their Myelin Sheaths.- 4.4. Connective Tissue Sheaths.- 5. References.- 2 The Nerve Impulse.- 1. Introduction.- 2. Passive Electrical Properties.- 3. Voltage-Clamp Analysis of the Ionic Current.- 4. Momentary Current-Voltage Relations.- 5. The Threshold Conditions for Excitation.- 6. Factors Determining Conduction Velocity.- 7. References.- 3 Axoplasmic Transport-Energy Metabolism and Mechanism.- 1. Introduction.- 2. Fast Axoplasmic Transport.- 2.1. Characterization.- 2.2. Mechanism and Energy Supply.- 2.3. Transport and Membrane Function.- 3. Slow Axoplasmic Transport.- 3.1. Characterization.- 3.2. Mechanism.- 4. References.- Section IIA-Junctional Transmission-Structure.- 4 Neuromuscular Junctions and Electric Organs.- 1. Introduction.- 2. The Typical Neuromuscular Junction.- 2.1. Distribution and Location of Nerve Terminals.- 2.2. The Axon.- 2.3. The Synaptic Space.- 2.4. Postjunctional Muscle Fiber.- 3. Variations of Motor End Plates.- 3.1. Variations from Class to Class.- 3.2. Endings on Slow-Twitch and Rapid-Twitch Fibers.- 3.3. Endings on Slow Tonic Muscle Fibers.- 4. Electric Organs.- 4.1. Electrocytes.- 4.2. Innervation and Ultrastructure.- 5. References.- 5 The Peripheral Autonomic System.- 1. Anatomical Considerations: Sympathetic and Parasympathetic Divisions.- 2. Morphological Observations.- 2.1. Preganglionic Neurons.- 2.2. Postganglionic Neurons.- 2.3. Adrenal and Extra-Adrenal Chromaffin Cells.- 3. References.- 6 Ultrastructure of Ganglionic Junctions.- 1. General Considerations.- 2. Sympathetic Ganglia.- 2.1. Amphibia.- 2.2. Reptiles.- 2.3. Mammals.- 2.4. Some Effects of Different Fixatives.- 3. Parasympathetic Ganglia.- 3.1. Ciliary Ganglion.- 3.2. Otic Ganglion.- 3.3. Ganglia of the Enteric Plexuses.- 3.4. Cardiac Ganglion Cells.- 4. Summary and Comment.- 5. References.- Section IIB-Junctional Transmission-Function.- 7(i) Neuromuscular Transmission-Presynaptic Factors.- 1. Synthesis, Storage, and Release of Acetylcholine.- 1.1. Synthesis of ACh.- 1.2. Storage and Release.- 2. The Acceleration of Release by Nerve Impulses.- 2.1. The Role of the Nerve Impulse.- 2.2. The Role of Ca2+.- 2.3. After- Effects of Depolarization-Secretion Coupling.- 3. References.- 7 (ii) Neuromuscular Transmission-The Transmitter-Receptor Combination.- 1. Introduction.- 2. Molecular Basis of Chemoelectric Transduction.- 3. Pharmacology.- 4. Chemical Nature of the Acetylcholine Receptor.- 5. Desensitization.- 6. References.- 7 (iii) Neuromuscular Transmission-Enzymatic Destruction of Acetylcholine.- 1. Location and Measurement of Cholinesterases at the Junction.- 1.1. Histochemical Staining.- 1.2. Microchemical Methods.- 1.3. Assay of External AChE.- 1.4. Radioautographic Methods.- 2. Amounts and Types of Cholinesterase at the Junctions.- 3. Requirement for AChE in Impulse Transmission.- 4. Relation of AChE to ACh- Receptors.- 5. Quantitative Relation of AChE to ACh at the End Plate.- 6. References.- 8 Ganglionic Transmission.- 1. Introduction.- 2. Response of Autonomic Ganglia to Preganglionic Volleys.- 2.1. Response of Normal Ganglia.- 2.2. Response of Curarized Ganglia.- 2.3. Slow Ganglionic Responses and Afterdischarges.- 3. Electrical Constants of Ganglion Cell Membrane.- 4. Action Potentials of Single Ganglion Cells.- 4.1. Response to Antidromic Stimulation.- 4.2. Response to Direct Intracellular Stimulation.- 4.3. Response to Orthodromic Stimulation.- 4.4. Ionic Requirement for Generation of Action Potential.- 5. Nature and Electrogenesis of Postsynaptic Potentials.- 5.1. The "Fast" Excitatory Postsynaptic Potential.- 5.2. The "Slow" Excitatory Postsynaptic Potential.- 5.3. The "Late Slow" Excitatory Postsynaptic Potential.- 5.4. The "Slow" Inhibitory Postsynaptic Potential.- 6. Cholinergic and Adrenergic Receptors at Preganglionic Nerve Terminals.- 6.1. Cholinergic Receptor Site.- 6.2. Adrenergic Receptor Site.- 7. References.- 9 Function of Autonomic Ganglia.- 1. Introduction.- 2. Ganglia as Coordinating Centers.- 2.1. The Relay Hypothesis of Ganglionic Function.- 2.2. Development of a Stochastic Hypothesis.- 3. Experimental Evidence.- 3.1. Observed Patterns of Innervation.- 3.2. Ganglionic Activity and Factors Influencing It.- 3.3. Relative Autonomy of Ganglia.- 4. Conclusions.- 5. References.- 10 Peripheral Autonomic Transmission.- 1. Introduction.- 2. Definition of the Autonomic Neuromuscular Junction.- 2.1. Relation of Nerve Fibers to Muscle Effector Bundles.- 2.2. Relation of Nerve Fibers to Individual Smooth Muscle Cells.- 3. Adrenergic Transmission.- 3.1. Introduction.- 3.2. Structure of Adrenergic Neurons and Storage of Noradrenaline.- 3.3. Electrophysiology of Adrenergic Transmission.- 3.4. Ionic Basis of the Action of Catecholamines on the Postjunctional Membrane.- 3.5. Summary.- 4. Cholinergic Transmission.- 4.1. Introduction.- 4.2. Localization of Acetylcholinesterase.- 4.3. Electrophysiology of Cholinergic Transmission.- 4.4. Ionic Basis of the Action of ACh on the Postjunctional Membrane.- 4.5. Summary.- 5. Purinergic Transmission.- 5.1. Introduction.- 5.2. Electrophysiology of Purinergic Transmission.- 5.3. Summary.- 6. Conclusions.- 7. References.- 11 "Trophic" Functions.- 1. Introduction.- 2. Regulation of Taste Buds.- 3. Regulation of Amphibian Limb Regeneration.- 4. Regulation of Physiological and Metabolic Properties of Muscle.- 4.1. Resting Membrane Potential.- 4.2. Acetylcholine Sensitivity.- 4.3. Cholinesterase Activity.- 4.4. The Role of ACh Release.- 4.5. The Dynamic Nature of the Muscle Fiber.- 4.6. Plasticity of the Motor Unit.- 5. Mechanisms of Neural Regulation.- 6. References.- Section III-Receptors-Structure and Function.- 12 Cutaneous Receptors.- 1. Introduction.- 2. Morphology of Cutaneous Nerves.- 2.1. Uniformity of Cutaneous Axons.- 2.2. Relative Numbers of Myelinated and Nonmyelinated Axons.- 3. Morphology of Cutaneous Receptors.- 3.1. Encapsulated Receptors.- 3.2. Unencapsulated Corpuscular Receptors.- 3.3. Noncorpuscular Receptors.- 4. Physiology of Cutaneous Receptors.- 4.1. Cutaneous Mechanoreceptors.- 4.2. Cutaneous Thermoreceptors.- 4.3. Nociceptors.- 5. References.- 13 The Pacinian Corpuscle.- 1. Introduction.- 2. Morphology.- 3. Afferent Responses to Mechanical Stimuli.- 4. Mechanical Properties of the Corpuscle.- 5. Receptor Potentials.- 6. Impulse Activity in the Nerve Terminal.- 7. Distribution of Pacinian Corpuscles.- 8. Central Effects of Impulses from Pacinian Corpuscles.- 9. References.- 14 Receptors in Muscles and Joints.- 1. Introduction.- 2. Joint Receptors.- 3. Tendon Organs.- 4. Muscle Spindles.- 4.1. Reptiles.- 4.2. Amphibia.- 4.3. Birds.- 4.4. Mammals.- 5. Uncertain Origin of Adaptation.- 6. References.- 15 Enteroceptors.- 1. Introduction.- 2. Methods.- 2.1. Histology.- 2.2. Physiology.- 3. Cardiovascular Receptors.- 3.1. Systemic Arterial Baroreceptors.- 3.2. Pulmonary Arterial Baroreceptors.- 3.3. Ventricular Receptors.- 3.4. Atriovenous Receptors.- 4. Respiratory System Receptors.- 4.1. Cough and Irritant Receptors.- 4.2. Pulmonary Stretch Receptors.- 4.3. Type J Receptors.- 4.4. Other Receptors.- 5. Alimentary System Receptors.- 5.1. Muscular Receptors.- 5.2. Serosal Receptors.- 5.3. Muscularis Mucosae Receptors.- 5.4. Chemoreceptors.- 5.5 Hepatic Osmoreceptors.- 6. Urinary Tract Receptors.- 6.1. Bladder.- 6.2. Urethra.- 7. Other Enteroreceptors.- 8. References.- 16 Arterial Chemoreceptors.- 1. Introduction.- 2. Structure.- 2.1. Light Microscopy.- 2.2. Electron Microscopy.- 2.3. Degeneration Studies.- 3. Function.- 3.1. Types of Activity in the Nerve Supply to the Receptor Complex.- 3.2. The Type I Cell.- 4. The Identity of the Receptor.- 4.1. The Received View.- 4.2. A New Hypothesis.- 5. References.- 17 Taste Receptors.- 1. Introduction.- 2. Gustatory Nerve Fiber Response to Chemical Stimuli.- 2.1. Multiple Sensitivity of Single Chorda Tympani Fibers.- 2.2. Neural Code for Quality of Taste and "Across-Fiber Pattern" Theory.- 3. Electrical Responses of Gustatory Cells to Chemical Stimuli.- 3.1. Innervation and Structure of Taste Bud.- 3.2. How Do Gustatory Cells Respond to Chemical Stimuli?.- 4. References.

The Peripheral Nervous System

The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

A technique is described which permits the inscription of the ventilatory response to isocapnic hypoxia in man as a continuous curve relating alveolar oxygen tension and minute ventilation. The adjustment of ventilation to changes in alveolar oxygen tension is complete in 18-23 sec and this is sufficiently rapid to justify the use of a non-steady-state method. Changes in alveolar carbon dioxide tension are prevented by addition of carbon dioxide to the inspired gas. The resulting [unk]V(E)-P(Ao2) curves are hyperbolic such that falling P(Ao2) produces only slight rises in [unk]V(E) until a critical P(Ao2) range of 50-60 mm Hg is reached. With further fall in P(Ao2), [unk]V(E) increases steeply and the slope of the curve approaches infinity at a tension of 30-40 mm Hg. For purposes of quantitation these curves are approximated by a simple hyperbolic function, the parameters of which are evaluated by a least squares fit of the data. The parameter A denotes curve shape such that the higher the value of A. the greater the increase in ventilation for a given decrease in P(Ao2) and hence the greater the hypoxic drive. Curves are highly reproducible for each subject and curves from different subjects are similar. In 10 normal subjects at resting P(ACo2), A = 180.2 +/-14.5 (SEM). When P(ACo2) is adjusted to levels 5 mm Hg above and below control in six subjects A = 453.4 +/-103 and 30.2 +/-6.8 respectively. These latter values differed significantly from control (P < 0.05). These changes in curve shape provide a clear graphic description of interaction between hypercapnic and hypoxic ventilatory stimuli. At normal P(ACo2) the [unk]V(E)-P(Ao2) curve has an inflection zone located over the same P(o2) range as the inflection in the oxygen-hemoglobin dissociation curve. This indicated that ventilation might be a linear function of arterial oxygen saturation or content. Studies in four subjects have demonstrated that ventilation is indeed related to arterial oxygen content in a linear fashion. These data suggest, but do not prove, that oxygen tension in chemoreceptor tissue as in part determined by circulatory oxygen delivery may be an important factor in controlling the ventilatory response to hypoxia.

/pdf/hypoxic-ventilatory-drive-in-normal-man-3kuc4203gz.pdf

Hypoxic ventilatory drive in normal man

Stimulus interaction in the responses of carotid body chemoreceptor single afferent fibers.

Respiratory insensitivity to hypoxia in chronically hypoxic man

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1954.sp005143

Observations on the volume of blood flow and oxygen utilization of the carotid body in the cat.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1952.sp004732

The effect of carotid occlusion upon the intrasinusal pressure with special reference to vascular communications between the carotid and vertebral circulations in the dog, cat and rabbit

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1952.sp004753

The blood supply of the carotid body in cats, dogs and rabbits

Roy & Brown (1885) showed that,in dogs, asphyxia could cause bronchoconstriction or bronchodilatation, but they did not localize the origin of these effects. Evidence that changes in gaseous composition of the blood influences the bronchial musculature by a central mechanism was first obtained by Einthoven (1892). He found that, in dogs, inhalation of high concentrations of carbon dioxide caused bronchoconstriction which was abolished by section of the vagus nerves. This was confirmed, in cats, by Dixon & Brodie (1903), although in one experiment they found that section of the vagus nerve on the same side as the lung lobe from which they were recording bronchomotor responses did not entirely abolish the bronchoconstrictor response to inhalation of carbon dioxide. They concluded that there might be both a central and peripheral effect. In the light of more recent work, it is possible that the lung lobe still received a vagal innervation from the contralateral side, since it has been shown that there is a considerable crossed vagal innervation of the lungs in the dog (Braeucker, 1926; I. de B. Daly & Hebb, 1942), and cat (Dixon & Ransom, 1912; Daly & Mount, 1951). In one experiment, Einthoven (1892) found that inhalation of nitrogen caused bronchoconstriction. Using the technique of perfusing the isolated head connected with its trunk only by the cervical vagosympathetic nerves, Houssay & Cruciani (1929) found that central anaemia caused bronchoconstriction in the trunk of the recipient. This was confirmed by Daly & Schweitzer (1952) using a similar technique, but a different method of recording bronchomotor responses. Intracarotid injections of blood containing a low oxygen content but a normal carbon

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1953.sp004848

The effects upon the bronchial musculature of altering the oxygen and carbon dioxide tensions of the blood perfusing the brain.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1952.sp004814

A. Schweitzer

Papers

Observations on the volume of blood flow and oxygen utilization of the carotid body in the cat.

The effect of carotid occlusion upon the intrasinusal pressure with special reference to vascular communications between the carotid and vertebral circulations in the dog, cat and rabbit

The blood supply of the carotid body in cats, dogs and rabbits

The effects upon the bronchial musculature of altering the oxygen and carbon dioxide tensions of the blood perfusing the brain.

The blood supply of the superior cervical sympathetic and the nodose ganglia in cats, dogs and rabbits.