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

We studied the ultrastructure of the rat carotid body and found that glomus cells (Type I cells) are of two types (A and B) based on the size of their dense-cored vesicles. Dense-cored vesicles in type A cells have a mean diameter nearly 30% larger than those in type B cells. Although we seldom found nerve endings on type B cells, at least two types of nerves end on type A cells. Axonal degeneration studies showed that more than 95% of these nerves are afferent axons which leave the carotid body in the carotid sinus nerve and have their cell bodies in the sensory (petrosal) ganglion of the glossopharyngeal nerve. Less than 5% are preganglionic efferent axons from the cervical sympathetic trunk which enter the carotid body with axons from the superior cervical sympathetic ganglion. We found no efferent axons from the glossopharyngeal nerve which end on glomus cells, although some do end on ganglion cells. Afferent and efferent nerve endings can be distinguished morphologically, although both types contain many synaptic vesicles and few large dense-cored vesicles. Synaptic vesicles in afferent nerve endings are 15% larger but 60% less numerous than those in efferent nerve endings. Large densecored vesicles in afferent nerve endings are similar in size but 80% less numerous than those in efferent nerve endings. Some regions of afferent nerve endings are presynaptic to glomus cells, some are postsynaptic, and some form reciprocal synapses. Efferent nerve endings are presynaptic to glomus cells but not in synaptic contact with afferent nerve endings. Blood vessels in the carotid body have both a parasympathetic and a sympathetic innervation. Most parasympathetic vasomotor nerves arise within the carotid body from ganglion cells whose preganglionic innervation is from the glossopharyngeal nerve. Terminals of these vasomotor nerves contain clear-cored synaptic vesicles. Sympathetic vasomotor nerves, most of which come from ganglion cells in the superior cervical ganglion (and from a few ganglion cells in the carotid body) have dense-cored synaptic vesicles. We postulate that (I) afferent nerve endings, which are interconnected with glomus cells by reciprocal synapses, are chemoreceptors; (2) glomus cells are dopaminergic interneurons which modulate the sensitivity of chemoreceptive nerve endings; (3) glomus cells and afferent nerves interact through reciprocal synapses which form an inhibitory feedback loop: sensory nerves release an excitatory transmitter when stimulated, the transmitter causes glomus cells to release dopamine, and dopamine inhibits the sensory nerves; (4) the feedback loop may contribute to the hyperbolic nature of the curve described by the relationship between arterial oxygen pressure and the rate of chemo-receptor firing; (5) by enhancing dopamine release from some glomus cells, preganglionic sympathetic nerves decrease chemoreceptor activity, an effect opposite from that of vasoconstriction produced by postganglionic sympathetic nerves on blood vessels j (6) synaptic interconnections enable glomus cells to influence one another. We cannot exclude the possibility that glomus cells, like afferent nerve endings, are chemoreceptors sensitive to hypoxia and hypercapnia or that glomus cells, in addition to their other functions, secrete a polypeptide hormone.

The innervation of glomus cells, ganglion cells and blood vessels in the rat carotid body: A quantitative ultrastructural analysis

Regulation of respiration (first of three parts).

This review deals with drug-induced lipidoses and the possible underlying mechanisms. A variety of drugs, widely differing in their main pharmacological actions, but closely resembling each other with respect to particular physiochemical properties, have been found to cause in animals and man cytological alterations that are reminiscent of the inherited lipid-storage diseases of man. Ultrastructurally, the alterations are characterized by multilamellated or crystalloid cytoplasmic inclusions, i.e., residual bodies resulting from an intralysosomal accumulation of polar lipids. Biochemically, some of the most severely affected tissues have been demonstrated to contain increased amounts of phospholipids and of the drug applied. All drugs hitherto found to induce such alterations are cationic amphiphilic (amphipathic) compounds; they possess a highly apolar ring system and a cationic hydrophilic side chain (e.g., triparanol, chloroquine, chlorzyclizine, 4,4′-diethylaminoethoxyhexestrol, chlorphentermine, ipri...

Drug-induced phospholipidoses. II. Tissue distribution of the amphiphilic drug chlorphentermine.

The sections in this article are:


1
Structure
1.1
General Anatomy, Histology, and Embryology of Carotid Body

1.2
Carotid Body Ultrastructure

1.3
Pathological Changes and Physiologically Induced Changes in Carotid Body Morphology




2
Response of Chemoreceptors
2.1
Resting Chemoreceptor Discharge

2.2
Chemoreceptor Response to Hypoxia

2.3
Chemoreceptor Response to Partial Pressure of CO2 and pH

2.4
Chemoreceptor Response to Temperature and Osmolarity

2.5
Carotid Body Blood Flow, O2 Consumption, and Chemoresponse

2.6
Efferent Modulation of Chemosensory Discharge




3
Mechanisms of Chemoreception
3.1
Transducer Element(s) in Carotid Body

3.2
Biophysical Aspects of Chemoreception

3.3
Role of Putative Neurotransmitters in Chemotransduction

3.4
Hypotheses on Mechanisms of Chemoreception




4
Addendum
4.1
Recent Advances in Carotid Body Chemoreception

4.2
Structure

4.3
Response of Chemoreceptors

4.4
Mechanisms of Chemoreception

Initiation and Control of Chemoreceptor Activity in the Carotid Body

Adult Syrian hamsters were given a subcutaneous injection of reserpine 3 days before an intraperitoneal injection of (3)H-3,4 dihydroxyphenylalanine or (3)H-5, hydroxytryptophan and the carotid bodies were subsequently prepared for electron microscopic radioautography. Other Syrian hamsters were given a subcutaneous injection of reserpine and the carotid bodies were subjected to a sensitive cytochemical test for the detection of unsubstituted amines. These studies were made to determine whether the labeled amine precursors were incorporated into the cells and to see whether the parenchymal cells were affected by reserpine treatment. Material from hamsters treated first with reserpine and subsequently injected with (3)H-3,4 dihydroxyphenylalanine or (3)H-5, hydroxytryptophan exhibited reduced grains of silver over the cells which were associated mainly with the dense cores of the cytoplasmic granules. These studies offer evidence that the granules of the carotid body incorporate catecholamine and indolamine precursors. Material from hamsters incubated for the presence of unsubstituted amines gave a positive reaction (opaque cytoplasmic granules) for catecholamines but not for indolamines. The latter substances may not be present in quantities sufficient to register a positive reaction in the cytochemical test. The opaque granules, indicative of the presence of catecholamines, decreased in density after reserpine treatment. 5 days after one reserpine injection the granules had regained opacity and were comparable to those seen in the control cells.

/pdf/electron-microscopic-radioautographic-studies-of-the-carotid-r56h1jv1vk.pdf

Electron microscopic radioautographic studies of the carotid body following injections of labeled biogenic amine precursors

The carotid bodies from control, reserpine-treated, and hypoxia-treated hamsters were fixed with phosphate-buffered glutaraldehyde and osmium tetroxide, s-Collidine-buffered osmium tetroxide, or phosphate-buffered glutaraldehyde followed by potassium dichromate incubation. Following glutaraldehyde-osmium tetroxide fixation no differences in density or population of the electron-opaque granules in the glomus cells of either control or experimental animals were observed. With s-Collidine-buffered osmium tetroxide and the glutaraldehyde-dichromate technique a marked decrease in density without an appreciable reduction in number of granules was noted after reserpine treatment, while in hypoxia-treated hamsters the density and population of the granules were not different from those of the controls. The results indicate that reserpine depletes the amines without granule disappearance and that hypoxia does not affect the amine content of the granules. It is suggested that following glutaraldehyde-osmium tetroxide double fixation, persistence of the density of the granules in reserpine-treated animals is due primarily to the nonamine content, and that the amines in the glomus cells are probably not directly involved in the respiratory reflex.

https://rupress.org/jcb/article-pdf/42/3/804/1069223/804.pdf

The effects of reserpine and hypoxia on the amine-storing granules of the hamster carotid body.

The administration of triparanol caused an hypertrophy of smooth membranes and the occurrence of numerous cytoplasmic bodies in smooth muscle fibers and parasympathetic ganglion cells in the myenteric plexus of the hamster ileum. The hypertrophied membranes were more evident in the early stages of treatment when the cytoplasmic bodies were relatively few in number. The cytoplasmic bodies were tentatively divided into four types as follows: whorls of membranes (type I), labyrinthine aggregates of smooth membranes (type II), dense bodies with a reticular internal structure (type III) and crystalline bodies showing a regular lattice pattern (type IV). There were also many intermediate types of cytoplasmic bodies which exhibited more than one characteristic of the types mentioned above. The relative numbers of the cytoplasmic bodies seemed to be increased in the order of type I (or type II), type III, and type IV in proportion to the period of treatment. It is suggested that type IV cytoplasmic bodies are formed through the stages of type I (or type II) and type III, and that types I, II, and III in turn, form from hypertrophied smooth membranes. The formation of crystalline bodies from hypertrophied membranes may represent the inclusion of cytoplasmic organelles into autophagic vacuoles (lysis). After certain degrees of lysis, more resistant components of the hypertrophied membranes remain as residues. These residues, rich in phospholipids, are probably represented as crystalline bodies.

An ultrastructural study of opaque cytoplasmic inclusions induced by triparanol treatment

A variety of age-related changes occur in the structure of neurons in the cerebral cortex of Wistar-Kyoto and spontaneously hypertensive rats. The most marked alteration associated with increasing age was the deposition of lipofuscin pigment, primarily at the bases of apical dendrites of pyramidal neurons. While no strain-related differences in the amount of lipofuscin pigment were observed in the youngest (3 months) and in the aged (22-27 months) groups of rats, it appeared that hypertensive rats had larger pigment deposits at 12 months of age. At the ultrastructural level, neurons of the aged brains exhibited numerous nuclear invaginations and filamentous nuclear inclusions, increased amounts of Golgi complex and two types of cytoplasmic inclusions. The number of degenerative structures in the neuropil (membranous whorls, dystrophic axons and alterations in myelin sheaths) was also apparently increased in the aged brains. Neurofibrillary tangles were observed in dendritic processes of a 27-month-old Wistar-Kyoto rat. Glial cells accumulated distinctive pigment granules by which the three types of glia could be identified.

Brain aging in normotensive and hypertensive strains of rats. II. Ultrastructural changes in neurons and glia.

The sinus nerve or sympathetic trunk was stimulated unilaterally in one group of adult cats or Syrian hamsters while in another group the sinus nerve or sympathetic trunk was cut unilaterally and the animals were given reserpine. In a third group, atropine was administered prior to sinus nerve stimulation. All tissues were processed for the detection of primary monoamines. The carotid bodies on the operated sides were compared with those on the unoperated sides of the same animal in order to determine if amine depletion occurred following the experimental procedures. After sinus nerve stimulation alone, the density of the granules in the glomus cells was decreased, but changes were not noted in the granules following sympathetic nerve stimulation. Sinus nerve stimulation after atropine administration resulted in no change in granule density. Sinus nerve transection followed by reserpine treatment resulted in a greater decrease in granule density on the unoperated than on the operated side. Transection of the sympathetic components to the carotid body followed by reserpine injections resulted in a decrease in granule density in the glomus cells on both the operated and unoperated sides. These results suggest that the sinus nerve must be intact for reserpine to exert an effect and that the sinus nerve may contain efferent fibers which modulate amine secretion.

/pdf/effects-of-sinus-nerve-stimulation-on-carotid-body-glomus-3bhii5xq4p.pdf

I-Li Chen

Papers

Electron microscopic radioautographic studies of the carotid body following injections of labeled biogenic amine precursors

The effects of reserpine and hypoxia on the amine-storing granules of the hamster carotid body.

An ultrastructural study of opaque cytoplasmic inclusions induced by triparanol treatment

Brain aging in normotensive and hypertensive strains of rats. II. Ultrastructural changes in neurons and glia.

Effects of sinus nerve stimulation on carotid body glomus cells