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 migration and differentiation of neural crest cells.

Modern views on an ancient chemical: serotonin effects on cell proliferation, maturation, and apoptosis.

Publisher Summary This chapter focuses on the morphology of specialized neuronal contacts in general and of synaptic contacts in particular. The term “synapse” is used as a morphological term to describe specialized regions of contact between nerve cells and between nerve cells and effector organs. The structure of this specialized region is of crucial importance. Whereas epithelial cells in general show symmetrical contact regions such as the desmosomes and tight junctions the nervous system shows, in addition, asymmetrical contact regions, the “synaptic thickenings”. It is emphasized that, in addition to transmission of impulses, the organization of neuroneuronal junctions is likely to include other important properties. The interaction between neurons by which a nerve cell can maintain or even stimulate the growth and maturation of an innervated structure is likely to involve neuronal contacts, as is the ability of developing and regenerating axons to grow to and make contact with specific cell groups. Although relatively little is known about these aspects of neuroneuronal interaction they cannot be ignored when the morphology of synaptic contacts is being considered.

Synaptic Morphology in the Normal and Degenerating 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

Adult Syrian hamsters were given daily subcutaneous injections of reserpine (1 mg/kg) for one or three days in order to study the fine structural changes in adreno-medullary cells. Initial alterations of fine structure in animals given one injection and sacrificed 15 hours later. Hamsters treated for three days were adrenalectomized on the left side 24 hours after the last reserpine injection. Following adrenalectomy, animals were allowed to recover for 48 or 96 hours after which the cells of the right adrenal medulla were compared with those of the left.



Medullary cell changes 15 hours following one injection of reserpine included partial loss of electron opaque granules and an increase in the number of cytoplasmic vesicles and vacuoles. Medullary cells from the left adrenal glands removed following three subcutaneous injections of reserpine were characterized by a marked loss of electron opaque granules and by the presence of many vesicles and vacuoles distributed throughout the cytoplasm.



Forty-eight hours following unilateral adrenalectomy medullary cells from the remaining right glands exhibited slightly electron opaque granules within the cytoplasm, each of which was surrounded by a smooth surfaced membrane. Cytoplasmic vesicles and vacuoles had decreased in number. Ninety-six hours following unilateral adrenalectomy medullary cells from the right glands showed further decreases in numbers of vesicles and vacuoles, and granules which possessed an electron opaqueness comparable to control medullary cells had reappeared within the cytoplasm.

An electron microscopic study of the effects of reserpine on adreno-medullary cells of the syrian hamster†

Typical vagal paraganglia of Syrian hamsters are encapsulated in connective tissue and consist of groups of epithelial cells. Ganglion cells, a few fenestrated capillaries, and bundles of unmyelinated nerve fibers are intermingled among the parenchymal cells. The parenchymal cells are of two types: chief or paraganglion and sustentacular or supporting cells. The processes of the supporting cells partly or completely surround the paraganglion cells. In addition to the nucleus, Golgi complex, mitochondria, parallel-arrayed granular endoplasmic reticulum, and lipofuscin pigment, the chief cells are characterized by the presence of numerous membrane-bound, electron opaque granules. After an injection of 3H-dopa, labelings were concentrated over the chief cells and were associated predominantly with the granules. Following glutaraldehyde-dichromate treatment the granules gave a positive reaction for unsubstituted amines. These results suggest that the chief cells contain catecholamines in the electron opaque granules.

Ultrastructural studies of vagal paraganglia in Syrian hamsters.

The medullae from the right adrenal glands of hamsters given one or three injections of reserpine were prepared for electron microscopy by fixation in buffered osmic acid while the contralateral left glands were fixed in formol-dichromate for light microscopic determinations of the chromaffin reaction. The adreno-medullary cells of these animals were compared with cells of untreated hamsters in order to determine if catecholamine loss was accompanied by changes in the electron opaque cytoplasmic granules.



Ten and 15 hours following one reserpine injection (1 mg/kg) the chromaffin reaction was positive, whereas after 20 hours the reaction was negative, reflecting a catecholamine reduction. The negative chromaffin reaction was accompanied by alterations in granule ultrastructure. The dense central core of the granules was less electron opaque compared with those of control medullary cells. The decreased density likely reflected a catecholamine loss since the opaque appearance of the granules is attributed to the presence of the amines. Following three injections (1 mg/kg daily; three days) the chromaffin reaction was negative and most granules had disappeared from the cytoplasm. The results give evidence that, after limited reserpine injections (1 mg/kg; one injection), catecholamines can be released from the medullary cells without granule disappearance.

A light and electron microscopic study correlating the chromaffin reaction and granule ultrastructure in the adrenal medulla of the Syrian hamster

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 study of cell division in chick embryonic ganglia.

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Robert D. Yates

Author Tools

Chat about Author