What contains bundles of axons called tracts that carry impulses from one part of the nervous system to another?

In myelinated axons, an exquisite matching between the internodal electrotonic properties and the nodal active properties ensures that the electrotonic potential reaching a node has an adequate amplitude and the node has sufficient Na+ channels to generate an action potential that will spread to the next node.

From: From Molecules to Networks, 2004

Muscle Pain and Cramps

Joseph Jankovic MD, in Bradley and Daroff's Neurology in Clinical Practice, 2022

Nociceptive Axons

Many of the afferent axons that transmit painful stimuli from muscle (nociceptors) have free nerve endings (see review byMense and Gerwin, 2010). These free nerve endings do not have corpuscular receptive structures such as pacinian or paciniform corpuscles. They appear as a “string of beads,” thin stretches of axon (with diameters of 0.5–1.0 μm) with intervening varicosities. Most free nerve endings are ensheathed by a single layer of Schwann cells that leave bare some of the axon membranes, where only the basal membrane of the Schwann cell separates the axon membrane from the interstitial fluid. A single fiber has several branches that extend over a broad area. These terminal axons (nerve endings) end near the perimysium, adventitia of arterioles, venules, and lymphatic vessels, but do not contact muscle fibers (Fig. 29.1,A). It is not clear whether nociceptive afferents can have both cutaneous and muscle branches. The varicosities in the free terminals contain granular or dense core vesicles containing glutamate and neuropeptides such as SP, vasoactive intestinal peptide (VIP), CGRP, and somatostatin. When the afferents are activated, neuropeptides are released into the interstitial tissue and may activate other nearby muscle nociceptors.

Action potentials arising in nociceptor terminals induce or potentiate pain by two mechanisms:centripetal conduction to central branches of afferent axons brings nociceptive signals directly to the CNS.Centrifugal conduction of action potentials along peripheral axon branches causes indirect effects by activating other unstimulated nerve terminals of the same nerve and causing release of glutamate and neuropeptides into the extracellular medium. These chemical substances can stimulate or sensitize terminals on other nociceptive axons. This is the basis for the axon reflex and the wheal and flare around a cutaneous lesion.

Group III (class Aδ cutaneous afferent) thinly myelinated and group IV (class C cutaneous afferent) unmyelinated afferent axons conduct the pain-inducing stimuli from muscle to the CNS. Group III nociceptive axons are thinly myelinated and conduct impulses at moderately slow velocities (3–13 m/sec). Group III fibers can end in free nerve terminals (possibly for mediating a more spontaneous pain) or other receptors such as paciniform corpuscles. Group IV fibers are unmyelinated, conduct impulses at very slow velocities (0.6–1.2 m/sec), end as free nerve endings, and are the main mediators of the diffuse, dull, or burning muscle pain.

Group II axons are large and myelinated, and conduct impulses at rapid velocities, mainly from muscle spindles. They normally mediate innocuous stimuli, and stimulation may reduce the perception of pain (by acting on the nociceptive afferents in the spinal cord). Inflammation or repetitive stimulation can sensitize group II afferents (phenotypic switch), which then mediate mechanical allodynia in some tissues.

Neuro-ophthalmology

TIMOTHY J. MARTIN, in Primary Care Ophthalmology (Second Edition), 2005

Visual Field Loss Patterns in Lesions of the Chiasm and Posterior Visual Pathways

Axons from retinal ganglion cells that represent right visual space are routed through the chiasm to form the left optic tract, synapsing in the left lateral geniculate body (and vice versa for left visual space) (Fig. 12-1). Anatomically, this means that axons originating in the nasal half of the retina (which map the temporal visual field) cross in the chiasm to the opposite side. Therefore, mass lesions compressing the chiasm disrupt these crossing fibers, causing temporal visual field defects in both eyes. Lesions posterior to the chiasm (optic tract and posterior visual pathways) produce homonymous (on the same side in both eyes) visual field defects that respect the vertical meridian. From the chiasm posteriorly, corresponding axons from the right and left eyes that represent the same point in visual space move closer together as they converge on a common point in the occipital cortex. Thus, the more posterior a lesion is, the more congruous the resultant visual field defects become: the homonymous visual defects in each eye look more alike in shape and depth.

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Developmental Disorders of the Nervous System

Joseph Jankovic MD, in Bradley and Daroff's Neurology in Clinical Practice, 2022

Growth of Axons and Dendrites

During the course of neuroblast migration, neurons remain largely undifferentiated cells, and the embryonic cerebral cortex at midgestation consists of vertical columns of tightly packed cells between radial blood vessels and extensive extracellular spaces. Cytodifferentiation begins with a proliferation of organelles, mainly endoplasmic reticulum and mitochondria in the cytoplasm, and clumping of condensed nuclear chromatin at the inner margin of the nuclear membrane. Rough endoplasmic reticulum becomes swollen, and ribosomes proliferate.

The outgrowth of the axon always precedes the development of dendrites, and the axon forms connections before the differentiation of dendrites begins. Ramón y Cajal first noted the projection of the axon toward its destination and named this growing process thecone d’accroissement (growth cone). The tropic factors that guide the growth cone to its specific terminal synapse, whether chemical, endocrine, or electrotaxic, have been a focus of controversy for many years. However, we now know that diffusible molecules secreted along their pathway by the processes of fetal ependymal cells and perhaps some glial cells guide growth cones during their long trajectories. Some molecules (e.g., brain-derived neurotropic growth factor, netrin, S-100β protein) attract growing axons, whereas others (e.g., the glycosaminoglycan keratan sulfate—not to be confused with another very different protein, keratin) strongly repel them and thus prevent aberrant decussations and other deviations.

The proteoglycan keratan sulfate has been known since 1990 to be an important molecule in the dorsal median septum of the spinal cord that prevents rostrally growing dorsal column axons from crossing the midline before their intended destinations in the nuclei gracilis and cuneatus at the caudal medulla oblongata; aberrant decussation would confuse the brain about laterality of sensory stimuli (Snow et al., 1990). Keratan sulfate is selective, however, repelling excitatory glutamatergic axons while facilitating inhibitory GABAergic axons. The great majority of dorsal root ganglion neurons that project axons into the dorsal columns are glutamatergic, by contrast with spinothalamic fibers that mainly are GABAergic; ascending axons of the nuclei gracilis and cuneatus to the thalamus also are GABAergic. Another repulsive factor for guidance of olfactory axons away from septal receptors is a secreted protein calledSlit, which is the ligand for theSlit receptorRobo (Brose et al., 1999; Li et al., 1999; Rothberg et al., 1990). Commissural axons also are enabled to cross the ventral median septum of the spinal cord that repulses longitudinal axons growing rostrally or caudally in the longitudinal axis of the neural tube and early fetal spinal cord (Bovolenta and Dodd, 1990)

Keratan sulfate also occurs in the forebrain and is strongly expressed in early fetal life in the thalamus and globus pallidus, later appearing in the molecular zone and later diffusely in the cortical plate, finally becoming more localized in the deep cortical laminae and the U-fiber layer, where it impedes the penetration of axons from deep white-matter heterotopia so that they cannot integrate into cortical synaptic circuitry and epileptic networks (Sarnat, 2019). Granulofilamentous keratan sulfate also binds to neuronal somatic membranes, but not to dendritic spines, explaining why axosomatic synapses are inhibitory and axodendritic synapses are excitatory (Sarnat, 2019). An additional function of keratan sulfate in the brain, where is it secreted by astrocytes into the intercellular matrix, is to surround axonal fascicles so that axons can neither enter nor exit the fascicles except at programmed places. Both large and long fascicles, such as the corticospinal tract, and short fascicles, such as the coarse local axonal bundles within the globus pallidus and similar but smaller “pencil fibers of Wilson” within the corpus striatum, are insulated (Sarnat, 2019). Keratan sulfate also has a wider distribution in the body in organs other than the CNS. It is strongly expressed in cornea, cartilage, bone, synovium, connective tissues, and other sites (Caterson and Melrose, 2018; Pomin, 2015, 2018). It may explain why cartilage is not penetrated by nerves except at designated foramina.

White Matter Pathophysiology

Bruce R. Ransom, ... Selva Baltan, in Stroke (Seventh Edition), 2022

Activation of Intracellular Ca2+ Release

Axons exposed to ischemia show rapid increases in [Ca2+]i.64,96 A significant portion of this increase occurs in the absence of [Ca2+]o and has been linked to Ca2+ release from intracellular stores, specifically from axonal endoplasmic reticulum (ER) and possibly also mitochondria.96,97 The mechanisms of [Ca2+]i release during ischemia have proved complex. Axon depolarization can lead to activation of L-type Ca2+ channels92 coupled to ryanodine receptors, leading to Ca2+ release from axonal ER.96 Other pathways may also operate, including Ca2+ activation of second messenger cascades leading to nitric oxide formation and release of Ca2+ from mitochondria.97 Pharmacologic blockade of these several pathways during ischemia improves functional outcome. Given the powerful effect that age has on ischemic injury mechanisms and outcomes in the rodent optic nerve,42 it will be important to explore [Ca2+]i release mechanisms in older animals.

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Late Responses

David C. Preston MD, in Electromyography and Neuromuscular Disorders, 2021

Axon Reflex

The axon reflex (A wave), although not a true reflex, is another late potential that often is recognized during the recording of F responses. The axon reflex typically occurs between the F response and the direct M response (Fig. 4.14). An axon reflex is identified as a small motor potential that is identical in latency and configuration with each successive stimulation. This is in contrast to the F response, which varies slightly in latency and configuration from stimulation to stimulation. It often is useful to acquire these potentials on a rastered trace, which can be superimposed. Axon reflexes, unlike F responses, superimpose perfectly on one another. Axon reflexes typically are seen in reinnervated nerves, especially when a submaximal stimulus is given.

An axon normally divides into its terminal divisions very close to the muscle, which usually is distal to the common distal stimulation sites for most nerves studied in the EMG laboratory. In reinnervated nerves, however, terminal branching points from collateral sprouting may occur proximal to the distal stimulation site. It is in this latter situation, with submaximal stimulation, that an axon reflex may occur. As a nerve is stimulated, the action potential travels both distally and proximally. If the proximally traveling antidromic pulse passes a terminal branching point, the pulse might then travel back down that branching nerve fiber to the muscle to create an axon reflex, which occurs after the M potential but before the F response (Fig. 4.15). With supramaximal stimulation, the antidromic volley usuallycollides with the orthodromically traveling axon reflex, and the axon reflex is not seen. If all the distal nerve fibers have not been supramaximally stimulated, however, there may be no antidromic volley in the branching fibers to collide with the orthodromically traveling axon reflex, in which case the potential is free to travel back down the branching fiber to the muscle, creating the axon reflex. Axon reflexes are important to identify because they often suggest reinnervation along the nerve, as well as the possibility that the stimulation is not supramaximal. Most important, axon reflexes should not be confused with the F response, which usually occurs later. Rarely, the axon reflex will follow rather than precede the F response if the regenerating collateral fibers are conducting very slowly.

Although axon reflexes are most often associated with reinnervation following axonal loss lesions, they also can be seen in demyelinating neuropathies. Most classic is Guillain-Barré syndrome in which axon reflexes are often seen in the first several days of the illness. Their etiology in this setting remains a topic of debate but has been speculated to occur from ephaptic spread from one nerve fiber to another at a point of inflammation and demyelination (ephaptic meaning direct spread from one nerve membrane to another).

Neuroanatomy and Mechanisms of Visceral Pain

Benjamin L. Katz MD, MBA, ... A. Sassan Sabouri MD, in Interventional Management of Chronic Visceral Pain Syndromes, 2021

Sympathetic Nervous System

General sympathetic nervous system functions include vasoconstriction, increased heart rate, inhibition of glandular secretion and smooth muscle contraction in organs, and contraction of smooth muscle sphincters.

Except for sympathetic nerve fibers that synapse directly on chromaffin cells in the adrenal medulla, all autonomic visceral efferent pathways consist of at least two neurons.

The nerve cell bodies of sympathetic presynaptic neurons are found in the lateral gray horn of spinal cord segments T1 through L2 (Fig. 2.2). The sympathetic chain, also known as the sympathetic trunk, consists of a series of interconnected ganglia that run from the base of the skull to the coccyx lateral to the vertebral column (Fig. 2.3). The sympathetic chain allows the axons of sympathetic presynaptic neurons to synapse at ganglia above or below their spinal cord segmental origin.

The myelinated axons of all sympathetic presynaptic neurons leave the spinal cord in the ventral roots of the thoracic, lumbar spinal nerves and enter the sympathetic trunk through white rami communicantes. Sympathetic visceral motor impulses may take several pathways at this point.

1.

The axons of presynaptic sympathetic neurons carrying impulses to peripheral blood vessels, skin glands, and smooth muscles synapse at the sympathetic chain ganglia. The axons of the corresponding postsynaptic neurons then join spinal nerves through gray rami communicantes to reach their targets.

2.

The axons of presynaptic sympathetic neurons carrying impulses to structures in the head and neck ascend within the sympathetic chain from upper thoracic spinal cord levels and synapse on cervical sympathetic ganglia. The axons of the corresponding postsynaptic neurons typically follow branches of the carotid arteries to their targets.

3.

The axons of presynaptic sympathetic neurons carrying impulses to thoracic viscera such as the heart, lungs, and esophagus enter the ventral rami of spinal nerves and typically synapse at adjacent sympathetic chain ganglia. The axons of the corresponding postsynaptic neurons typically travel by direct branches to the cardiac, pulmonary, and esophageal autonomic plexuses.

4.

The axons of most sympathetic presynaptic neurons to abdominal and pelvic viscera pass through the sympathetic trunk without synapsing, form distinct thoracic splanchnic or lumbar splanchnic nerves, and synapse at ganglia within one of the many autonomic nerve plexuses clustered around the major branches of the abdominal aorta. The axons of the corresponding postsynaptic neurons typically follow the appropriate visceral branches of the aorta to reach their targets.

5.

The axons of some lower lumbar presynaptic neurons carrying impulses to the distal portions of the urogenital organs and the perineal erectile tissue may descend in the sympathetic chain to synapse at the sacral sympathetic chain ganglia. The axons of the corresponding postsynaptic neurons, the “sacral splanchnic nerves,” travel anteriorly by direct, and possibly vascular, branches to reach their targets.

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Molecular Properties of Ion Channels

Lily Yeh Jan, Yuh Nung Jan, in From Molecules to Networks, 2004

Different potassium channels are targeted to axons and dendrites.

Myelinated axons have voltage-gated sodium channels confined to the node of Ranvier (Salzer, 1997), flanked by certain isoforms of voltage-gated potassium channels (Kv1.1 and Kv1.2) forming two rings in the juxtaparanodal regions (Rasband et al., 1998; Wang et al., 1993; Zhou et al., 1999). Another member of the same family, Kv1.4, is found in patches along the axon and near the nerve terminals (Cooper et al., 1998), whereas members of a closely related family such as Kv4.2 are located on the dendrite and on the postsynaptic membrane (Alonso and Widmer, 1997; Sheng et al., 1993; Tkatch et al., 2000). Large conductance (BK) calcium-activated potassium channels, on the other hand, are present on the presynaptic membrane (Wanner et al., 1999). Heteromeric channels formed by different α and β subunits may be localized to different domains of the neuronal membrane, thereby further increasing the diversity of these channels (Rhodes et al., 1995; Veh et al., 1995).

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COLORECTAL CANCER IN ULCERATIVE COLITIS

In Surgery of the Anus, Rectum & Colon (Third Edition), 2008

Overall assessment of colonoscopic surveillance

Axon (1994) reviewed the outcome of 12 separate colonoscopic cancer surveillance programmes for colitis with total or extensive disease of more than 10 years duration by specialists with a particular interest in detecting early cancers (Table 38.26). A total of 1916 patients were entered and 92 cancers detected as a result of 3807 colonoscopies. However, only 52 (57%) were early lesions so the remainder represent lesions that would soon have become symptomatic. Of the 52 favourable lesions, only 22 were found by colonoscopy but of these, only eight were actually detected in high-risk individuals at first colonoscopy; that is 1 per 476 examinations. Axon concluded that it was difficult to justify the time and expense for such a small return. Thus, not only are colonoscopic surveillance programmes ineffective for most individuals with colitis, but they might be positively disadvantageous when surveillance involves bowel preparation and a painful examination. Surveillance is a constant reminder of asymptomatic, on-going disease; no wonder recruitment and compliance is poor. Hence, until newer and more effective surveillance techniques are available, we simply advise total colonoscopy in patients with total colonic disease of 10 years duration, together with regular clinical follow-up and repeat colonoscopy when new symptoms arise.

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Peripheral Nerve Stimulation

Michael Stanton-Hicks, in Neurostimulation for the Treatment of Chronic Pain, 2012

Neuroanatomy

The axon is the functional unit of a peripheral nerve. Both afferent and efferent axons with their Schwann cells are enclosed in a delicate layer of endoneurial tissue (endoneurium). This is connective tissue that allows the free diffusion of fluids to and from neural structures. Each bundle of axons is enclosed by the perineurium. Cell bodies in the dorsal root ganglion are the source of an axon with a long branch that extends to its peripheral functional source and a shorter branch that passes from its cell body to the spinal cord. Sensory axons are unipolar and transmit sensory information from receptors in the periphery to second-order neurons in the spinal cord. On the other hand, motor neurons arise from the cell bodies in the ventral horn of the spinal cord and in contrast are multipolar with many dendrites. In addition, an axon carries impulses peripherally to activate their specific effector organs. Both dendrites and cell bodies of these neurons are highly specialized to integrate postsynaptic currents that modulate effector organs.

Myelinated nerve fibers have many concentric laminae that form from a single Schwann cell. The nodes of Ranvier are interruptions in the myelin sheath where the inward currents during depolarization are regenerated. An axon of a sensory neuron varies in diameter from as little as 2 µm to 11.75 µm.34,35 To facilitate regional distribution and therefore sensory coverage, nerve fibers divide into many branches, thereby allowing the innervation of a significant tissue mass by a single neuron. Clinically this results in referred pain that may originate in a single neuron being transmitted by branches to other tissues in the same region. The axon reflex is another mechanism that allows pain to be felt in undisturbed tissue. In this case antidromic transmission passes to other adjacent tissue, causing an expansion of the painful area. Table 17-2 lists the diameters of nerve fibers and their conduction velocities and function. The fascicular anatomy within nerve trunks is shown in Fig. 17-1. Figs. 17-1 and 17-2 show nerve fibers grouped within a thin laminated sheet (epineurium) that covers the axons.

A collection of nerve fibers (axon bundles) are known as fascicles. Each fascicle containing many axons is encased by a connective tissue layer and perineurium. The entire nerve is contained within a loose outer covering, the epineurium. Although fascicles vary in size from 0.04 to 4 mm, the majority are found between 0.04 and 2 mm in diameter. As nerves proceed distally, their fascicles begin to divide into smaller and smaller units and become more numerous. In addition, this organization takes on a topographically discrete nature, particularly in mixed (motor and sensory) nerves, and is responsible for providing an intimate view of the fascicular architecture.36-39 For example, in the ulnar nerve behind the medial epicondyle many nerve fibers are grouped into a single fascicle. A similar arrangement is found in the radial nerve in the spinal groove, the axillary nerve behind the humerus, and the common peroneal nerve in the lower thigh.

The histology of nerve fibers has considerable bearing on the ability to selectively stimulate the sensory or motor nerve fibers. The cross sectional area of a nerve trunk is comprised of 25% to 75% epineurial tissue, the highest amount being in the sciatic nerve in the gluteal region and the lowest in the ulnar nerve at the medial epicondyle. This characteristic influences the effect of neurostimulation. The greater the thickness (higher impedance), the greater is the attenuation of the electric field. In a similar manner, this effects the diffusion of local anesthetics and therefore the amount necessary to achieve their mechanism of action at the axon.

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Small Intestinal Motor and Sensory Function and Dysfunction

Jane M. Andrews, L. Ashley Blackshaw, in Sleisenger and Fordtran's Gastrointestinal and Liver Disease (Ninth Edition), 2010

Efferent Supply

The axons of the intrinsic motor neurons that supply small intestinal smooth muscle exit the intramural ganglia and enter either the circular or the longitudinal muscle layer, where they pass in close proximity to both the myocytes and ICC. No specific neuromuscular junctions are present in small intestinal smooth muscle as in skeletal muscle, although the multiple varicosities along the motor axons probably represent specialized areas of neurotransmission. The motor axons discharge along their length, potentially activating large numbers of myocytes through ICC but possibly also directly activating them. The lack of exclusive, specific neuromuscular junctions, the electrical gap junctions among myocytes, and the overlap of innervation of myocytes from more than one motor axon mean that functionally discrete motor units in the intestinal smooth muscle do not appear to exist, in contrast with skeletal muscle. The ENS motor supply itself is both inhibitory and excitatory, and intrinsic motor neurons generally contain both a fast and a slow neurotransmitter. The predominant excitatory transmitters are acetylcholine (fast) and substance P (slow), and the predominant inhibitory transmitters are nitric oxide (fast), vasoactive intestinal polypeptide (VIP) (slow), adenosine triphosphate (ATP) (fast), and the nucleotide β-nicotinamide adenine dinucleotide (β-NAD).12

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What matter contains bundles of axons called tracts that carry impulses from one part of the nervous system to another?

White Matter in the Brain and Spinal Cord The white matter of your brain and spinal cord is composed of bundles of axons. These axons are coated with myelin, a mixture of proteins and lipids, that helps conduct nerve signals and protect the axons.

What is a bundle of axons within a nerve called?

In the peripheral nervous system a bundle of axons is called a nerve. In the central nervous system a bundle of axons is called a tract. Each axon is surrounded by a delicate endoneurium layer.

What bundles of axons carry impulses from the central nervous system to effectors?

Efferent neurons transmit signals from the central nervous system to the effector cells and are sometimes called motor neurons. Interneurons connect neurons within specific regions of the central nervous system.

Which structure contains bundles of axons organized into tracts?

The CNS is composed of the brain and spinal cord. In the CNS, there are localized collection of neuron cell bodies called nuclei within the gray matter and bundles of axons called tracts within the white matter. The PNS is made of collections of neuron cell bodies called ganglia, and bundle of axons called nerves.

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