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I. THE NEURON is the structural and functional unit of the nervous system. The neuron consists of a perikaryon (cell body), dendrite, and axon, each of which contains certain ul-trastructural components (Table 7-1). The axon arises from an extension of the perikaryon called rhe axon hillock. The part of the axon between the axon hillock and the start of the myelin sheath is called the initial segment and is where the action potential is initiated.

A. Axonal transport

1. Fast anterograde transport is responsible for transporting synaptic vesicles from the perikaryon to the synaptic terminal and uses kinesin, which has adenosine triphosphatase (ATPase) activity.

2. Slow anterograde transport is responsible for transporting cytosol and cytoskele-tal elements from the perikaryon to the synaptic terminal.

3. Fast retrograde transport is responsible for transporting nerve growth factor, tetanus toxin, polio virus, rabies virus, and herpes simplex virus from the synaptic terminal to the perikaryon and uses dynein, which has ATPase activity.

B. Action potential (Figure 7-1)

1. Within the neuronal cytoplasm, the sodium ion concentration is low and the potassium ion concentration is high. Within the extracellular milieu, the sodium ion concentration is high and the potassium ion concentration is low.

2. Because of potassium ion leakage from the cytoplasm into the extracellular milieu and the Na+-K+-ATPase pump, a resting membrane potential (-70 mV) is established.

3. When the membrane potential reaches threshold (-55 mV), an action potential occurs.

4. At the peak of the action potential, the membrane potential reaches approximately +50 mV because of a depolarization due to an influx of sodium ions.

5. At the nadir of the action potential, the membrane potential reaches approximately -80 mV because of a hyperpolarization due to an efflux of potassium ions.

6. Tetrodotoxin (a poison found in puffer fish) and saxitoxin [a poison found in di-noflagellates ("red tides")] are potent sodium ion channel blockers.

7. Tetraethylammonium (a poison) is a potent potassium ion channel blocker.

C. Synapse (axodendritic)

1. Synapses are areas of interaction between two neurons; for example, an axon and dendrite, forming an axodendritic synapse.

Table 7-1

Ultrastructural Components of Neuron

Cell Part

Ultrastructural Components

Perikaryon

Nucleus with prominent nucleolus, rER and polyribosomes (Nissl substance), Golgi complex, some sER, mitochondria, lysosomes, microfilaments (actin), neurofilaments (intermediate), microtubules, and inclusion bodies

Dendrite

Similar to perikaryon

Axon

Some sER, mitochondria, neurofilaments (intermediate), microtubules, and neurosecretory vesicles [rER, polyribosomes (Nissl substance), Golgi complex, and lysosomes are absent]

rER = rough endoplasmic reticulum; sER = smooth endoplasmic reticulum.

2.

The presynaptic membrane of the axon releases the neurotransmitter.

3.

The postsynaptic membrane of the dendrite has receptors for the neurotransmitter.

4.

Binding of the neurotransmitter to receptor alters the conductance of the postsynaptic membrane to ions.

5.

An influx of sodium ions depolarizes the postsynaptic neuron, producing an excitatory postsynaptic potential (EPSP).

6.

An influx of chloride ions hyperpolarizes the postsynaptic neuron, producing an inhibitory postsynaptic potential (IPSP).

7.

The EPSPs and IPSPs spread over the postsynaptic neuron by electrotonic conduction. If the momentary sum of the EPSPs and IPSPs reaches -55 mV (thresh-

old), an action potential occurs at the initial segment of the axon. Note that an action potential does not occur at the synapse.

old), an action potential occurs at the initial segment of the axon. Note that an action potential does not occur at the synapse.

D. Node of Ranvier

1. This is a segment of the axon exposed to the extracellular milieu due to gaps in the myelin sheath.

2. It is the site where action potentials are regenerated due to the presence of sodium ion channels.

E. Neurotransmitters (Table 7-2)

F. Fuel sources. Glucose is the major fuel source for neurons. During starvation, ketones can be metabolized by neurons.

II. NEUROGLIAL CELLS are the nonneural cells of the nervous system.

A. Oligodendrocytes produce myelin in the central nervous system (CNS). One oligodendrocyte can myelinate several axons.

B. Astrocytes have the following characteristics and functions:

1. Project foot processes to capillaries

2. Play a role in the metabolism of neurotransmitters [e.g., glutamate, 7-aminobutyric acid (GABA), serotonin]

Influx of Na+

-70mV

Electrotonic conduction

Electrotonic conduction ol Ranvier - Direction ol AP —

Influx of Na+

-70mV

Figure 7-1. (A) Diagram depicting the sodium (Na+) and potassium (K+) ion concentrations in the neuron and extracellular milieu. (G) Diagram of an action potential. The influx of Na+ (thick clashed line) and efflux of K+ (t/im dashed line) are indicated. (C) Synapse and generation of action potential. Two synapses (1 and 2) are shown. Synapse 1 allows for the influx of Na+ (depolarization), causing an excitatory postsynaptic potential (EPSP). Synapse 2 allows for the influx of chloride ions (hyperpolarization), causing an inhibitory postsynaptic potential (IPSP). The EPSPs and IPSPs spread over the postsynaptic neuron by electrotonic conductance (dotted lines). If the sum reaches -55 mV (threshold), an action potential (AP) is generated at the initial segment of the axon. The AP is conducted along the axon and propagated, which means "new" APs are regenerated at the nodes of Ranvier due to an influx of sodium ions. (D) Diagram of a neuron cut so as to sever the perikaryon from the axon. If an AP is experimentally induced at mid-axon, the AP will be propagated along the axon in both directions; that is, toward both the perikaryon and synaptic terminal.

Table 7-2

Various Neurotransmitters

Neurotransmitter

Chemical Structure

Characteristics

Acetylcholine (ACh)

Catecholamines Epinephrine oh ch,

Uses the nicotinic ACh receptor (nAChR), which is a transmitter-gated ion channel that is permeable to Na+, K+, and Ca2+ ions

Uses the muscarinic ACh receptor (mAChR), which is a G protein-linked receptor

Is the neurotransmitter of the peripheral nervous system (PNS), neuromuscular junction, parasympathetic system, preganglionic sympathetic neurons, basal and visceral motor nuclei in the brain stem, and basal nucleus of Meynert (involved in Alzheimer's disease)

Uses alt a2, or (31( p2, p3-adrenergic receptors, which are 6 protein-linked receptors

Plays an insignificant role in the central nervous system (CNS)

Is found in the adrenal medulla

Norepinephrine ch,

Uses otlt a2, or (51, p2, p3-adrenergic receptors, which are G protein-linked receptors

Is the transmitter of postganglionic sympathetic neurons and CNS (locus ceruleus)

Plays a role in anxiety states, panic attacks, and depression

Uses D1 and D2 dopamine receptors, which are G protein-linked receptors

Is depleted in Parkinson disease

Is increased in schizophrenia

Serotonin (5-hydroxy-tryptamine; 5-HT)

Uses the 5-HT receptor, which is a transmitter-gated ion channel that is permeable to Na+ and K+ ions Is the neurotransmitter of the raphe nuclei of the brain stem whose neurons project to widespread areas of the CNS

7-Aminobutyric acid (GABA)

Uses the GABAa receptor, which is a transmitter-gated ion channel that is permeable to CI" ions Uses the GABAb receptor, which is a G

protein-linked receptor Is the major inhibitory neurotransmitter of the CNS

Glycine cooh

Uses the glycine receptor, which is a transmitter-gated ion channel that is permeable to CI" ions Is the major Inhibitory neurotransmitter of the spinal cord

(continued)

Table 7-2

Various Neurotransmitters

Neurotransmitter

Chemical Structure Characteristics

Glutamate

Opioid peptides Neuropeptides

Uses the N-methyl-D-asparate (NMDA), kainate, or quisqualate A receptors, all of which are transmitter-gated ion channels that are permeable to Na+, K+, and Ca2+ ions

Is the major excitatory neurotransmitter of the CNS

Use receptors that are G protein-linked receptors

Use receptors that are G protein-linked receptors

3. Buffer the potassium ion concentration of the CNS extracellular space

4. Form glial scars in a damaged area of the CNS (i.e., astrogliosis)

5. Undergo hypertrophy and hyperplasia in reaction to CNS injury

6. Contain the glial fibrillary acidic protein (GFAP)

C. Microglia are derived from monocytes and have phagocytic function.

D. Epcndymal cells line the ventricles of the brain.

E. Tanycytes are a modified type of ependymal cell that transports cerebrospinal fluid (CSF) to neurons in the hypothalamus.

F. Choroid epithelial cells line (he choroid plexus and produce CSF.

G. Schwann cells produce myelin in the peripheral nervous system (PNS). One Schwann cell myelinates only one axon. Schwann cells invest all myelinated and unmyelinated axons of the PNS and are separated from each other by nodes of Ranvier.

III. THE BLOOD-BRAIN BARRIER

A. The blood-brain barrier represents an anatomic and physiologic separation of blood from the CNS extracellular fluid.

B. It consists of tight junctions between nonfenestrated endothelial cells with few pinocytic vesicles.

C. It does not exist in some areas of the CNS, such as the median eminence, neurohypophysis, lamina terminalis, pineal gland, area postrema, and choroid plexus.

IV. THE BLOOD-CSF BARRIER consists of tight junctions between choroid epithelial cells of the choroid plexus.

V. NERVE DEGENERATION AND REGENERATION

1. Degeneration. Anterograde (Wallerian) degeneration of the axon and myelin sheath occurs distal to the site of injury. Macrophages infiltrate to remove cellular debris.

a. Chromatolysis |loss of rough endoplasmic reticulum (rER)], movement of nucleus to the periphery, and hypertrophy of the perikaryon occurs.

b. During this time, muscle fasciculations (small irregular contractions) occur caused hy release of acetylcholine (ACh) from the degenerating synaptic terminal.

2. Regeneration. Schwann cells proliferate and form a cord that is penetrated by the growing axon. The axon grows at 3 mm/day until it reaches the skeletal muscle.

a. If the axon docs not penetrate the cord of Schwann cells, the axon will not reach the skeletal muscle.

b. During this time, muscle fibrillations (spontaneous repetitive contractions) occur caused by a supersensitivity of the muscle to ACh.

1. Degeneration. Microglia phagocytose myelin and injured axons. Glial scars (as-trogliosis) form.

2. Regeneration. Effective regeneration does not occur in the CNS.

VI. CLINICAL CONSIDERATIONS

A. Huntington disease (HD) is an autosomal dominant mutation of the HD gene, which is located on the short (p) arm of chromosome 4 (i.e., 4p) and encodes a protein called Huntington.

1. The characteristic dysfunction is cell death of cholinergic and GABA-ergic neurons within the caudate nucleus. This results clinically in choreic (dance-like) movements, mood disturbances, and loss of mental activity.

2. The mechanism for neuronal cell death may involve a hyperactive glutamate re-ccptor [the N-methyl-D-aspartate (NMDA) receptor], resulting in glutamate toxicity.

3. Glutamate toxicity results from an excessive influx of calcium ions into the neuron.

B. Parkinson disease is a degenerative disease that results in the depletion of dopamine and loss of melanin-containing dopaminergic neurons within the substantia nigra. This results clinically in bradykinesia, stooped posture, shuffling gait, and masked fades.

C. Motor neuron disease is a progressive disease caused by the death of motor neurons, the pathogenesis of which is not known.

1. Death of upper motor neurons in the brain stem is called progressive bulbar palsy.

2. Death of lower motor neurons in the spinal cord is called progressive muscular atrophy.

3. Death of upper motor neurons of the corticospinal tract, corticobulbar tract, and brain stem, along with lower motor neurons of the spinal cord, is called amyotrophic lateral sclerosis (also called Lou Gehrig disease). Amyotrophic lateral sclerosis results clinically in hyperreflexia, spasticity, and Babinski reflex, along with muscle atrophy, weakness, and fasiculations.

D. Multiple sclerosis may be a type of autoimmune disease in which the myelin of the CNS is destroyed. This results clinically in paralysis, loss of sensation, and loss of coordination. The exact nature of the defect depends on the specific area of the CNS involved. Interferon beta-la (Avonex) and interferon beta-lb (Betaseron) are used clinically to ameliorate the autoimmune attack on myelin.

E. Astrocytoma is a tumor of astrocytes that accounts for approximately 80% of adult primary brain tumors. Its hallmark is a proliferation of astrocytic cell processes of varying size that displace normal neurons. This results clinically in seizures, headaches, and focal neurologic deficits depending on the area of the CNS involved.

VII. SELECTED PHOTOMICROGRAPHS

A. Blood-brain barrier (Figure 7-2; sec III)

Figure 7-2. (A) An electron micrograph of a capillary within the central nervous system (CNS). A zonula occludens (arrows) between two endothelial cells prevents the escape of macromolecules into the brain. This is the basis of the blood-brain barrier. A paucity of pinocytotic vesicles and astrocytic foot processes also may play a role in the barrier. (B) High magnification of the boxed area in A showing the zonula occludens (arrow) between two endothelial cells.

Figure 7-2. (A) An electron micrograph of a capillary within the central nervous system (CNS). A zonula occludens (arrows) between two endothelial cells prevents the escape of macromolecules into the brain. This is the basis of the blood-brain barrier. A paucity of pinocytotic vesicles and astrocytic foot processes also may play a role in the barrier. (B) High magnification of the boxed area in A showing the zonula occludens (arrow) between two endothelial cells.

B. Oligodendrocyte (Figure 7-3; see II A)

Figure 7-3. Electron micrograph of an oligodendrocyte (OL). Note the cell processes of the oligodendrocyte extending to two axons within the CNS and providing the myelin sheath. Note that one oligodendrocyte can myelinate several axons. (Reprinted with permission from Siegel GJ, Agranoff BW, Albers RW, et al: Basic Neu-rochemistry, 6th ed. Philadelphia, Lippincott-Raven, 1988, p 22.)

Figure 7-3. Electron micrograph of an oligodendrocyte (OL). Note the cell processes of the oligodendrocyte extending to two axons within the CNS and providing the myelin sheath. Note that one oligodendrocyte can myelinate several axons. (Reprinted with permission from Siegel GJ, Agranoff BW, Albers RW, et al: Basic Neu-rochemistry, 6th ed. Philadelphia, Lippincott-Raven, 1988, p 22.)

Figure 7-4. Electron micrograph of a longitudinal section of a myelinated axon of the adult sciatic nerve [i.e., peripheral nervous system (PNS)]. The myelin sheath in the PNS is formed by a Schwann cell (SC). The axon (Ax) with microtubules (m) and neurofilaments (nf) can be observed. The myelin sheath terminates at the node of Ranvier (brackets). The node of Ranvier is where action potentials are regenerated due to the presence of sodium ion channels that allow an influx of sodium ions to occur. (Reprinted with permission from Peters A, Palay SL, Webster HF: The Fine Structure of the Nervous System: Neurons and Their Suptxrrting Cells, 3rd ed. London, Oxford University Press, 1990. © 1990 by Alan Peters. Used by permission of Oxford University Press, Inc.)

Figure 7-4. Electron micrograph of a longitudinal section of a myelinated axon of the adult sciatic nerve [i.e., peripheral nervous system (PNS)]. The myelin sheath in the PNS is formed by a Schwann cell (SC). The axon (Ax) with microtubules (m) and neurofilaments (nf) can be observed. The myelin sheath terminates at the node of Ranvier (brackets). The node of Ranvier is where action potentials are regenerated due to the presence of sodium ion channels that allow an influx of sodium ions to occur. (Reprinted with permission from Peters A, Palay SL, Webster HF: The Fine Structure of the Nervous System: Neurons and Their Suptxrrting Cells, 3rd ed. London, Oxford University Press, 1990. © 1990 by Alan Peters. Used by permission of Oxford University Press, Inc.)

Figure 7-5. Electron micrograph of an axodendritic synapse [i.e., between an axon (Ax) and a dendrite (D)]. Synaptic vcsicles (arrow I), mitochondria (arrow 2), and a postsynaptic density (arrow 3) arc identified. (Reprinted with permission from Chazel G, Baude A, Barbe A, et al: Ultrastructural organization of the interstitial subnucleus of the nucleus of the tractus solitarius in the cat: identification of vagal afferents. ] Neurocytol 20:859, 1991.)

Figure 7-5. Electron micrograph of an axodendritic synapse [i.e., between an axon (Ax) and a dendrite (D)]. Synaptic vcsicles (arrow I), mitochondria (arrow 2), and a postsynaptic density (arrow 3) arc identified. (Reprinted with permission from Chazel G, Baude A, Barbe A, et al: Ultrastructural organization of the interstitial subnucleus of the nucleus of the tractus solitarius in the cat: identification of vagal afferents. ] Neurocytol 20:859, 1991.)

E. Myelinated and unmyelinated axons (Figure 7-6)

Figure 7-6. Electron micrograph of adult sciatic nerve (PNS) reveals a myelinated axon (asterisk) surrounded by a myelin sheath, Schwann cell cytoplasm, basal lamina (B), and collagen of the endoneurium (Co/). Unmyelinated axons (arrows) are separately embedded within Schwann cell cytoplasm (SC) with no myelin sheath. SN = Schwann cell nucleus. (Reprinted with permission from Peters A, Palay SL, Webster HF: The Fine Structure of the Nervous System: Neurons and Their Supporting Cells, 3rd ed. London, Oxford University Press, 1990. © 1990 by Alan Peters. Used by permission of Oxford University Press, Inc.)

Figure 7-6. Electron micrograph of adult sciatic nerve (PNS) reveals a myelinated axon (asterisk) surrounded by a myelin sheath, Schwann cell cytoplasm, basal lamina (B), and collagen of the endoneurium (Co/). Unmyelinated axons (arrows) are separately embedded within Schwann cell cytoplasm (SC) with no myelin sheath. SN = Schwann cell nucleus. (Reprinted with permission from Peters A, Palay SL, Webster HF: The Fine Structure of the Nervous System: Neurons and Their Supporting Cells, 3rd ed. London, Oxford University Press, 1990. © 1990 by Alan Peters. Used by permission of Oxford University Press, Inc.)

F. Astrocytoma (Figure 7-7; see VII E)

Figure 7-7. Astrocytoma (glioblastoma multiforme). (A) Coronal brain section shows a glioma in the left frontal cortex containing pigmentation due to hemorrhage. This 65-year-old woman demonstrated personality/behavioral changes during a period of several months. Her condition became increasingly more serious and eventually led to institutionalization for the last 2 weeks of her life. (Reprinted with permission from Woodard JS: Complete Legend of Histologic Neuropathology Illustrations. Orange, CA, California Medical Publications, 1982.) (J3) Light micrograph indicating areas of necrosis (N) that are surrounded by areas of hypercellularity with highly anaplastic tumor cells crowded along the edges of the necrotic regions producing so-called pseudopal-isading (PP). (Courtesy of the East Carolina University School of Medicine, Department of Pathology slide collection.) (C) Light micrograph of the vascular proliferation associated with astrocytoma. Tufts of endothelial may bulge into the vascular lumen with extreme examples forming glomeruloid structures. (Courtesy of the East Carolina University School of Medicine, Department of Pathology slide collection.)

Figure 7-7. Astrocytoma (glioblastoma multiforme). (A) Coronal brain section shows a glioma in the left frontal cortex containing pigmentation due to hemorrhage. This 65-year-old woman demonstrated personality/behavioral changes during a period of several months. Her condition became increasingly more serious and eventually led to institutionalization for the last 2 weeks of her life. (Reprinted with permission from Woodard JS: Complete Legend of Histologic Neuropathology Illustrations. Orange, CA, California Medical Publications, 1982.) (J3) Light micrograph indicating areas of necrosis (N) that are surrounded by areas of hypercellularity with highly anaplastic tumor cells crowded along the edges of the necrotic regions producing so-called pseudopal-isading (PP). (Courtesy of the East Carolina University School of Medicine, Department of Pathology slide collection.) (C) Light micrograph of the vascular proliferation associated with astrocytoma. Tufts of endothelial may bulge into the vascular lumen with extreme examples forming glomeruloid structures. (Courtesy of the East Carolina University School of Medicine, Department of Pathology slide collection.)

G. Multiple sclerosis (Figure 7-8; see Vll D)

Figure 7-8. Multiple sclerosis. A cross-section through the pons is stained for myelin (black). Note the focal areas (X) where demyelination has occurred. (Reprinted with permission from Stevens A, Lowe J: Human Histology, 2nd ed. London, Mosby, 1997, p 87.)

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