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[PDF] Clinical Neuroanatomy 26th Edition eBook Free clinical neuroanatomy 26th edition by stephen waxman Clinical Neuroanatomy, 26th Edition PDF. Correlative Neuroanatomy pdf by Stephen G. Waxman. Vmpfc is correlated with recovery even the number of alternative treatments these studies. The locus of. New York Chicago San Francisco Lisbon London Madrid Mexico City. Milan New Delhi San Juan Seoul Singapore Sydney Toronto. Stephen G. Waxman, MD.

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Author: Stephen Waxman | Stephen G. Waxman Gray's Clinical Neuroanatomy: The Anatomic Basis for Clinical Neuroscience · Read more. Clinical Neuroanatomy - Free ebook download as PDF File .pdf), Text File .txt) or Tan AM, Waxman SG: Spinal cord injury, dendritic spine remodel. Clinical Neuroanatomy, 28e. Stephen G. Waxman. Go to Review Questions · Go to Cases. Search Textbook Autosuggest Results. Show Chapters Hide Chapters.

Synapses are the junctions between neurons that permit them to communicate with each other. No sensory deficits were found. This syndrome results from dys dysfunction in spinal cord injury, and destruction of myelin as function of clustered nuclei and tracts in the lateral medulla a result of infl amm atory processes leads to the abnormal func and is usually due to infarction resulting from occlusion of the tion in multiple sclerosis. In contrast to ac tion potentials see the next section , which are all-or-none responses, generator potentials are graded the larger the stimulus [stretch or pressure] , the larger the depolarization and additive two small stimuli, close together in time, pro duce a generator potential larger than that made by a single small stimulus. Many other p rocesses a round this cel l a re myeli nated axons M. Together with the body resulting from a hemispheric lesion such as a stroke, or Clinical Illustrations and Cases placed throughout this a third nerve palsy suggesting an intracranial mass.

Oxford Univ Press, 1 Toga A, Mazziotta J: The Systems. The Central Nervous System: Structure and Function. Oxford Univ Press, 1 98 1.

Pdf waxman neuroanatomy

Damasio H: Human Brain Anatomy i n Computerized Images. Motor neurons are usually larger than sensory neurons. The cellular elements of the tube appear undifferentiated lower spinal cord, a distance of less than 2 ft in infants or 4 ft at first, but they later develop into various types of neurons or more in adults; others have very short processes, reaching, and supporting glial cells. These small neurons, with short axons that terminate locally, are called interneurons. Layers of the Neura l Tu be Extending from the nerve cell body are usually a num The embryonic neural tube has three layers Fig 2- 1: Most neu tricular zone, later called the ependyma, around the lumen rons give rise to a single axon which branches along its central canal of the tube; the intermediate zone , which is course and to many dendrites which also divide and subdi formed by the dividing cells of the ventricular zone including vide, like the branches of a tree.

The receptive part of the the earliest radial glial cell type and stretches between the neuron is the dendrite, or dendritic zone see Dendrites ventricular surface and the outer pial layer; and the external section.

The conducting propagating or transmitting part marginal zone, which is formed later by processes of the is the axon, which may have one or more collateral branches. The downstream end of the axon is called the synaptic ter The intermediate zone, or mantle layer, increases in cellu minal, or arborization.

The neuron's cell body is called the larity and becomes gray matter. The nerve cell processes in the soma, or perikaryon. Cel l Bodies The cell body is the metabolic and genetic center of a neuron Differentiation and M i g ration see Fig Although its size varies greatly in different neu The largest neurons, which are mostly motor neurons, differen ron types, the cell body makes up only a small part of t he neu tiate first.

Sensory and small neurons, and most of the glial cells, ron's total volume. Newly formed neurons may The cell body and dendrites constitute the receptive pole of migrate extensively through regions of previously formed neu the neuron. Synapses from other cells or glial processes tend to rons. When glial cells appear, they can act as a framework that cover the surface of a cell body Fig Because the axonal process of a neuron may begin growing toward its target Dend rites during migration, nerve processes in the adult brain are often curved rather than straight.

The newer cells of the future cere Dendrites are branches of neurons that extend from the cell bral cortex migrate from the deepest to the more superficial lay body; they receive incoming synaptic information and thus, ers. The small neurons of the incipient cerebellum migrate first together with the cell body, provide the receptive pole of the to the surface and later to deeper layers, and this process con neuron.

Most neurons have many dendrites see Figs , , tinues for several months after birth. The receptive surface area of the dendrites is usually far larger than that of the cell body. Because most dendrites are long and thin, they act as resistors, isolating electrical NEURONS events, such as postsynaptic potentials, from one another see Chapter 3.

The branching pattern of the dendrites can be Neurons vary in size and complexity. For example, the nuclei very complex and determines how the neuron integrates of one type of small cerebellar cortical cell granule cell are synaptic inputs from various sources. Some dendrites give rise only slightly larger than the nucleoli of an adjacent large to dendritic spines, which are small mushroom-shaped. Mantle layer Dend rites cellular: Peri karyon Axon hillock I n itial segment of axon.

Early stag e with large centra l canal. Later stage with smal ler central canal. Col lateral branch. Dendritic spines are currently of great interest to researchers. The shape of a spine regulates the strength of the synaptic signal that it receives.

A synapse onto the tip of a spine with a thin "neck'' will have a smaller influ ence than a synapse onto a spine with a thick neck. Dendritic spines are dynamic, and their shape can change. Changes in dendritic spine shape can strengthen synaptic connections so as to contribute to learning and memory.

The mye l i n sheath is prod uced by oligodendrocytes in the centra l nervous system and by Schwa n n cel ls in the peri p heral nerv Receptive zone Transm ission Terminal zone axon ous system.

N ote the three motor end-p lates, which transmit the nerve i m pu l ses t o striated skeleta l m u scle fi bers. Arrows show the d i rection of the nerve i m p u l se. A Axon s A single axon or nerve fiber arises from most neurons. The axon is a cylindrical tube of cytoplasm covered by a membrane, t he axolemma. A cytoskeleton consisting of neurofilaments and microtubules runs through the axon.

The rnicrotubules provide a framework for fast axonal transport see Axonal Transport sec tion. Specialized molecular motors kinesin molecules bind to Preganglionic vesicles containing molecules eg, neurotransmitters destined B cel l for transport and "walk'' via a series of adenosine triphosphate FIGURE Schematic illustration of nerve cel l types.

ATP -consuming steps along the microtubules. Central nervous system cells: Autonomic cel l s to smooth m u scle. Notice how the po axon, near the cell body to the synaptic terminals. The initial sition of the cell body with r espect to the axon varies. The neuronal su rface is completely cov e red by either syna ptic endings of other neurons 5 or p rocesses of glial cells. Many other p rocesses a round this cel l a re myeli nated axons M.

Courtesy of Dr. DM McDonald. The axolemma of the initial by Schwann cells in the peripheral nervous system PNS and segment contains a high density of sodium channels, which by oligodendrocytes a type of glial cell in the central nervous permit the initial segment to act as a trigger zone.

In this system CNS Figs to 2- 1 1. The myelin sheath is divided zone, action potentials are generated so that they can travel into segments about 1 mm long by small gaps 1 11m long along the axon, finally invading the terminal axonal branches where myelin is absent; these are the nodes of Ranvier. The and triggering synaptic activity, which impinges on other neu smallest axons are unmyelinated.

As noted in Chapter 3 , rons. The initial segment does not contain Nissl substance myelin functions as a n insulator. I n general, myelination see Fig In large neurons, the initial segment arises con serves to increase the speed of impulse conduction along the spicuously from the axon hillock, a cone-shaped portion of axon.

Axons range in length from a f ew microns in interneurons to well over a meter ie, in a lumbar motor neu B. Axonal Tra nsport ron that projects from the spinal cord to the muscles of the In addition to conducting action potentials, axons transport foot and in diameter from 0. Myelin body retrograde transport. Because ribosomes are not Many axons are covered b y myelin. The myelin consists of present in the axon, new protein must be synthesized and multiple concentric layers of lipid-rich membrane produced moved to the axon.

Retrograde transport is similar to rapid anterograde transport. Fast transport involves microtubules extending through the cytoplasm of the neuron. An axon can be injured by being cut or severed, crushed, or compressed. After injury to the axon, the neuronal cell body responds by entering a phase called the axon reaction, or chromatolysis. In general, axons within peripheral nerves can regenerate quickly after they are severed, whereas those within the CNS do not tend to regenerate.

The axon reaction and axonal regeneration are further discussed in Chapter Syna pses Transmission of information between neurons occurs at synapses. Communication between neurons usually occurs from the axon terminal of the transmitting neuron presyn aptic side to the receptive region of the receiving neuron postsynaptic side Figs and This specialized in terneuronal complex is a synapse, or synaptic j unction. As outlined in Table 2- 1 , some synapses are located between an axon and a dendrite axodendritic synapses, which tend to be excitatory , or a thorn, or mushroom-shaped dendritic spine.

Note the spi nes on the main dend rite and on its smaller branches. Micrograph courtesy of Dr. Andrew Tan, Yale University.

Dend rites 1 rad iate from the neuronal cell B. Note the i ncreased n u m be r of dendritic spi nes and their alte red body, which conta ins the nucleus 3. The axon arises from the ce l l shape fol l owing nerve i nj u ry. Modified from Tan AM et al: Axodend ritic 4 a n d axosomatic Rac1 -reg u l ated dendritic spine remodeling contributes to neuropathic pain after 5 synapses a re p resent.

M ye l i n sheaths 6 a re present a round some peripheral nerve i nju ry, Exper Neurol 1 ; Schwann cell nucleus have several distinctive characteristics: Synaptic vesicles contain neurotransmitters, and each vesicle contains a small packet, or quanta, of transmitter. When the synaptic terminal is depo larized by an action potential in i ts parent axon , there is an influx of calcium. This calcium influx leads to phosphoryla tion of a class of proteins called synapsins.

After phosphory lation of synapsins, synaptic vesicles dock at t he presynaptic membrane facing the synaptic cleft, fuse with i t, and release their transmitter see Chapter 3. Synapses are very diverse in their shapes and other prop erties. Some are inhibitory and some excitatory; in some, the Schwann cell nucleus transmitter is acetylcholine; in others, it is a catecholamine, A amino acid, or other substance see Chapter 3. Some synaptic vesicles are large, some small; some have a dense core, whereas others do not.

Flat synaptic vesicles appear to contain an in hibitory mediator; dense-core vesicles contain catecholarnines. In addition to calcium-dependent, vesicular neurotrans mitter release, there is also a second, nonvesicular mode of neurotransmitter release that is not calcium-dependent.

This mode of release depends on transporter molecules , which usually serve to take up transmitter from the synaptic cleft. B Inner mesaxon Outer mesaxon Nerve cell bodies are grouped characteristically in many parts of the nervous system. In the peri phera l nervou s system PN S , cortices, cell bodies aggregate to form layers called laminas. These axons a re not, however, insu lated by a mye l i n brum form compact groups, or nuclei.

Each nucleus contains sheath. Mye l i nated PNS fi bers a re su rrounded b y a mye l i n sheath that is formed by a spiral wra pping of the axon by a Schwann cell. Reproduced, with permission, from J u nq ueira LC, short relays within the nucleus. Basic Histology, 1 1 th ed. McGraw Hill, Groups of nerve cells are connected by pathways formed which protrudes from the dendrite Fig 2- 1 3.

Other synapses by bundles of axons. In some pathways, the axon bundles are are located between an axon and a nerve cell body axoso sufficiently defined to be identified as tracts, or fasciculi; in matic synapses, which tend to be inhibitory. Still other others, there are no discrete bundles of axons. Aggregates of synapses are located between an axon terminal and another tracts in the spinal cord are referred to as columns, or funi axon; these axoaxonic synapses modulate transmitter release culi see Chapter 5.

Within the brain, certain tracts are re by the postsynaptic axon. Synaptic transmission permits in ferred to as lemnisci. In some regions of the brain, axons are formation from many presynaptic neurons to converge on a intermingled with dendrites and do not r un in bundles so that single postsynaptic neuron.

Some large cell bodies receive sev pathways are difficult to identify. These networks are called eral thousand synapses see Fig Impulse transmission at most synaptic sites involves the release of a chemical transmitter substance see Chapter 3 ; at other sites, current passes directly from cell to cell through NEUROGLIA specialized junctions called electrical synapses, or gap junctions.

Electrical synapses are most common in inverte Neuroglial cells, commonly called glial cells, outnumber brate nervous systems, although they are found in a small neurons in the brain and spinal cord 1 0: They do not form number of sites in the mammalian CNS.

Chemical synapses synapses. Schwann cel l s 5 may s u rround one myeli nated or severa l u n myel i nated axons. X 1 6, There are two cytes, both of which are derived from ectoderm. In contrast broad classes of glial cells, macroglia and microglia to neurons, these cells may have the capability, under some Table Axodend ritic Axon terminal Dend rite Usually excitatory.

Axosomatic Axon terminal Cell body Usually inhibitory. Axoaxonic Axon terminal Axon term inal Presynaptic i n h ibition modu l ates transmitter release in postsynaptic axon. Astrocytes provide structural support to nervous tissue and act during development as guidewires that direct neu ronal migration. Astrocytes may also play a role in synaptic transmission. Many synapses are closely invested by astrocytic processes, which appear to participate in the reup take of neurotransmitters.

Astrocytes also surround endothe lial cells within the CNS, which are joined by tight junctions that impede the transport of molecules across the capillary ep ithelium, and contribute to the formation of the blood-brain barrier see Chapter 1 1.

Although astrocytic processes around capillaries do not form a functional barrier, they can selectively take up materials to provide an environment opti mal for neuronal function. Astrocytes form a covering on the entire CNS surface and proliferate to aid in repairing damaged neural tissue Fig 5. These reactive astrocytes are larger, are more eas ily stained, and can be definitively identified in histological sections because they contain a characteristic, astrocyte-spe cific protein: Chronic astrocytic proliferation leads to gliosis, sometimes called glial scarring.

Whether glial scarring is beneficial, or inhibits regeneration of injured neurons, is currently being FIGURE 2 - 1 0 Oligodendrocytes form myelin i n t h e centra l studied. There is l ittl e oligodendrocyte cytop l a s m Cyt i n the o l igodend rocyte p rocesses that s p i ra l around the axon Ol igodendrocytes to fo rm mye l i n , and the mye l i n sheaths a re connected to t h e i r p a r Oligodendrocytes predominate in white matter; they extend ent oligodendrocyte cel l body by o n l y t h i n tongues of cyto p l a s m.

The mye l i n is period ica l l y of myelin which acts as an insulator around axons in the CNS. Redrawn and reproduced with permission from the neurons they envelop. A single oligodendrocyte may wrap Bunge M, Bunge R. Pappas G: Ultrastructural study of r emyelination in an experimen tal lesion in adult cat spinal cord, J Biophys Biochem Cytol May; 1 0: In peripheral nerves, by contrast, myelin is formed by Schwann cells.

Each Schwann cell myelinates a single axon, and remyelination can occur at a brisk pace after Astrocytes injury to the myelin in the peripheral nerves. There are two broad classes of astrocytes: Protoplasmic astrocytes are more delicate, and their many processes are branched.

Neuroanatomy pdf waxman

They occur in gray matter. Fi Microg l ia brous astrocytes are more fibrous, and their processes con Microglial cells are the macrophages, or scavengers, of the taining glial fibrils are seldom branched.

Astrocytic processes CNS. They constantly survey the brain and spinal cord, acting radiate in all directions from a small cell body. They surround as sentries designed so as to detect, and destroy, invaders. Glial cel l s f Macroglia Oligodendrocytes. Astrocytes Myelin formation i n CNS.

Clinical Neuroanatomy, 28e

Reg u late ionic environment; reuptake of neu rotransm itters; guidance of. X The inset shows axon A1 and its mye l i n sheath at higher magn ification. The myel i n is a spira l of ol igodendrocyte mem brane that surro u nds the axon.

M ost of the ol igodendrocyte cytoplasm is extruded from the myelin. Beca use the mye l i n is com pact, it has a high electrical resistance and low capacitance so that it can fu nction as a n insulator around the axon.

When an area of the brain or spinal cord is Extrace l l u l a r Space damaged or infected, microglia activate and migrate to the site There is some fluid-fill e d space between the various cellular of injury to remove cellular debris. Some microglia are always components of the CNS.

Microglia play an of the total volume of the brain and spinal cord. Their role after endogenous insults, portant in electrical signaling in the nervous system see including stroke or neurodegenerative diseases such as Chapter 3 , regulation of the levels of these ions in the extra Alzheimer disease, is less well understood, and it is not clear cellular compartment ionic homeostasis is an important at this time whether activation of microglia in these disorders function, which is, at least in part, performed by astrocytes.

Bielschowsky si lver membrane sta i n. Postsynaptic membrane The capillaries within the CNS are completely invested by glial Synaptic cleft or neural processes. Moreover, capillary endothelial cells in the brain in contrast to capillary endothelial cells in other or FIGURE 2 Schematic drawing of a synaptic terminal. This barrier iso molecules i nto the synaptic cleft so that they can bind t o receptors in lates the brain extracellular space from the intravascular the postsyna ptic mem brane.

Postsynaptic cell C l i n ica l Correlation In cerebral edema , there is an increase in the bulk of the. Cerebral edema can be either vasogenic primarily ex tracellular or cytotoxic primarily intracellular. The cell body maintains the functional and anatomic integrity of the axon Fig If the axon is cut, the part distal to the cut degenerates wallerian degeneration , because materials for maintaining the axon mostly proteins are formed in the Axosomatic cell body and can no longer be transported down the axon axoplasmic transport.

FIGURE 3 Axodend ritic synapses termi nate on dend ri ties or mushroom-shaped "dendritic spines;' and tend to be exci tatory. Axosomatic synapses termi nate on neuronal cel l bodies and FIGURE 5 M icrog raphs showi ng astrocytes with i n t h e nor tend to be i n h i bitory. Axoaxonal synapses termi nate o n a n axon, mal human bra i n A , and within glial sca rs in patients with m u ltiple often close to synaptic term i n a ls, and modu late the release of neuro sclerosis B and fol lowi ng stroke C.

Note the hypertrop hied transmitters. Reprod uced, with permission, from Ganong WF: Review of Medical astrocytes with i n g l i a l scars i n B and C. Courtesy of Physiology, 22nd ed. McGraw-H ill, Several months. Normal nerve fi ber, with its perika ryon and the effector cel l stri ated skeletal m u scle.

N otice the position of the n e u ro n n ucleus and the a m o u nt and d i stribution of N i ssl bodies. When the fi ber is i nj u red, the n e u ro n a l n ucleus m oves to the cel l periphery, Nissl bodies beco m e g reatly red uced i n n u m be r chromatolysis , and the nerve fi ber d i sta l to the i nj u ry degenerates a l o n g with its mye l i n sheath.

Debris is p h a g ocytized by m a c rophages. The m uscle fi ber shows p ro n o u nced disuse atrop hy.

Clinical Neuroanatomy

Schwa n n cel l s prolife rate, forming a com pact cord that is penetrated by the g rowi n g axon. The axon g rows at a rate of 0. In this exa m ple, the n erve fi ber regeneration was successfu l, and the m uscle fi ber was a l s o regenerated after rece iving nerve sti m u l i.

When the axon does not penetrate the cord of Schwa n n ce l l s, its g rowt h i s not organ ized and s u ccessfu l regenera tion does n ot occ u r. The Principles of Pathology and Bacteriology, 3rd ed. Butterworth, 1 Distal to the level of axonal transection when a peripheral swelling of nearby astrocytes, and activation of microglia.

To Successful axonal regeneration does not commonly occur af gether with macrophages, they phagocytize the remnants of ter injury to the CNS.

Many neurons appear to be dependent the myelin sheaths, which lose their integrity as the axon on connection with appropriate target cells; if t he axon fails degenerates. The changes include swelling of the cell body and nucleus, which is usu ally displaced from the center of the cell to an eccentric loca Reg eneration tion.

The regular arrays of ribosome-studded endoplasmic A. Periphera l Nerves reticulum, which characterize most neurons, are dispersed Regeneration denotes a nerve's ability to regrow to an appro and replaced by polyribosomes. The ribosome-studded en priate target, including the reestablishment of functionally doplasmic reticulum, which had been termed the Nissl sub useful connections see Figs 2 - 1 6 and 2 - 1 7. Shortly 1 -3 stance by classical neuroanatomists, normally stains densely days after an axon is cut, the tips of the proximal stumps form with basic dyes.

The loss of staining of the Nissl substance, as enlargements, or growth cones. The growth cones send out a result of dispersion of the endoplasmic reticulum during exploratory pseudopodia that are similar to the axonal growth the axon reaction, led these early scientists to use the term cones formed in normal development.

Each axonal growth "chromatolysis: Axon branch Receptor now appreciated that molecules such as NoGo act as "stop. Neutralization of NoGo has been shown to pro mote the regeneration of axons within t he spinal cord in ex perimental animals. When confronted with a permissive envi Retrograde Receptor ronment eg, when the transected axons of CNS neurons are degeneration hypersensitive permitted to regrow into a peripheral nerve, or transplanted Site of injury into the CNS as a "bridge" , CNS axons can regenerate for dis.

Retrograde Regenerative Orthograde reaction: Remyeli nation In a number of disorders of the peripheral nervous system FIGURE 7 S u m m a ry of changes occurring in a neuron and such as the Guillain-Barre syndrome , there is demyelina the structure it innervates when its axon is crushed or cut at the tion, which interferes with conduction see Chapter 3. This point ma rked X. Modified from Ries D. Reproduced, with permission, from condition is often followed by remyelination by Schwann cells, Ganong WF: Review of Medical Physiology, 22nd ed.

In contrast, remyelination occurs can cross the scar tissue and enter the distal nerve stump, suc much more slowly if at all in the CNS. Little remyelination cessful regeneration with restoration of function may occur.

A different form of plasticity Schwarm cell tubes surrounded by basal lamina Biingner's ie, the molecular reorganization of the axon membrane that bands in the distal stump explains the different degrees of re acquires sodium channels in demyelinated zones appears to generation that are seen after nerve crush compared with nerve underlie clinical remissions in which there is neurological transection.

After a crush injury to a peripheral nerve, the ax improvement in patients with multiple sclerosis. Col latera l Sprouti ng sion, facilitating regeneration of axons through the injured This phenomenon has been demonstrated in the CNS as well nerve. In contrast, if the nerve is cut, the continuity of these as in the peripheral nervous system see Fig It occurs pathways is disrupted. Even with meticulous surgery, it can be when an innervated structure has been partially denervated. This kind of regen Peripheral system axons will reinnervate both muscle and eration demonstrates that there is considerable plasticity in sensory targets; however, motor axons will not connect to sen the nervous system and that one axon can take over the synap sory structures, or sensory axons to muscle.

Although a motor tic sites formerly occupied by another. Such movements include "j aw It has classically been believed t hat neurogenesis-the capa winking;' in which motor axons destined for the jaw muscles bility for production of neurons from undifferentiated, prolif reinnervate muscles around the eye after injury. According to this B.

Centra l Nervous System traditional view, after pathological insults t hat result in neu Axonal regeneration is typically abortive in the CNS. The rea ronal death, the number of neurons is permanently reduced. Classi However, recent evidence has indicated that a small number cal neuropathologists suggested that the glial scar, which is of neuronal precursor cells, capable of dividing and t hen dif largely formed by astrocytic processes, may be partly respon ferentiating into neurons, may exist in t he forebrain of adult sible.

The properties of the oligodendroglial cells in contrast mammals, including humans. These rare precursor cells re to those of the Schwarm cells of peripheral nerves may also side in the subventricular zone. For example, there is some ev account for the difference in regenerative capacity: Recent idence for postnatal neurogenesis in the dentate gy. An inhibitory fac eration of new neurons in this critical region can be acceler tor produced by oligodendrocytes, CNS myelin, or both may ated in an enriched environment.

While the number of new interfere with regeneration of axons through the CNS. Neuroglia, 2nd ed. Oxford Univ Press, suggest strategies for restoring function after inj ury to the This is an area of intense research.

Kordower J, Tuszynski M: CNS Regeneration. Laming PR: Glial Cells. Cambridge Univ Press, 1 The Neuron: Cell and Molecular Biology, 3rd ed. Oxford Univ Press, 1. The Fine Structure o f the peutics: Trends Neurosci Nervous System, 3rd ed. Rakic P: A century of progress in corticoneurogenesis: Cereb Cortex ; 1 6 vol 2. Librairie Maloine, 1 9 1 1. Hall ZW editor: An Introduction t o Molecular Neurobiology.

Development of the Nervous System. Sinauer, NY, Strittmatter SM: Remyelination of developmental guidance during recovery from spinal cord the injured spinal cord. Prog Brain Res ; 1 6 1: Nat Rev Neurosci ;7: Comparative views of neuro Neurochemisry. The Neurologist ;6: Basic Histology, 9th ed. Exp Neurol 2; The Axon: Structure, Injury. Humana, 1. Function, and Pathophysiology. More hippocampal neurons Yuste R: Dendritic spines MIT. Press, Nature 1 ; Si gnaling in the Nervous System Along with muscle cells, neurons are unique in that they are see Table 3 - 1.

The Nernst equation, which would be used to excitable; that is, they respond to stimuli by generating elec determine membrane potential across a membrane permeable trical impulses.

Electrical r esponses of neurons modifications only to r ions, is as follows: Propa gated electrical impulses are termed action potentials. Cell membranes are highly permeable to most At physiologic temperatures inorganic ions, but they are almost impermeable to proteins and many other organic ions.

For these membranes, potential is the weighted average membrane into the cell. In carrying out this essential activity, of the equilibrium potentials for each permeable ion, with the the pump consumes adenosine triphosphate ATP. When the chemical and electrical forces are equally strong, an equilibrium potential exists. The generator receptor potential is a local, nonpropagated response that occurs in some sensory receptors eg, muscle stretch receptors and pacinian corpuscles, which are touch pressure receptors where mechanical energy is converted into electric signals.

The generator potential is produced in a small area of the sensory cell: Most generator potentials are depolarizations, in which membrane potential becomes less negative. In contrast to ac tion potentials see the next section , which are all-or-none responses, generator potentials are graded the larger the stimulus [stretch or pressure] , the larger the depolarization and additive two small stimuli, close together in time, pro duce a generator potential larger than that made by a single small stimulus.

When the magnitude of mem brane. The Physiology of Nerve Cells. Johns nerve. Hopkins U niversity Press, 1 If permeability to a Neurons communicate by producing electrical impulses called certain ion increases eg, by the opening of pores or channels action potentials. Action potentials are self-regenerative elec specifically permeable to that ion , membrane potential trical signals that tend to propagate throughout a neuron and moves closer to the equilibrium potential for that ion.

Con along its axon. The action potential is a depolarization of a bout versely, if permeability to that ion decreases eg, by closing of 1 00 mV a large signal for a neuron. The action potential is all pores or channels permeable to that ion , membrane potential or none. Its size is constant for each neuron. The strongest sti m u l u s Reproduced, with permission, from Ganong WF: Review of Med ical Physiology, 18th ed.

Essentials of H u m a n Physi p rod uced a n action potential i n t h e sensory nerve, originating i n the ology. Ross G editor. Year Book, The refrac Katz equation, thus causing further depolarization. When a tory period limits the ability of the axon to conduct high depolarization from a generator potential, synaptic potential, frequency trains of action potentials. If a sufficient number of sodium channels are activated, there is a depolarization of about 1 5 mV, and Voltage-sensitive ion channels are specialized protein mole threshold is reached so that the rate of depolarization in cules that span the cell membrane.

These doughnut-shaped creases sharply to produce an action potential Fig The tential. As the impulse passes, repolarization occurs rapidly channel also possesses a voltage sensor, which, in response to at first and then more slowly. Membrane potential thus re changes in potential across the membrane, either opens acti turns to resting potential.

The action potential tends to last for vates or closes inactivates the channel. Because these channels open in brane toward EK. In the wake of an action potential, t here is a response to depolarization, and because by opening they drive refractory period of decreased excitability. If a suffi cient number of these channels are opened, there is an explo sive, ali-or-none response, termed the action potential see Fig Latent Iperiod enter cell open. Axon Microelectrode inside axon.

In the resting state, the mem brane potential resting potential i s about - 70 mV. The action potential a p p roaches EN and overshoots permea b i l ity of the membra ne, causing fu rthe r depolarization and the 0-mV level.

When a sufficient n u mber of aga i n settl ing at resting potential. McGraw- H i l l, In the resting axon, there is a d ifference of - 70 mV between the i nterior of the axon and the outer su rface of its mem brane rest ing potential.

Basic Histology, 7th ed. Myelination has profound effects on the conduction of action potentials along the axon. As the action potential invades a given region of the axon, it depolarizes the region in front of it, so that the im pulse crawls slowly and continuously along t he entire length of the axon Fig The myelin has a high electrical resistance and low ca ternodal axon m e m brane u nder the myelin, so that they a re masked.

The myelin sheath Reproduced with permission from Waxman SG: Saltatory conduction in a mye l i nated axon. The myelin fu nctions as an insu lator beca use of its high r esista n ce and low ca pacitance. Thus, when the action potential cross-hatching is at a given node of Ranvier, the majority of the electrical cu rrent is shu nted t o the next node a long the pathway shown by the broken arrow.

Conduction of the action potentia l proceeds i n a disconti nuous m a n ner, j u m ping from node to node with a high conduction velocity. I n demyelinated axons there is loss of cu rrent t h rough the damaged myelin. As a r esu lt, it either ta kes longer t o reach t h reshold and conduction velocity is r educed, or threshold is n ot reached a n d the actio n potential fa ils to propa gate. Reproduced, with permission, from Waxman SG: Membranes, myelin and the pathophysiology of mu ltiple sclerosis.

Because the current flow through the insulating myelin is large and myelinated, conduct rapidly, and carry various mo very small and physiologically negligible, t he action potential tor or sensory impulses.

They are most susceptible to injury in myelinated axons jumps from one node to the next in a by mechanical pressure or lack of oxygen. B fibers are mode of conduction that has been termed saltatory Fig These fibers serve autonomic functions. C fibers are mode of conduction in myelinated fibers. First, the energy re the smallest and are nonmyelinated; they conduct impulses quirement for impulse conduction is lower in myelinated the slowest and serve pain conduction and autonomic func fibers; therefore, the metabolic cost of conduction is lower.

An alternative classification, used t o describe sensory Second, myelination results in an increased conduction ve axons in peripheral nerves, is shown in Table Figure shows conduction velocity as a function of diameter for nonmyelinated and myelinated axons. For non myelinated axons, conduction velocity is proportional to diameter In contrast, conduction velocity in myelinated axons increases linearly with diameter. A myelinated axon can 8 conduct impulses at a much higher conduction velocity t han a nonmyelinated axon of the same size.

To conduct as rapidly as a 1 0 -! By increasing the con duction velocity, myelination reduces the time it takes for im pulses to travel from one region to another, thus reducing the time needed for reflex activities and permitting the brain to operate as a high-speed computer.

Types of Fi bers Fiber diameter J. Nerve fibers within peripheral nerves have been divided into FIGURE Relationship between cond uction velocity and di three types according to their diameters, conduction veloci a m eter i n mye l i nated and non mye l i nated axons. Myelinated axons ties, and physiologic characteristics Table A fibers are conduct more rapidly than non myelinated axons of the same size. Neuropathy C. Twenty-fo u r Peri p h e ra l n e u ropath ies-diseases affect i n g periphera l hours later, her vision h a d d i mmed, and a day later, she was nerves-a re a very common cause o f disabil ity.

Peri pheral tota lly blind in her left eye.

A neurologist found a normal neu neuropathy occu rs, for exa mple, i n a bout one-half of indi rologic exa m i n ation. A magnetic resonance scan demon vid u a l s with d i a betes, a n d can occur as a co m p l ication of strated severa l a reas of demye l i nation in the s u bcortical treatment with medications that include cancer chemother wh ite matter of both cerebral hemispheres.

Despite the per a pies. Many n e u ropathies affect l a rge mye l i n ated n erve sistence of these a bnorma l ities, C. Her physician told her that of deep ten d o n refl exes a n k l e jerk, knee jerk etc.

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The she probably had m u ltiple sclerosis. She recovered 3 weeks longest fi bers a re affected first, and thus the feet and hands later with only mild resid ual wea kness. The After a sym ptom-free i nterva l for 2 years, C.

Conduction b l ock, she atte m pted to perform vo l u nta ry acti o n s "inte n t i o n whereby i m p u l ses fa il to propagate past a point of axonal tremor". On exa mination, the neurologist found signs s u g inju ry, can a l so occur. The red uction i n conduction velocity gesti ng demye l i nation i n the b ra i n s t e m a n d cerebe l l u m. Slowing in rem itting form of m u ltiple sclerosis. Th i s s o m e chronic or hered itofa m i l i a l neuropathies. Demyelination a re d i s s e m i n ated i n s pace and i n time h e n ce, the term "multiple sclerosis".

Remye l i n ation, with i n the core of the Demyeli nation, or damage to the mye l i n sheath, is seen in a demyeli nation plaq ues, occurs sl uggishly if at a l l. The most common is mu lti The relapsi ng-remitting cou rse exempl ified by C. How does recovery occur? Recent stud nisms. This perm its i m p u lses to propagate in a C l i n ical I l l u stration descri bes a patient with m u lti conti n uous, slow manner si m i l a r to nonmyelinated axons ple sclerosis.

The slowly con ducted i m p u lses ca rry enough information t o suppo rt clin ical recovery of some fu nctions, such as vision, even though the axons remain demye l inated.

Synapses are the junctions between neurons that permit them to communicate with each other.

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Some synapses are excita tory increasing the probability that the postsynaptic neuron does not involve neurotransmitters. Synaptic delay is will fire , whereas others are inhibitory decreasing the prob shorter at electrical synapses than at chemical synapses. Whereas electrical synapses occur commonly in t he CNS of In the most general sense, there are two broad inframammalian species, they occur only rarely in the anatomic classes of synapses Table 3 - 4.

Electrical or mammalian CNS. At a chem Gap junctions act as conductive pathways, so electrical cur ical synapse a distinct cleft about 30 nm wide represents rent can flow directly from the presynaptic axon into the an extension of the extracellular space, separating the pre postsynaptic neuron. Transmission at electrical synapses and p ostsynaptic membranes.

Peri pheral neuropathies affect the longest nerve fi bers fi rst, and the f eet and hands thus a re affected i n early stages of the d isease. Catherina Faber. Release of neuro system in Table 3 - 5. As a result of depolarization of the transmitter occurs when the presynaptic vesicles fuse with presynaptic ending by action potentials, neurotransmitter the presynaptic membrane, permitting release of their con molecules are released from the presynaptic ending, diffuse tents by exocytosis.

As a result of t his activity-in channels. These depolarizations and phosphorylation of proteins called synapsins, which appear hyperpolarizations are integrated by the neuron and deter- to cross-link vesicles to the cytoskeleton, thereby preventing. A a Proprioception; somatic motor 1 C dorsal root Pain, reflex responses 0.

Reproduced, with permission, from Ganong WF: Neurotransm itters. I a Muscle spindle, a n n u l ospira l ending A cr Acetylcholine ACh Neuromuscular j unction, a utonomic ganglia, parasympathetic neurons, b Golgi tendon organ A cr motor nuclei of cranial nerves, caudate Muscle spindle, flower-spray A J3 nucleus and putamen, basal nucleus of ending; touch, pressure Meynert, portions of the limbic system.

Ill Pa i n and temperature receptors; A 'O Norepinephrine N E Sympathetic nervous system, locus some touch receptors ceruleus, lateral tegmentum. Review of Medica l Physiology, 22nd ed. McGraw-Hiil, Serotonin 5-HT Parasympathetic neurons in g ut, pineal gla nd, nucleus raphe magnus of pons. Gamma-a m i nobutyric Cerebe l l u m, h ippocam pus, cerebral their movement. This action permits fusion of vesicles with acid GABA cortex, striatonigra l system the presynaptic membrane, resulting in a rapid release of Glycine Spinal cord neurotransmitter.

The release process and diffusion across Gl utamic acid Spinal cord, bra i n stem, cerebellum, the synaptic cleft account for the synaptic delay of 0. This sequence is shown in diagram matic form at the neuromuscular j unction, a prototypic synapse, in Figure 3 - 1 0. Transmitter molecules carry information from the presynap tic neuron to the postsynaptic neuron by binding at the post Second-Messenger Mediated Slow synaptic membrane with either of two types of postsynaptic A second mode of chemical synaptic transmission, which is receptor.

The first type is found exclusively in the nervous sys closely related to endocrine communication in nonneural tem and is directly linked to an ion channel a ligand-gated cells, uses receptors that are not directly linked to ion chan ion channel. By binding to the postsynaptic receptor, the nels; these receptors open or close ion channels or change the transmitter molecule acts directly on the postsynaptic ion levels of intracellular second messengers via activation of G channel.

Moreover, the transmitter molecule is rapidly proteins and production of second messengers. The cascade of molecular mediated slow I events, leading from binding of transmitter at these recep l I n hibitory tors to opening or closing of channels, takes hundreds of milliseconds to seconds, and the effects on channels are rel atively long-lasting seconds to minutes.

This mode of synaptic transmission has, therefore, been termed "slow: This tends to cause hyperpolarization and most commonly occurs at axosomatic synapses, where it is called postsynaptic inhibition Fig 3- 1 1.

Information processing by neurons involves the integra tion of synaptic inputs from many other neurons. As a neu Synaptic --m j! J ron integrates the incoming synaptic information, i t weighs vesicles the excitatory and inhibitory signals.

Depending on whether or not threshold is reached at the impulse initiation zone usually the axon initial segment , an action potential is ei ther generated or not. If an action potential is initiated, i t propagates along the axon t o impinge, via its synapses, o n still Muscle other neurons.

The rate and pattern of action potentials membrane carry information. Acetylcho line ACh is the transm itter at this syna pse. Part of the can learn and store information in the form of memories. It has nerve terminal is shown, lying i n close a pposition t o a m uscle end long been suspected that memory has its basis in the strength p late. Synthesis of ACh occurs l oca l ly, i n the p resyna ptic t erminal, ening of particular synaptic connections. In the past few years, from acetyl-coenzyme A CoAl and choline 1.

AC h is then incorpo much progress has been made in understanding synaptic plas rated i nto membra ne-bound syna ptic vessels 2. Release of ACh oc ticity. Long-term potentiation, characterized by the enhanced curs by exocytosis, which i nvolves fusion of the vesicles with the transmission at synapses t hat follow high-frequency stimula presynaptic mem brane 3.

The contents of a pproxi mately play a role in associative learning. Long-term potentiation de synaptic vesicles a re released i nto the syna ptic cleft in r esponse to a pends on the presence of N-methyl-D-aspartate NMDA re single action potential. The rel eased ACh d iffuses ra pidly across the ceptors in the postsynaptic membrane. When the channel closes, to binding of the transmitter glutamate but only if the postsy the ACh d i ssociates and is hyd rolyzed by acetylcholinesterase 6.

Thus, these synapses sense the "pairing" of two synaptic inputs in a manner analogous t o second-messenger-linked transmission is slower and may af conditioning to behavioral stimuli. Recent work suggests that, fect a wider range of postsynaptic neurons. These structural changes, triggered by specific patterns of synaptic activity, may provide a basis for memory. Thus, second messengers can activate en Excitatory postsynaptic potentials EPSPs are produced by zymes that modify preexisting proteins or induce the expres the binding of neurotransmitter molecules to receptors that sion of new proteins.

This is an example of plasticity within the depolarization. In general, excitatory synapses tend to be axo nervous system. These changes in protein synthesis in the dendritic.

In contrast, inhibitory postsynaptic potentials postsynaptic cell may participate in learning and memory and IPSPs in many cases are caused by a localized increase in are probably important in nervous system development. Glyci ne Opens Cl - channels I n h ibitory.

It is localized to Presynaptic inhibition provides a mechanism for controlling the myoneural junction. The transmitter at the neuromuscular the efficacy of transmission at individual synapses. It is medi synapse is ACh. Small amounts of ACh are released randomly ated by a. Binding of neuro from the nerve cell membrane at rest; each release produces a transmitters to the receptors mediating presynaptic inhibition minute depolarization, a miniature end-plate potential, about leads to a reduction in the amount of neurotransmitter 0.

These miniature end-plate potentials, secreted by the postsynaptic axon. This reduction is caused ei also called quanta, reflect the random discharge of ACh from ther by a decrease in the size of the action potential in the single synaptic vesicles. This causes a full end-plate potential release. Presynaptic inhibition thus provides a mechanism that exceeds the fuing level of the muscle fiber. Some presynaptic nerves can release more The axons of lower motor neurons project through peripheral than one transmitter; differences in the frequency of nerve nerves to muscle cells.

These motor axons terminate at a stimulation probably control which transmitter is released. The nerve impulse is transmitted to the muscle ters; others appear to be hormones.

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Some relatively well-un across the neuromuscular synapse also called the neuromus derstood neurotransmitters and their distributions are dis cular junction. The end-plate potential is the prolonged cussed next. Circulating hormones Angiotensin Calcitonin Gl ucagon Insulin. Schematic i l l u stration of two types of inhi Dynorphin bition i n the spinal cord. In d i rect i n h i bition a lso called postsynaptic Beta-endorphin i n h i bition , a chemica l mediator released from a n i n h i bitory neuro n Met-en kephalin cau ses hyperpola rization i n h i bitory postsynaptic potential of a Leu-en kepha l i n m otor neuron.

I n p resynaptic i n h i bition, a second chem i ca l media Kyotorphin tor released onto the ending axon of a n excitatory neuro n causes Others a red uction in the size of the postsy n a ptic excitatory potential. Bradyki nin Bottom: Diagram of a s pecific i n h i b itory system involving an Carnosine i n h i b itory i nterneuron Renshaw cel l. Functional Neuroanatomy.

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Computational Neuroanatomy: Principles and Methods. Recommend Documents. Neuroanatomy Through Clinical Cases