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6 Tissue Growth, Development, Repair, and Degeneration
signals arrive at the output neuron at different times,
and the output neuron may go on firing for some time
after input has ceased. Unlike a reverberating circuit,
this type has no feedback loop. Once all the neurons
in the circuit have fired, the output ceases. Continued
firing after the stimulus stops is called after-discharge.
It explains why you can stare at a lamp, then close
your eyes and continue to see an image of it for a
while. Such a circuit is also important in withdrawal
reflexes, in which a brief pain produces a longerlasting output to the limb muscles and causes you to
draw back your hand or foot from danger.
Memory and Synaptic Plasticity
You may have wondered as you studied this chapter, How
am I going to remember all of this? It seems fitting that we
end with the subject of how memory works, for you now
have the information necessary to understand its cellular
and chemical basis.
The things we learn and remember are not stored in
individual “memory cells” in the brain. We do not have
a neuron assigned to remember our phone number and
another assigned to remember our grandmother’s face, for
example. Instead, the physical basis of memory is a pathway through the brain called a memory trace (engram30),
in which new synapses have formed or existing synapses
have been modified to make transmission easier. In other
words, synapses are not fixed for life; in response to
experience, they can be added, taken away, or modified
to make transmission easier or harder. Indeed, synapses
can be created or deleted in as little as 1 or 2 hours. The
ability of synapses to change is called synaptic plasticity.
Think about when you learned as a child to tie your
shoes. The procedure was very slow, confusing, and laborious at first, but eventually it became so easy you could
do it with little thought—like a motor program playing
out in your brain without requiring your conscious attention. It became easier to do because the synapses in a
certain pathway were modified to allow signals to travel
more easily across them than across “untrained” synapses.
The process of making transmission easier is called synaptic potentiation (one form of synaptic plasticity).
Neuroscientists still argue about how to classify the
various forms of memory, but three kinds often recognized are immediate memory, short-term memory, and
long-term memory. We also know of different modes of
synaptic potentiation that last from just a few seconds to
a lifetime, and we can correlate these at least tentatively
with different forms of memory.
Immediate memory is the ability to hold something in
mind for just a few seconds. By remembering what just
en = inner; gram = mark, trace, record
happened, we get a feeling for the flow of events and a
sense of the present. Immediate memory is indispensable
to the ability to read; you must remember the earliest
words of a sentence until you get to its end in order to
extract any meaning from the sentence. You could not
make any sense of what you read if you forgot each word
as soon as you moved on to the next one. Immediate
memory might be based on reverberating circuits. Our
impression of what just happened can thus reecho in our
minds for a few seconds as we experience the present
moment and anticipate the next one.
Short-term memory (STM) lasts from a few seconds to a
few hours. Information stored in STM may be quickly forgotten if we stop mentally reciting it, we are distracted, or
we have to remember something new. Working memory is
a form of STM that allows us to hold an idea in mind long
enough to carry out an action such as calling a telephone
number we just looked up, working out the steps of a mathematics problem, or searching for a lost set of keys while
remembering where we have already looked. It is limited
to a few bits of information such as the digits of a telephone
number. It has long been thought that working memory is
based on persistent activity in a reverberating circuit of
neurons, but recent evidence leans toward the storage of
working memory in a circuit of facilitated synapses that
can remain quiescent (consuming no energy) most of the
time, but be reactivated by a new sensory input.
Such synaptic facilitation, as it is called (different
from the facilitation of one neuron by another that we
studied earlier in the chapter), can be induced by tetanic
stimulation, the rapid arrival of repetitive signals at a
synapse. Each signal causes a certain amount of Ca2+ to
enter the synaptic knob. If signals arrive very rapidly, the
neuron cannot pump out all the Ca2+ admitted by one
action potential before the next action potential occurs.
More and more Ca2+ accumulates in the knob. Since Ca2+
is what triggers the release of neurotransmitter, each new
signal releases more neurotransmitter than the one before.
With more neurotransmitter, the EPSPs in the postsynaptic cell become stronger and stronger, and that cell is more
likely to fire.
Memories lasting for a few hours, such as remembering what someone said to you earlier in the day or
remembering an upcoming appointment, may involve
posttetanic potentiation. In this process, the Ca2+ level
in the synaptic knob stays elevated for so long that
another signal, coming well after the tetanic stimulation has ceased, releases an exceptionally large burst of
neurotransmitter. That is, if a synapse has been heavily
used in the recent past, a new stimulus can excite the
postsynaptic cell more easily. Thus, your memory may
need only a slight jog to recall something from several
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Integration and Control
Long-term memory (LTM) lasts up to a lifetime and is
less limited than STM in the amount of information it
can store. LTM allows you to memorize the lines of a play,
the words of a favorite song, or (one hopes!) textbook
information for an exam. On a still longer timescale, it
enables you to remember your name, the route to your
home, and your childhood experiences.
There are two forms of long-term memory: declarative
and procedural. Declarative memory is the retention of
events and facts that you can put into words—numbers,
names, dates, and so forth. Procedural memory is the
retention of motor skills—how to tie your shoes, play a
musical instrument, or type on a keyboard. These forms
of memory involve different regions of the brain but are
probably similar at the cellular level.
Some LTM involves the physical remodeling of synapses or the formation of new ones through the growth
and branching of axon terminals and dendrites. In the
pyramidal cells of the brain, the dendrites are studded with
knoblike dendritic spines that increase the area of synaptic
contact. Studies on fish and other experimental animals
have shown that social and sensory deprivation causes
these spines to decline in number, while a richly stimulatory environment causes them to proliferate—an intriguing
clue to the importance of a stimulating environment to
infant and child development. In some cases of LTM, a new
synapse grows beside the original one, giving the presynaptic cell twice as much input into the postsynaptic cell.
LTM can also be grounded in molecular changes
called long-term potentiation. This involves NMDA31
receptors, which are glutamate-binding receptors found
on the synaptic knobs of pyramidal cells. NMDA receptors
are usually blocked by magnesium ions (Mg2+), but when
they bind glutamate and are simultaneously subjected
to tetanic stimulation, they expel the Mg2+ and open to
DEEPER INSIGHT 12.4
Alzheimer and Parkinson Diseases
Alzheimer and Parkinson diseases are the two most common degenerative disorders of the brain. Both are associated with neurotransmitter deficiencies.
Alzheimer32 disease (AD) may begin before the age of 50 with
signs so slight and ambiguous that early diagnosis is difficult. One of
its first signs is memory loss, especially for recent events. A person with
AD may ask the same questions repeatedly, show a reduced attention
span, and become disoriented and lost in previously familiar places.
admit Ca2+ into the dendrite. When Ca2+ enters, it acts as
a second messenger that leads to a variety of effects:
The neuron produces even more NMDA receptors,
which makes it more sensitive to glutamate in the
It synthesizes proteins concerned with physically
remodeling a synapse.
It releases nitric oxide, which diffuses back to the
presynaptic neuron and triggers still more glutamate
You can see that in all of these ways, long-term potentiation can increase transmission across “experienced”
synapses. Remodeling a synapse or installing more neurotransmitter receptors has longer-lasting effects than
facilitation or posttetanic potentiation.
The anatomical sites of memory are discussed in
chapter 14 in connection with brain anatomy. Regardless
of the sites, however, the cellular mechanisms are as
Before You Go On
Answer the following questions to test your understanding of the
22. Contrast the two types of summation at a synapse.
23. Describe how the nervous system communicates quantitative
and qualitative information about stimuli.
24. List the four types of neural circuits and describe their similarities
and differences. Discuss the unity of form and function in these
four types—that is, explain why each type would not perform as
it does if its neurons were connected differently.
25. How does long-term potentiation enhance the transmission
of nerve signals along certain pathways?
Family members often feel helpless and confused as they watch their
loved one’s personality gradually deteriorate beyond recognition. The
AD patient may become moody, confused, paranoid, combative, or
hallucinatory—he or she may ask irrational questions such as, Why is
the room full of snakes? The patient may eventually lose even the ability to read, write, talk, walk, and eat. Death ensues from pneumonia or
other complications of confinement and immobility.
AD affects about 11% of the U.S. population over the age of 65;
the incidence rises to 47% by age 85. It accounts for nearly half of all
nursing home admissions and is a leading cause of death among the
elderly. AD claims about 100,000 lives per year in the United States.
Diagnosis of AD can be confirmed by autopsy. There is atrophy of
some of the gyri (folds) of the cerebral cortex and the hippocampus,
N-methyl-D-aspartate, a chemical similar to glutamate
Alois Alzheimer (1864–1915), German neurologist
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an important center of memory. Nerve cells exhibit neurofibrillary
tangles—dense masses of broken and twisted cytoskeleton (fig. 12.31).
Alois Alzheimer first observed these in 1907 in the brain of a patient
who had died of senile dementia. The more severe the signs of disease,
the more neurofibrillary tangles are seen at autopsy. In the intercellular
spaces, there are senile plaques consisting of aggregations of cells,
altered nerve fibers, and a core of β-amyloid protein—the breakdown
product of a glycoprotein of plasma membranes. Amyloid protein is
rarely seen in elderly people without AD. It is now widely believed to
be the crucial factor that triggers all the other aspects of AD pathology.
Intense biomedical research efforts are currently geared toward
identifying the causes of AD and developing treatment strategies.
Three genes on chromosomes 1, 14, and 21 have been implicated in
various forms of early- and late-onset AD. Interestingly, persons with
Down syndrome (trisomy-21), who have three copies of chromosome
21 instead of the usual two, tend to show early-onset Alzheimer disease. Nongenetic (environmental) factors also seem to be involved.
As for treatment, considerable attention now focuses on trying
to halt β-amyloid formation or stimulate the immune system to
clear β-amyloid from the brain tissue, but clinical trials in both of
these approaches have been suspended until certain serious side
effects can be resolved. AD patients show deficiencies of acetylcholine (ACh) and nerve growth factor (NGF). Some patients show
improvement when treated with NGF or cholinesterase inhibitors,
but results so far have been modest.
Parkinson33 disease (PD), also called paralysis agitans or parkinsonism, is a progressive loss of motor function beginning in a person’s
50s or 60s. It is due to degeneration of dopamine-releasing neurons
in a portion of the brain called the substantia nigra. A gene has
recently been identified for a hereditary form of PD, but most cases
are nonhereditary and of little-known cause; some authorities suspect
Dopamine (DA) is an inhibitory neurotransmitter that normally
prevents excessive activity in motor centers of the brain called the
basal nuclei. Degeneration of dopamine-releasing neurons leads to an
excessive ratio of ACh to DA, causing hyperactivity of the basal nuclei.
As a result, a person with PD suffers involuntary muscle contractions.
These take such forms as shaking of the hands (tremor) and compulsive “pill-rolling” motions of the thumb and fingers. In addition, the
facial muscles may become rigid and produce a staring, expressionless
face with a slightly open mouth. The patient’s range of motion diminishes. He or she takes smaller steps and develops a slow, shuffling gait
with a forward-bent posture and a tendency to fall forward. Speech
becomes slurred and handwriting becomes cramped and eventually
illegible. Tasks such as buttoning clothes and preparing food become
Patients cannot be expected to recover from PD, but its effects
can be alleviated with drugs and physical therapy. Treatment with
dopamine is ineffective because it cannot cross the blood–brain barrier, but its precursor, levodopa (L-dopa), does cross the barrier and
has been used to treat PD since the 1960s. L-dopa affords some relief,
but it does not slow progression of the disease and it has undesirable
side effects on the liver and heart. It is effective for only 5 to 10 years
of treatment. A newer drug, deprenyl, is a monoamine oxidase (MAO)
inhibitor that retards neural degeneration and slows the development
A surgical technique called pallidotomy has been used since
the 1940s to quell severe tremors. It involves the destruction of a
small portion of cerebral tissue in an area called the globus pallidus.
Pallidotomy fell out of favor in the late 1960s when L- dopa came into
common use. By the early 1990s, however, the limitations of L-dopa
had become apparent, while MRI- and CT-guided methods had
improved surgical precision and reduced the risks of brain surgery.
Pallidotomy has thus made a comeback. Other surgical treatments for
parkinsonism target brain areas called the subthalamic nucleus and the
ventral intermediate nucleus of the thalamus, and involve either the
destruction of tiny areas of tissue or the implantation of a stimulating
electrode. Such procedures are generally used only in severe cases
that are unresponsive to medication.
FIGURE 12.31 Alzheimer Disease. (a) Brain of a person who
died of AD. Note the shrunken folds of cerebral tissue (gyri) and
wide gaps (sulci) between them. (b) Cerebral tissue from a person
with AD. Neurofibrillary tangles are present within the neurons, and
a senile plaque is evident in the extracellular matrix.
James Parkinson (1755–1824), British physician
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Effects of the
on Other Organ Systems
Cutaneous nerves regulate
piloerection, sweating, cutaneous
vasoconstriction and vasodilation,
and heat loss through the
body surface, and provide for
cutaneous sensations such as
touch, itch, tickle, pressure,
heat, and cold.
Nerves to lymphatic organs influence the
development and activity of immune cells;
emotional states influence susceptibility to
infection and other failures of immunity.
Nervous stimulation maintains
the muscle tension that
stimulates bone growth and
remodeling; nerves in the bones
respond to strains and fractures.
Skeletal muscles cannot contract
without nervous stimulation; the
nervous system controls all body
movements and muscle tone.
The brainstem regulates the
rhythm of breathing, monitors
blood pH and blood gases, and
adjusts the respiratory rate and
depth to control these within
Sympathetic nerves modify the
rate of urine production by the
kidneys; nervous stimulation
of urinary sphincters aids in
urine retention in the bladder,
and nervous reflexes control its
The hypothalamus controls
the pituitary gland; the
sympathetic nervous system controls
the adrenal medulla; neuroendocrine
cells are neurons that secrete
hormones such as oxytocin; sensory
and other nervous input influences
the secretion of numerous other
The nervous system regulates the rate
and force of the heartbeat, regulates
blood vessel diameters, monitors and
controls blood pressure and blood gas
concentrations, routes blood to organs
where needed, and influences blood
The nervous system regulates
appetite, feeding behavior,
digestive secretion and motility,
The nervous system regulates sex
drive, arousal, and orgasm; the
brain regulates the secretion of
pituitary hormones that control
spermatogenesis in males and the
ovarian cycle in females; the nervous
system controls various aspects of
pregnancy and childbirth; the brain
produces oxytocin, which is involved
in labor contractions and lactation.
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Assess Your Learning Outcomes
To test your knowledge, discuss the following topics with a study partner or in
writing, ideally from memory.
12.1 Overview of the Nervous System
1. What the nervous and endocrine systems have in common
2. Three fundamental functions of the
nervous system; the roles of receptors
and effectors in carrying out these
3. Difference between the central nervous system (CNS) and peripheral
nervous system (PNS); between the
sensory and motor divisions of the
PNS; and between the somatic and
visceral subdivisions of both the sensory and motor divisions
4. The autonomic nervous system and
its two divisions
12.2 Properties of Neurons (p. 441)
1. Three fundamental physiological
properties of neurons
2. Differences between sensory (afferent) neurons, interneurons (association neurons), and motor (efferent)
3. The parts of a generalized multipolar
neuron, and their functions
4. Differences between multipolar, bipolar, unipolar, and anaxonic neurons;
an example of each
5. Ways in which neurons transport
substances between the neurosoma
and the distal ends of the axon
12.3 Supportive Cells (Neuroglia) (p. 446)
1. Six kinds of neuroglia; the structure
and functions of each; and which
kinds are found in the CNS and
which ones in the PNS
2. Structure of the myelin sheath,
and how CNS and PNS glial cells
3. How fiber diameter and the presence
or absence of myelin affect the conduction speed of a nerve fiber
4. The regeneration of a damaged nerve
fiber; the role of Schwann cells, the
basal lamina, and neurilemma in
regeneration; and why CNS neurons
12.4 Electrophysiology of Neurons
1. The meanings of electrical potential and resting membrane potential
(RMP); the typical voltage of an RMP
2. What an electrical current is, and how
sodium ions and gated membrane
channels generate a current
3. How stimulation of a neuron generates a local potential; the physiological properties of a local potential
4. Special properties of the trigger zone
and unmyelinated regions of a nerve
fiber that enable these regions to generate action potentials
5. The mechanism of an action potential; how it relates to ion flows and
the action of membrane channels;
and what is meant by depolarization and repolarization of the plasma
membrane during local and action
6. The all-or-none law and how it
applies to an action potential; other
properties of action potentials in contrast to local potentials
7. The basis and significance of the
refractory period that follows an
8. How one action potential triggers
another; how a chain reaction of
action potentials constitutes a nerve
signal in an unmyelinated nerve
fiber; and what normally prevents the
signal from traveling backward to the
9. Saltatory conduction in a myelinated
nerve fiber; differences in conduction mechanisms of the nodes of
Ranvier and the internodes; and why
signals travel faster in myelinated
fibers than in unmyelinated fibers of
12.5 Synapses (p. 460)
1. The structure and locations of
2. The role of neurotransmitters in
3. Categories of neurotransmitters and
common examples of each
4. Why the same neurotransmitter can
have different effects on different cells
5. Excitatory synapses; how acetylcholine and norepinephrine excite a
6. Inhibitory synapses; how
γ-aminobutyric acid (GABA)
inhibits a postsynaptic neuron
7. How second-messenger systems
function at synapses
8. Three ways in which synaptic
transmission is ended
9. Neuromodulators, their chemical
nature, and how they affect synaptic
12.6 Neural Integration (p. 466)
1. Why synapses slow down nervous
communication; the overriding
benefit of synapses
2. The meaning of excitatory and inhibitory postsynaptic potentials (EPSPs
3. Why the production of an EPSP
or IPSP may depend on both the
neurotransmitter released by the
presynaptic neuron and the type of
receptor on the postsynaptic neuron
4. How a postsynaptic neuron’s decision
to fire depends on the ratio of EPSPs
5. Temporal and spatial summation,
where they occur, and how they
determine whether a neuron fires
6. Mechanisms of facilitation and
presynaptic inhibition, and how
communication between two
neurons can be influenced by a
third neuron employing one of
7. Mechanisms of neural coding; how a
neuron communicates qualitative and
8. Why the refractory period sets a limit
to how frequently a neuron can fire
9. The meanings of neural pool and
10. The difference between a neuron’s
discharge zone and facilitated zone,
and how this relates to neurons
working in groups
11. Diverging, converging, reverberating,
and parallel after-discharge circuits of
neurons; examples of their relevance
to familiar body functions
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Integration and Control
12. The cellular basis of memory; what
memory consists of in terms of neural
pathways, and how it relates to synaptic plasticity and potentiation
13. Types of things remembered in immediate memory, short-term memory
(STM), and long-term memory (LTM),
and in the declarative and procedural
forms of LTM
14. Neural mechanisms thought to be
involved in these different forms of
Testing Your Recall
1. The integrative functions of the nervous system are performed mainly by
a. afferent neurons.
b. efferent neurons.
d. sensory neurons.
6. An IPSP is
of the postsynaptic
a. a refractory period
b. an action potential
c. a depolarization
d. a repolarization
e. a hyperpolarization
2. The highest density of voltage-gated
ion channels is found on the
of a neuron.
c. nodes of Ranvier
e. synaptic knobs
7. Saltatory conduction occurs only
a. at chemical synapses.
b. in the initial segment of an axon.
c. in both the initial segment and
d. in myelinated nerve fibers.
e. in unmyelinated nerve fibers.
3. The soma of a mature neuron lacks
a. a nucleus.
b. endoplasmic reticulum.
4. The glial cells that fight infections in
the CNS are
b. satellite cells.
c. ependymal cells.
5. Posttetanic potentiation of a synapse
increases the amount of
b. neurotransmitter receptors
c. facilitated circuits.
d. diverging circuits.
e. converging circuits.
11. Neurons that convey information to
the CNS are called sensory, or
12. To perform their role, neurons must
have the properties of excitability,
is a period of time in
which a neuron is producing an
action potential and cannot respond
to another stimulus of any strength.
8. Some neurotransmitters can have
either excitatory or inhibitory effects
depending on the type of
a. receptors on the postsynaptic cell.
b. synaptic vesicles in the axon.
c. synaptic potentiation that occurs.
d. postsynaptic potentials on the synaptic knob.
e. neuromodulator involved.
14. Neurons receive incoming signals by
way of specialized extensions of the
9. Differences in the volume of a sound
are likely to be encoded by differences in
in nerve fibers from
the inner ear.
b. signal conduction velocity
c. types of postsynaptic potentials
d. firing frequency
e. voltage of the action potentials
17. The trigger zone of a neuron consists
10. Motor effects that depend on repetitive output from a neural pool are
most likely to use
a. parallel after-discharge circuits.
b. reverberating circuits.
15. In the CNS, myelin is produced by
glial cells called
16. A myelinated nerve fiber can produce
action potentials only in specialized
18. The neurotransmitter secreted at an
adrenergic synapse is
19. A presynaptic nerve fiber cannot
cause other neurons in its
fire, but it can make them more sensitive to stimulation from other presynaptic fibers.
are substances released along
with a neurotransmitter that modify
the neurotransmitter’s effect.
Answers in appendix B
Building Your Medical Vocabulary
State a medical meaning of each word
element below, and give a term in which
it or a slight variation of it is used.
1. antero2. -aps
10. somatoAnswers in appendix B
11/15/10 8:59 AM
True or False
Determine which five of the following
statements are false, and briefly explain
4. During an action potential, most of
the Na+ and K+ exchange places
across the plasma membrane.
1. A neuron never has more than one
5. Excitatory postsynaptic potentials
lower the threshold of a neuron and
thus make it easier to stimulate.
2. Oligodendrocytes perform the same
function in the brain as Schwann
cells do in the peripheral nerves.
3. A resting neuron has a higher concentration of K+ in its cytoplasm than in
the extracellular fluid surrounding it.
6. The absolute refractory period sets an
upper limit on how often a neuron
7. A given neurotransmitter has the
same effect no matter where in the
body it is secreted.
8. Myelinated nerve fibers conduct
signals more rapidly than unmyelinated ones because they have nodes of
9. Learning occurs by increasing the
number of neurons in the brain
10. Mature neurons are incapable of
Answers in appendix B
Testing Your Comprehension
1. Schizophrenia is sometimes treated
with drugs such as chlorpromazine
that inhibit dopamine receptors.
A side effect is that patients begin
to develop muscle tremors, speech
impairment, and other disorders
similar to Parkinson disease. Explain.
3. Suppose a poison were to slow down
the Na+–K+ pumps of nerve cells.
How would this affect the resting
membrane potentials of neurons?
Would it make neurons more excitable than normal, or make them more
difficult to stimulate? Explain.
2. Hyperkalemia is an excess of potassium in the extracellular fluid. What
effect would this have on the resting
membrane potentials of the nervous
system and on neural excitability?
4. The unity of form and function is an
important concept in understanding
synapses. Give two structural reasons why nerve signals cannot travel
backward across a chemical synapse.
What might be the consequences
if signals did travel freely in both
5. The local anesthetics lidocaine
(Xylocaine) and procaine (Novocaine)
prevent voltage-gated Na+ channels
from opening. Explain why this
would block the conduction of pain
signals in a sensory nerve.
Answers at www.mhhe.com/saladin6
Improve Your Grade at www.mhhe.com/saladin6
Download mp3 audio summaries and movies to study when it fits your schedule. Practice quizzes, labeling activities, games,
and flashcards offer fun ways to master the chapter concepts. Or, download image PowerPoint files for each chapter to create
a study guide or for taking notes during lecture.
11/15/10 8:59 AM
THE SPINAL CORD,
Cross section through two fascicles (bundles) of nerve fibers in a nerve
13.1 The Spinal Cord 479
• Functions 479
• Surface Anatomy 479
• Meninges of the Spinal Cord 480
• Cross-Sectional Anatomy 482
• Spinal Tracts 483
13.2 The Spinal Nerves 487
• General Anatomy of Nerves
and Ganglia 488
• Spinal Nerves 490
• Nerve Plexuses 493
• Cutaneous Innervation and
13.3 Somatic Reflexes 500
• The Nature of Reflexes 500
• The Muscle Spindle 501
• The Stretch Reflex 503
• The Flexor (Withdrawal) Reflex 504
• The Crossed Extension Reflex 505
• The Tendon Reflex 505
Study Guide 508
13.1 Clinical Application: Spina Bifida 482
13.2 Clinical Application: Poliomyelitis and
Amyotrophic Lateral Sclerosis 488
13.3 Clinical Application: Shingles 494
13.4 Clinical Application: Nerve Injuries 497
13.5 Clinical Application: Spinal Cord
Module 7: Nervous System
11/15/10 9:00 AM
• A knowledge of basic neuron structure (p. 442) is indispensable for
understanding this chapter.
• In this chapter’s discussion of spinal reflexes, it is necessary to be
familiar with the ways muscles work in groups at a joint, especially
antagonistic muscles. You can review that at page 318.
• An understanding of excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) (p. 466) and the parallel after-discharge type
of neural circuit (p. 470) are also important for understanding spinal
very year in the United States, thousands of people become
paralyzed by spinal cord injuries, with devastating effects on
their quality of life. The treatment of such injuries is one of
the most lively areas of medical research today. Therapists in this
specialty must know spinal cord anatomy and function to understand their patients’ functional deficits and prospects for improvement and to plan an appropriate regimen of treatment. Such knowledge is necessary, as well, for understanding paralysis resulting from
strokes and other brain injuries. The spinal cord is the “information
highway” that connects the brain with the lower body; it contains
the neural routes that explain why a lesion to a specific part of the
brain results in a functional loss in a specific locality in the lower
In this chapter, we will study not only the spinal cord but also
the spinal nerves that arise from it with ladderlike regularity at
intervals along its length. Thus, we will examine components of
both the central and peripheral nervous systems, but these components are so closely related, structurally and functionally, that it
is appropriate to consider them together. Similarly, the brain and
cranial nerves will be considered together in the following chapter.
Chapters 13 and 14 therefore elevate our study of the nervous
system from the cellular level (chapter 12) to the organ and system
13.1 The Spinal Cord
Expected Learning Outcomes
When you have completed this section, you should be able to
a. state the three principal functions of the spinal cord;
b. describe its gross and microscopic structure; and
c. trace the pathways followed by nerve signals traveling up
and down the spinal cord.
The spinal cord serves four principal functions:
1. Conduction. It contains bundles of nerve fibers
that conduct information up and down the cord,
The Spinal Cord, Spinal Nerves, and Somatic Reflexes
connecting different levels of the trunk with each
other and with the brain. This enables sensory
information to reach the brain, motor commands to
reach the effectors, and input received at one level of
the cord to affect output from another level.
2. Neural integration. Pools of spinal neurons receive
input from multiple sources, integrate the information, and execute an appropriate output. For
example, the spinal cord can integrate the stretch
sensation from a full bladder with cerebral input
concerning the appropriate time and place to urinate
and execute control of the bladder accordingly.
3. Locomotion. Walking involves repetitive,
coordinated contractions of several muscle groups
in the limbs. Motor neurons in the brain initiate
walking and determine its speed, distance,
and direction, but the simple repetitive muscle
contractions that put one foot in front of another,
over and over, are coordinated by groups of neurons called central pattern generators in the cord.
These neural circuits produce the sequence of outputs to the extensor and flexor muscles that cause
alternating movements of the lower limbs.
4. Reflexes. Reflexes are involuntary stereotyped
responses to stimuli, such as the withdrawal of a
hand from pain. They involve the brain, spinal cord,
and peripheral nerves.
The spinal cord (fig. 13.1) is a cylinder of nervous tissue
that arises from the brainstem at the foramen magnum of
the skull. It passes through the vertebral canal as far as the
inferior margin of the first lumbar vertebra (L1) or slightly
beyond. In adults, it averages about 45 cm long and 1.8 cm
thick (about as thick as one’s little finger). Early in fetal
development, the cord extends for the full length of the
vertebral column. However, the vertebral column grows
faster than the spinal cord, so the cord extends only to L3
by the time of birth and to L1 in an adult. Thus, it occupies
only the upper two-thirds of the vertebral canal; the lower
one-third is described shortly.
The cord gives rise to 31 pairs of spinal nerves. The
first pair passes between the skull and vertebra C1, and the
rest pass through the intervertebral foramina. Although the
spinal cord is not visibly segmented, the part supplied by
each pair of nerves is called a segment. The cord exhibits
longitudinal grooves on its anterior and posterior sides—
the anterior median fissure and posterior median sulcus,
respectively (fig. 13.2b).
The spinal cord is divided into cervical, thoracic,
lumbar, and sacral regions. It may seem odd that it has
a sacral region when the cord itself ends well above the
sacrum. These regions, however, are named for the level
of the vertebral column from which the spinal nerves
emerge, not for the vertebrae that contain the cord itself.
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Integration and Control
FIGURE 13.1 The Spinal Cord, Posterior Aspect. (a) Overview
of spinal cord structure. (b) Detail of the spinal cord and associated
Spinal nerve rootlets
Posterior median sulcus
Posterior root ganglion
In two areas, the cord is a little thicker than elsewhere.
In the inferior cervical region, a cervical enlargement gives
rise to nerves of the upper limbs. In the lumbosacral region,
there is a similar lumbar enlargement that issues nerves to
the pelvic region and lower limbs. Inferior to the lumbar
enlargement, the cord tapers to a point called the medullary cone (conus medullaris). Arising from the lumbar enlargement and medullary cone is a bundle of nerve roots
that occupy the vertebral canal from L2 to S5. This bundle,
named the cauda equina1 (CAW-duh ee-KWY-nah) for its
resemblance to a horse’s tail, innervates the pelvic organs
and lower limbs.
cauda = tail; equin = horse
Apply What You Know
Spinal cord injuries commonly result from fractures of vertebrae C5 to C6, but never from fractures of L3 to L5. Explain
Meninges of the Spinal Cord
The spinal cord and brain are enclosed in three fibrous
connective tissue membranes called meninges2 (meh-NINjeez)—singular, meninx (MEN-inks) (fig. 13.2). These membranes separate the soft tissue of the central nervous system
menin = membrane
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The Spinal Cord, Spinal Nerves, and Somatic Reflexes
Dura mater (dural sheath)
Spinous process of vertebra
Fat in epidural space
Posterior root ganglion
(a) Spinal cord and vertebra (cervical)
Posterior root of spinal nerve
Posterior root ganglion
Anterior median fissure
of spinal nerve
Dura mater (dural sheath)
(b) Spinal cord and meninges (thoracic)
(c) Lumbar spinal cord
FIGURE 13.2 Cross-Sectional Anatomy of the Spinal Cord. (a) Relationship to the vertebra, meninges, and spinal nerve. (b) Detail of the spinal
cord, meninges, and spinal nerves. (c) Cross section of the lumbar spinal cord with spinal nerves.
from the bones of the vertebrae and skull. From superficial to deep, they are the dura mater, arachnoid mater, and
The dura mater3 (DOO-ruh MAH-tur) forms a loosefitting sleeve called the dural sheath around the spinal
dura = tough; mater = mother, womb
cord. It is a tough collagenous membrane about as thick as
a rubber kitchen glove. The space between the sheath and
vertebral bones, called the epidural space, is occupied by
blood vessels, adipose tissue, and loose connective tissue.
Anesthetics are sometimes introduced to this space to
block pain signals during childbirth or surgery; this procedure is called epidural anesthesia.
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