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6 Tissue Growth, Development, Repair, and Degeneration

6 Tissue Growth, Development, Repair, and Degeneration

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CHAPTER 12



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

Immediate memory is the ability to hold something in

mind for just a few seconds. By remembering what just

30



en = inner; gram = mark, trace, record



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Nervous Tissue



471



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

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

hours earlier.



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PART THREE



Integration and Control



Long-Term Memory

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



Clinical Application



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.



31

32



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

future.

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

release.



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

described here.



Before You Go On

Answer the following questions to test your understanding of the

preceding section:

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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CHAPTER 12



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

environmental neurotoxins.

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

increasingly laborious.

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)



33



Nervous Tissue



473



inhibitor that retards neural degeneration and slows the development

of PD.

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.



Shrunken

gyri

Wide sulci



(a)



Neurons with

neurofibrillary

tangles



Senile plaque



(b)



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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CONNECTIVE

ISSUES

Effects of the

NERVOUS SYSTEM

on Other Organ Systems



INTEGUMENTARY SYSTEM

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.



LYMPHATIC/IMMUNE SYSTEM

Nerves to lymphatic organs influence the

development and activity of immune cells;

emotional states influence susceptibility to

infection and other failures of immunity.



RESPIRATORY SYSTEM

SKELETAL SYSTEM

Nervous stimulation maintains

the muscle tension that

stimulates bone growth and

remodeling; nerves in the bones

respond to strains and fractures.



MUSCULAR SYSTEM

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

normal ranges.



URINARY SYSTEM

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

emptying.



ENDOCRINE SYSTEM

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

hormones.



CIRCULATORY SYSTEM

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

clotting.



DIGESTIVE SYSTEM

The nervous system regulates

appetite, feeding behavior,

digestive secretion and motility,

and defecation.



REPRODUCTIVE SYSTEM

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.



474



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Nervous Tissue



475



STUDY GUIDE



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

(p. 440)

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

functions

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)

neurons

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

produce it

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

cannot regenerate



sal78259_ch12_439-477.indd 475



12.4 Electrophysiology of Neurons

(p. 451)

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

potentials

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

action potential

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

neurosoma

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

comparable size

12.5 Synapses (p. 460)

1. The structure and locations of

synapses

2. The role of neurotransmitters in

synaptic transmission

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

postsynaptic neuron

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

transmission

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

and IPSPs)

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

to IPSPs

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

these mechanisms

7. Mechanisms of neural coding; how a

neuron communicates qualitative and

quantitative information

8. Why the refractory period sets a limit

to how frequently a neuron can fire

9. The meanings of neural pool and

neural circuit

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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PART THREE



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

memory



Testing Your Recall

1. The integrative functions of the nervous system are performed mainly by

a. afferent neurons.

b. efferent neurons.

c. neuroglia.

d. sensory neurons.

e. interneurons.



6. An IPSP is

of the postsynaptic

neuron.

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.

a. dendrites

b. soma

c. nodes of Ranvier

d. internodes

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

axon hillock.

d. in myelinated nerve fibers.

e. in unmyelinated nerve fibers.



3. The soma of a mature neuron lacks

a. a nucleus.

b. endoplasmic reticulum.

c. lipofuscin.

d. centrioles.

e. ribosomes.

4. The glial cells that fight infections in

the CNS are

a. microglia.

b. satellite cells.

c. ependymal cells.

d. oligodendrocytes.

e. astrocytes.

5. Posttetanic potentiation of a synapse

increases the amount of

in the

synaptic knob.

a. neurotransmitter

b. neurotransmitter receptors

c. calcium

d. sodium

e. NMDA



c. facilitated circuits.

d. diverging circuits.

e. converging circuits.

11. Neurons that convey information to

the CNS are called sensory, or

,

neurons.

12. To perform their role, neurons must

have the properties of excitability,

secretion, and

.

is a period of time in

13. The

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

cell called

.



9. Differences in the volume of a sound

are likely to be encoded by differences in

in nerve fibers from

the inner ear.

a. neurotransmitters

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

of its

and

.



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

regions called

.



18. The neurotransmitter secreted at an

adrenergic synapse is

.

19. A presynaptic nerve fiber cannot

cause other neurons in its

to

fire, but it can make them more sensitive to stimulation from other presynaptic fibers.

20.



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



3. astro-



7. -grad



4. dendro-



8. neuro-



5. -fer



9. sclero-



6. gangli-



10. somatoAnswers in appendix B



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CHAPTER 12



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477



True or False

Determine which five of the following

statements are false, and briefly explain

why.



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

axon.



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

can fire.

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

Ranvier.

9. Learning occurs by increasing the

number of neurons in the brain

tissue.

10. Mature neurons are incapable of

mitosis.

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

directions?

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.



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CHAPTER



13

THE SPINAL CORD,

SPINAL NERVES,

AND SOMATIC

REFLEXES

Cross section through two fascicles (bundles) of nerve fibers in a nerve



CHAPTER OUTLINE

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

Dermatomes 500



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



DEEPER INSIGHTS

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

Trauma 507



Module 7: Nervous System



478



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CHAPTER 13



Brushing Up…

• 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

reflexes.



E



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

body.

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

levels.



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.



Functions

The spinal cord serves four principal functions:

1. Conduction. It contains bundles of nerve fibers

that conduct information up and down the cord,



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The Spinal Cord, Spinal Nerves, and Somatic Reflexes



479



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.



Surface Anatomy

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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480



PART THREE



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

structures.



C1



Cervical

enlargement



Cervical

spinal

nerves

C7



Dural

sheath

Subarachnoid

space

Thoracic

spinal

nerves



Spinal cord

Vertebra (cut)



Lumbar

enlargement



Spinal nerve

T12

Spinal nerve rootlets



Medullary

cone



Posterior median sulcus

Lumbar

spinal

nerves



Cauda equina



Subarachnoid space

Epidural space

Posterior root ganglion



L5



Rib

Arachnoid mater

Terminal

filum



Sacral

spinal

nerves



Dura mater



S5

Col



(b)



(a)



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.

1



cauda = tail; equin = horse



sal78259_ch13_478-510.indd 480



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

both observations.



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



2



menin = membrane



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CHAPTER 13



The Spinal Cord, Spinal Nerves, and Somatic Reflexes



481



Posterior



Meninges:

Dura mater (dural sheath)

Arachnoid mater

Pia mater



Spinous process of vertebra



Fat in epidural space

Subarachnoid space

Spinal cord

Denticulate ligament

Posterior root ganglion

Spinal nerve

Vertebral body



Anterior



(a) Spinal cord and vertebra (cervical)



Gray matter:

Posterior horn

Gray commissure

Lateral horn

Anterior horn



Central canal



Posterior

median sulcus



White matter:

Posterior column

Lateral column

Anterior column

Posterior root of spinal nerve

Posterior root ganglion

Spinal nerve



Anterior median fissure



Anterior root

of spinal nerve



Meninges:

Pia mater

Arachnoid mater

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

pia mater.

The dura mater3 (DOO-ruh MAH-tur) forms a loosefitting sleeve called the dural sheath around the spinal

3



dura = tough; mater = mother, womb



sal78259_ch13_478-510.indd 481



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.



11/15/10 9:00 AM



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