Excitation of Skeletal Muscle pdf - Membrane Physiology and Nerve and Muscle

muscle membrane and its subneural clefts below.

of the details of this mechanism can be seen in Figure 7–2, which shows an

of acetylcholine are released from the terminals into the synaptic space. Some

When a nerve impulse reaches the neuromuscular junction, about 125 vesicles

Secretion of Acetylcholine by the Nerve Terminals

vesicles.

acetylcholinesterase,

of which are normally in the terminals of a single end plate. In the synaptic

synaptic vesicles,

fiber membrane. Acetylcholine is synthesized in the cytoplasm of the terminal,

The acetylcholine in turn excites the muscle

acetylcholine.

phate (ATP), the energy source that is used for synthesis of an excitatory

subneural clefts,

This space is 20 to 30 nanometers wide. At the bottom of the gutter are numer-

a single axon terminal and the muscle fiber membrane. The invaginated mem-

Figure 7–1

surrounding fluids.

plate.

muscle fiber plasma membrane. The entire structure is called the

branching nerve

to a skeletal muscle fiber. The nerve fiber forms a complex of

shows the neuromuscular junction from a large, myelinated nerve fiber

Figure 7–1

of the muscle fibers, there is only one such junction per muscle fiber.

directions toward the muscle fiber ends. With the exception of about 2 per cent

with the muscle fiber near its midpoint. The

several hundred skeletal muscle fibers. Each nerve ending makes a junction,

entering the muscle belly, normally branches and stimulates from three to

horns of the spinal cord. As pointed out in Chapter 6, each nerve fiber, after

The skeletal muscle fibers are innervated by large,

The Neuromuscular

from Nerve Endings to

Transmission of Impulses

Neuromuscular Transmission and

Excitation of Skeletal Muscle:

Excitation-Contraction Coupling

Skeletal Muscle Fibers:

Junction

myelinated nerve fibers that originate from large motoneurons in the anterior

called the neuromuscular junction,
action potential initiated in the muscle fiber by the nerve signal travels in both

Physiologic Anatomy of the Neuromuscular Junction—The Motor End Plate.

and B

terminals that invaginate into the surface of the muscle fiber but lie outside the

motor end

It is covered by one or more Schwann cells that insulate it from the

C shows an electron micrographic sketch of the junction between

brane is called the synaptic gutter or synaptic trough, and the space between the
terminal and the fiber membrane is called the synaptic space or synaptic cleft.

ous smaller folds of the muscle membrane called

which greatly

increase the surface area at which the synaptic transmitter can act.

In the axon terminal are many mitochondria that supply adenosine triphos-

transmitter

but it is absorbed rapidly into many small

about 300,000

space are large quantities of the enzyme

which destroys

acetylcholine a few milliseconds after it has been released from the synaptic

expanded view of a synaptic space with the neural membrane above and the

molecular weight of 275,000. The complex is composed

into the synaptic space.

dense bar areas, where the acetylcholine is emptied

acetylcholine-gated ion channels,

membrane; these are

acetylcholine receptors

Figure 7–2 also shows many

brane to Open Ion Channels.

adjacent to the dense bars.

speculative, it is known that the effective stimulus for

exocytosis.

membrane adjacent to the dense bars. The vesicles

the acetylcholine vesicles, drawing them to the neural

in turn, are believed to exert an attractive influence on

to the interior of the nerve terminal. The calcium ions,

spreads over the terminal, these channels open and

When an action potential

gated calcium channels.

that penetrate the neural membrane; these are

To each side of each dense bar are protein particles

shown in cross section in Figure 7–2.

dense bars,

Membrane Physiology, Nerve, and Muscle

Unit II

On the inside surface of the neural membrane are

linear

voltage-

allow calcium ions to diffuse from the synaptic space

then fuse with the neural membrane and empty their
acetylcholine into the synaptic space by the process of

Although some of the aforementioned details are

causing acetylcholine release from the vesicles is entry
of calcium ions and that acetylcholine from the vesi-
cles is then emptied through the neural membrane

Effect of Acetylcholine on the Postsynaptic Muscle Fiber Mem-

very small

in the muscle fiber

and they are located almost entirely near the mouths
of the subneural clefts lying immediately below the

Each receptor is a protein complex that has a total

Terminal nerve

Teloglial cell

Axon

Myofibrils

branches

Muscle
nuclei

Myelin

sheath

Synaptic vesicles

Axon terminal in
synaptic trough

Subneural clefts

DW: A Textbook of Histology.

Couteaux R, in Bloom W, Fawcett

Fawcett DW, as modified from

fiber membrane. (Redrawn from

axon terminal and the muscle

micrographic appearance of the

Electron

Surface

through the end plate.

Different views of the motor end

Figure 7–1

plate. A, Longitudinal section

view of the end plate. C,

contact point between a single

Philadelphia: WB Saunders,
1986.)

Vesicles

Calcium
channels

Neural

membrane

Muscle

membrane

Release

sites

Dense bar

Basal lamina
and
acetylcholinesterase

Acetylcholine
receptors

Subneural cleft

receptors in the muscle membrane, at the mouths of the subneural

the release sites in the neural membrane to the acetylcholine

membrane of the neuromuscular junction. Note the proximity of

Release of acetylcholine from synaptic vesicles at the neural

Figure 7–2

clefts.

voltage changes, as recorded in the figure. By contrast,

potential, but they do produce weak local end plate

potentials A and C are too weak to elicit an action

shows three separate end plate potentials. End plate

potential initiating the action potential. This figure

Figure 7–4 shows the principle of an end plate

membrane.

to initiate more and more sodium channel opening,

much as 50 to 75 millivolts, creating a

The sudden insurgence of sodium ions into the muscle

End Plate Potential and Excitation of the Skeletal Muscle Fiber.

is sufficient to excite the muscle fiber. Then the rapid

The short time that the acetylcholine remains in the

to act on the muscle fiber membrane.

brane. (2) A small amount of acetylcholine diffuses out

acetylcholinesterase,

means: (1) Most of the acetylcholine is destroyed

in the space. However, it is removed rapidly by two

the synaptic space, continues to activate the acetyl-

The acetylcholine, once released into

In turn, this end plate potential initiates an

inside the muscle fiber membrane, called the

charges. This creates a local positive potential change

the fiber, carrying with them large numbers of positive

, the principal effect of

As shown in Figure 7–3

charged sodium ions to the inside of the fiber, while

membrane, –80 to –90 millivolts, pulls the positively

and potassium ions in the intracellular fluid. Second,

concentration: sodium ions in the extracellular fluid,

reasons. First, there are only two positive ions in large

acetylcholine channels than any other ions, for two

In practice, far more sodium ions flow through the

negative ions.

ions, do not pass through because of strong negative

opening. Conversely, negative ions, such as chloride

), and calcium (Ca

), potassium

about 0.65 nanometer, which is large enough to allow

The opened acetylcholine channel has a diameter of

section B of the figure.

tional change that opens the channel, as shown in

subunit proteins. This causes a conforma-

constricted, as shown in section A of the figure, until

channel, illustrated in Figure 7–3. The channel remains

brane, lying side by side in a circle to form a tubular

proteins. These protein

beta, delta,

of five subunit proteins, two

Excitation of Skeletal Muscle: Neuromuscular Transmission and Excitation-Contraction Coupling

Chapter 7

alpha proteins and one

each of

and gamma

molecules penetrate all the way through the mem-

two acetylcholine molecules attach respectively to the
two alpha

the important positive ions—sodium (Na

)—to move easily through the

charges in the mouth of the channel that repel these

the very negative potential on the inside of the muscle

simultaneously preventing efflux of the positively
charged potassium ions when they attempt to pass
outward.

opening the acetylcholine-gated channels is to allow
large numbers of sodium ions to pour to the inside of

end plate

potential.
action potential that spreads along the muscle mem-
brane and thus causes muscle contraction.

Destruction of the Released Acetylcholine by Acetyl-
cholinesterase.

choline receptors as long as the acetylcholine persists

by the enzyme

which is attached

mainly to the spongy layer of fine connective tissue
that fills the synaptic space between the presynaptic
nerve terminal and the postsynaptic muscle mem-

of the synaptic space and is then no longer available

synaptic space—a few milliseconds at most—normally

removal of the acetylcholine prevents continued
muscle re-excitation after the muscle fiber has re-
covered from its initial action potential.

fiber when the acetylcholine channels open causes the
electrical potential inside the fiber at the local area of
the end plate to increase in the positive direction as

local potential

called the end plate potential. Recall from Chapter 5
that a sudden increase in nerve membrane potential
of more than 20 to 30 millivolts is normally sufficient

thus initiating an action potential at the muscle fiber

end plate potential B is much stronger and causes
enough sodium channels to open so that the self-
regenerative effect of more and more sodium ions

Ach

–

channel mouth that prevent passage of negative ions such as

(Ach) has become attached and a conformational change has

Figure 7–3

Acetylcholine channel. A, Closed state. B, After acetylcholine

opened the channel, allowing sodium ions to enter the muscle
fiber and excite contraction. Note the negative charges at the

chloride ions.

fiber as does acetylcholine. The difference between

nicotine,

bachol,

methacholine, car-

Many compounds, including

Neuromuscular Junction

Block Transmission at the

release.

they are then ready for a new cycle of acetylcholine

is transported to the interior of these vesicles, and

vesicles. Within another few seconds, acetylcholine

to the interior of the membrane, thus forming new

original vesicles. Within about 20 seconds, the

nerve ending, especially the protein

membrane, caused by contractile proteins in the

over, “coated pits” appear in the terminal nerve

Within a few seconds after each action potential is

junction, new vesicles need to be re-formed rapidly.

few thousand nerve-to-muscle impulses. Therefore,

4. The number of vesicles available in the nerve

milliseconds.

reused to form new acetylcholine. This sequence of

into acetate ion and choline, and the choline is

action potential. Then, after a few milliseconds, the

of acetylcholine into the synaptic space.

fusion makes many of the vesicles rupture, allowing

the terminal membrane about 10,000-fold. This

increases about 100-fold, which in turn increases

calcium channels. As a result, the calcium ion

terminal, it opens many calcium channels in the

3. When an action potential arrives at the nerve

each vesicle.

form, about 10,000 molecules of acetylcholine in

interior, where it is stored in highly concentrated

2. Acetylcholine is synthesized in the cytosol of the

muscle end plate.

nerve fibers. About 300,000 of these small vesicles

are then transported by axoplasm that “streams”

the motoneuron in the spinal cord. These vesicles

1. Small vesicles, about 40 nanometers in size, are

cal transmission have been worked out. The formation

be studied easily, it is one of the few synapses of the

Acetylcholine Formation

exhausting levels of muscle activity.

junction occurs rarely, and even then only at the most

conditions, measurable fatigue of the neuromuscular

synapses are overexcited. Under normal functioning

lar junction, and it is the same effect that causes fatigue

muscle fiber. This is called

However, stimulation of the nerve fiber

safety factor.

required to stimulate the muscle fiber. Therefore, the

Ordinarily, each impulse that

Safety Factor for Transmission at the Neuromuscular Junction;

nerve terminals.

botulinum toxin,

peting for the acetylcholine receptor sites. The weak-

curare,

point A was caused by poisoning of the muscle fiber

potential. The weakness of the end plate potential at

Membrane Physiology, Nerve, and Muscle

Unit II

flowing to the interior of the fiber initiates an action

with

a drug that blocks the gating action of

acetylcholine on the acetylcholine channels by com-

ness of the end plate potential at point C resulted from
the effect of

a bacterial poison that

decreases the quantity of acetylcholine release by the

Fatigue of the Junction.

arrives at the neuromuscular junction causes about
three times as much end plate potential as that

normal neuromuscular junction is said to have a high

at rates greater than 100 times per second for several
minutes often diminishes the number of acetylcholine
vesicles so much that impulses fail to pass into the

fatigue of the neuromuscu-

of synapses in the central nervous system when the

Molecular Biology of

and Release

Because the neuromuscular junction is large enough to

nervous system for which most of the details of chemi-

and release of acetylcholine at this junction occur in the
following stages:

formed by the Golgi apparatus in the cell body of

through the core of the axon from the central
cell body in the spinal cord all the way to the
neuromuscular junction at the tips of the peripheral

collect in the nerve terminals of a single skeletal

nerve fiber terminal but is immediately transported
through the membranes of the vesicles to their

membrane of the nerve terminal because this
terminal has an abundance of voltage-gated

concentration inside the terminal membrane

the rate of fusion of the acetylcholine vesicles with

exocytosis
About 125 vesicles usually rupture with each

acetylcholine is split by acetylcholinesterase

reabsorbed actively into the neural terminal to be

events occurs within a period of 5 to 10

ending is sufficient to allow transmission of only a

for continued function of the neuromuscular

clathrin, which

is attached to the membrane in the areas of the

proteins contract and cause the pits to break away

Drugs That Enhance or

Drugs That Stimulate the Muscle Fiber by Acetylcholine-Like
Action.

and

have the same effect on the muscle

+ 20

+ 40

+ 60

Milliseconds

Millivolts

– 20

– 40

– 60

– 80

–100

toxin that decreases end plate release of acetylcholine, again too

Weakened end plate potential caused by botulinum

Normal end plate potential eliciting a muscle action

tial recorded in a curarized muscle, too weak to elicit an action

Weakened end plate poten-

Figure 7–4

End plate potentials (in millivolts). A,

potential. B,
potential. C,

weak to elicit a muscle action potential.

internal extensions of the cell membrane. Therefore,

lumens. In other words, the T tubules are actually

the extracellular fluid surrounding the muscle fiber,

Therefore, they communicate with

of the muscle fiber.

from the cell membrane, they are open to the exterior

where the T tubules originate

separate myofibrils. Also,

of T tubules interlacing among all the

side. Not shown in the figure is the fact that these

They begin at the cell membrane and penetrate all the

are very small and run transverse to the myofibrils.

tubule–sarcoplasmic reticulum system. The T tubules

Figure 7–5 shows myofibrils surrounded by the T

Reticulum System

Transverse Tubule–Sarcoplasmic

coupling.

ions then cause contraction. This overall process is

immediate vicinity of the myofibrils, and these calcium

Figure 7–5. The T tubule action potentials cause

from one side of the fiber to the other, as illustrated in

separate myofibrils. This is achieved by transmission of

cause maximum muscle contraction, current must pen-

almost no current flow deep within the fiber. Yet, to

The skeletal muscle fiber is so large that action poten-

“Transverse Tubules”

Interior of the Muscle Fiber by Way of

Spread of the Action Potential to the

nerve fibers that excite skeletal muscle.

3. Velocity of conduction: 3 to 5 m/sec—about 1/13

large myelinated nerves.

2. Duration of action potential: 1 to 5 milliseconds in

myelinated nerve fibers.

1. Resting membrane potential: about –80 to –90

for quantitative differences. Some of the quantitative

fibers applies equally to skeletal muscle fibers, except

few hours later.

normally, until a new dose of neostigmine is required a

mulate in the synaptic space. Within minutes, some of

or some other anticholinesterase drug, which allows

the respiratory muscles. The disease usually can be ame-

the patient dies of paralysis—in particular, paralysis of

late the muscle fibers. If the disease is intense enough,

Regardless of the cause, the end plate potentials that

acetylcholine-activated ion channels.

myasthenia gravis. Therefore, it is believed that myas-

fibers. Pathologically, antibodies that attack the acetyl-

20,000 persons, causes muscle paralysis because of

Myasthenia gravis,

tors, thus preventing sufficient increase in permeability

muscle. For instance, D-tubocurarine blocks the action

Drugs That Block Transmission at the Neuromuscular Junction.

cholinesterase for weeks, which makes this a particu-

as a powerful “nerve” gas poison, inactivates acetyl-

propyl fluorophosphate, which has military potential

esterase once again becomes active. Conversely, diiso-

for up to several hours, after which these drugs are

due to laryngeal spasm, which smothers the person.

reach the muscle. Unfortunately, it also can cause death

lates and stimulates the muscle fiber repetitively. This

sive nerve impulse, additional acetylcholine accumu-

hydrolyzes acetylcholine. Therefore, with each succes-

diisopropyl fluorophosphate,

neostigmine,

physostigmine,

known drugs,

Three particularly well-

virtue of leaking ions, initiate a new action potential,

from a previous contraction, these depolarized areas, by

are located. Then, every time the muscle fiber recovers

several hours. The drugs work by causing localized areas

Excitation of Skeletal Muscle: Neuromuscular Transmission and Excitation-Contraction Coupling

Chapter 7

these drugs and acetylcholine is that the drugs are not
destroyed by cholinesterase or are destroyed so slowly
that their action often persists for many minutes to

of depolarization of the muscle fiber membrane at the
motor end plate where the acetylcholine receptors

thereby causing a state of muscle spasm.

Drugs That Stimulate the Neuromuscular Junction by
Inactivating Acetylcholinesterase.

and

inactivate the acetyl-

cholinesterase in the synapses so that it no longer

causes muscle spasm when even a few nerve impulses

Neostigmine and physostigmine combine with acetyl-

cholinesterase to inactivate the acetylcholinesterase

displaced from the acetylcholinesterase so that the

larly lethal poison.

group of drugs known as curariform drugs can prevent
passage of impulses from the nerve ending into the

of acetylcholine on the muscle fiber acetylcholine recep-

of the muscle membrane channels to initiate an action
potential.

Myasthenia Gravis

which occurs in about 1 in every

inability of the neuromuscular junctions to transmit
enough signals from the nerve fibers to the muscle

choline-gated sodium ion transport proteins have been
demonstrated in the blood of most patients with

thenia gravis is an autoimmune disease in which the
patients have developed immunity against their own

occur in the muscle fibers are mostly too weak to stimu-

liorated for several hours by administering neostigmine

larger than normal amounts of acetylcholine to accu-

these paralyzed people can begin to function almost

Muscle Action Potential

Almost everything discussed in Chapter 5 regarding
initiation and conduction of action potentials in nerve

aspects of muscle potentials are the following:

millivolts in skeletal fibers—the same as in large

skeletal muscle—about five times as long as in

the velocity of conduction in the large myelinated

tials spreading along its surface membrane cause

etrate deeply into the muscle fiber to the vicinity of the

action potentials along transverse tubules (T tubules)
that penetrate all the way through the muscle fiber

release of calcium ions inside the muscle fiber in the

called excitation-contraction

Excitation-Contraction
Coupling

way from one side of the muscle fiber to the opposite

tubules branch among themselves so that they form
entire planes

and they themselves contain extracellular fluid in their

when an action potential spreads over a muscle fiber

Conversely, full excitation of the T tubule and

ited and maintains a relaxed state of the muscle.

little to elicit contraction. Therefore, the troponin-

ions in the cytosol that bathes the myofibrils is too

The normal resting

Excitatory “Pulse” of Calcium Ions.

the tubules. In addition, inside the reticulum is a

brils back into the sarcoplasmic tubules. This pump can

high concentration. However, a continually active

have diffused among the myofibrils, muscle contrac-

traction, as discussed in Chapter 6.

this time, enough calcium ions are released into the

channels remain open for a few milliseconds; during

well as their attached longitudinal tubules. These

ticular cisternae where they abut the T tubule. This in

Figure 7–6 shows that the action potential of the T

potential occurs in the adjacent T tubule.

calcium ions in high concentration, and many of these

Release of Calcium Ions by the

round all surfaces of the actual contracting myofibrils.

tubules, and (2) long longitudinal tubules that sur-

that abut the T

yellow. This is composed of two major parts: (1) large

Figure 7–5 also shows a

electrical currents surrounding these T tubules then

T tubules to the deep interior of the muscle fiber. The

membrane, a potential change also spreads along the

Membrane Physiology, Nerve, and Muscle

Unit II

elicit the muscle contraction.

sarcoplasmic reticulum, in

chambers called terminal cisternae

Sarcoplasmic Reticulum

One of the special features of the sarcoplasmic reticu-
lum is that within its vesicular tubules is an excess of

ions are released from each vesicle when an action

tubule causes current flow into the sarcoplasmic re-

turn causes rapid opening of large numbers of calcium
channels through the membranes of the cisternae as

sarcoplasm surrounding the myofibrils to cause con-

Calcium Pump for Removing Calcium Ions from the Myofibrillar
Fluid After Contraction Occurs.

Once the calcium ions

have been released from the sarcoplasmic tubules and

tion continues as long as the calcium ions remain in

calcium pump located in the walls of the sarcoplasmic
reticulum pumps calcium ions away from the myofi-

concentrate the calcium ions about 10,000-fold inside

protein called calsequestrin that can bind up to 40
times more calcium.

state concentration (less than 10

-7

molar) of calcium

tropomyosin complex keeps the actin filaments inhib-

sarcoplasmic reticulum system causes enough re-
lease of calcium ions to increase the concentration
in the myofibrillar fluid to as high as 2

¥ 10

-4

molar

Terminal

Transverse

Triad of the

A band

I band

Sarcotubules

Myofibrils

Z line

reticulum

Sarcolemma

tubule

cisternae

Mitochondrion

Sarcoplasmic
reticulum

Colard Keene.)

DW: A Textbook of Histology.

(Redrawn from Bloom W, Fawcett

two T tubules per sarcomere,

mammalian heart muscle, but

sarcomere, located at the Z line. A

This illustration was drawn from frog

tubules that surround all sides of

longitudinal sarcoplasmic reticulum

deep in the muscle fiber, each T

mic reticulum system. Note that

Transverse (T) tubule–sarcoplas-

Figure 7–5

the T tubules communicate with the
outside of the cell membrane, and

tubule lies adjacent to the ends of

the actual myofibrils that contract.

muscle, which has one T tubule per

similar arrangement is found in

mammalian skeletal muscle has

located at the A-I band junctions.

Philadelphia: WB Saunders, 1986.
Modified after Peachey LD: J Cell
Biol 25:209, 1965. Drawn by Sylvia

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Van der Kloot W, Molgo J: Quantal acetylcholine release at

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Toyoshima C, Nomura H, Sugita Y: Structural basis of ion

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Tang W, Sencer S, Hamilton SL: Calmodulin modulation of

Pharmacol Sci 23:569, 2002.

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Schiaffino S, Serrano A: Calcineurin signaling and neural

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Rekling JC, Funk GD, Bayliss DA, et al: Synaptic control of

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Allman BL, Rice CL: Neuromuscular fatigue and aging:

action potentials, as discussed in Chapter 6.

ruption for long intervals, a series of calcium pulses

occurs. If the contraction is to continue without inter-

During this calcium pulse, muscle contraction

about 1/3 of a second because of the long duration of

less in others. (In heart muscle, the calcium pulse lasts

lasts about 1/20 of a second, although it may last

this calcium “pulse” in the usual

depletes the calcium ions again. The total duration of

contraction. Immediately thereafter, the calcium pump

concentration, a 500-fold increase, which is about 10

Excitation of Skeletal Muscle: Neuromuscular Transmission and Excitation-Contraction Coupling

Chapter 7

times the level required to cause maximum muscle

skeletal muscle fiber

several times as long in some fibers and several times

the cardiac action potential.)

must be initiated by a continuous series of repetitive

References

Also see references for Chapters 5 and 6.

2003.

sion in skeletal muscle by slow conducting afferent fibers:

neurophysiological basis and implication for respiratory

pumping by Ca

ATP

Action potential

Calcium pump

required

Actin filaments

Sarcolemma

Myosin filaments

calcium pump.

mic reticulum and then (2) re-

calcium ions from the sarcoplas-

potential that causes release of

Figure 7–6

Excitation-contraction coupling in
the muscle, showing (1) an action

uptake of the calcium ions by a