Page 341 - Fundamentals of anatomy physiology

328 Unit 2 Support and Movement
Electrical Impulses and Excitable Membranes
10 As we learned in Chapter 3, all the cells of the body maintain a
membrane potential due to an unequal distribution of positive
and negative charges across their plasma membrane. p. 126
The unequal charge distribution means cells are polarized, much
like miniature batteries. In cells, the inner surface of the plasma
membrane is slightly negative compared to the outer surface.
The membrane potential is a measure of cellular polarization (in
­millivolt units) that compares the cytoplasmic membrane surface
charge to the extracellular membrane surface charge. In unstimu­
lated (resting) neurons and skeletal muscle fibers, typical resting
membrane potentials are −70 mV and −85 mV, respectively.
Recall that the main contributors of negative charges within
a cell are proteins that cannot cross the plasma membrane. There
is also an excess of sodium ions outside a cell and an excess of
potassium ions inside a cell. These ions can cross a membrane
through membrane channels that are specific for each ion.
Various stimuli can lead to a temporary change in the dis­
tribution of electrical charges across the plasma membranes of
all body cells. Differences in sodium ion and potassium ion
membrane permeability underlie such changes. An influx of
sodium ions leads to depolarization as the membrane potential
becomes less negative. The movement of potassium ions out of
a cell leads to hyperpolarization as the membrane potential be­
comes more negative. A return to the resting potential is called
repolarization. In most cells, the depolarization or hyperpolar­
ization of a plasma membrane is a localized change limited by
the presence or absence of stimulation. Called a graded poten-
tial, it does not continue to spread over the plasma membrane.
Neurons and skeletal muscle fibers, however, have electri­
cally excitable membranes. Excitable membranes permit rapid
communication between different parts of a cell. In neurons
and skeletal muscle fibers, the depolarization and repolarization
events produce an electrical impulse, or action potential, that is
propagated along their plasma membranes. Unlike the plasma
membranes of most cells, excitable membranes contain voltage-
gated channels that are activated and inactivated by changes in the
membrane potential. These electrical channels become activated
when the membranes of neurons and skeletal muscle fibers
first depolarize from the resting potential to a threshold potential site for calcium, and this site is empty when the muscle fiber is at
(from −70 to −60 mV for neurons and from −85 to −55 mV for
skeletal muscle fibers). Upon reaching the threshold potential,
voltage-gated sodium channels open and there is a rapid influx of
positively charged sodium ions into the cell. The inside of the
membrane reverses from a negative to positive charge, and the
depolarization peaks at a membrane potential of +30 mV with
the closure of the voltage-gated sodium channels. Repolarization
of the membrane then begins as voltage-gated potassium chan­
nels open and positively charged potassium ions leave the cell.
The loss of more positive charges than entered the cell causes
the membrane potential to become negative again. A “resting”
refractory period follows and the former concentrations of sodium
and potassium ions across the plasma membrane are restored
through the action of sodium–potassium ion pumps. p. 122
A further depolarization cannot occur until the refractory period
is over. As a result, the action potential travels in one direction
because the refractory period prevents it from propagating back
in the direction from where it was initiated.
The Control of Skeletal Muscle Activity
Skeletal muscle fibers begin contraction with the release of
their internal stores of calcium ions. That release is under the
control of the nervous system. Communication between a neu­
ron and another cell occurs at a synapse. When the other cell is a
skeletal muscle fiber, the synapse is known as a neuromuscular
junction (NMJ), or myoneural junction. The NMJ is made up of
an axon terminal (synaptic terminal) of a neuron, a specialized
region of the sarcolemma called the motor end plate, and, in
between, a narrow space called the synaptic cleft.
Motor neurons of the central nervous system (brain and
spinal cord) carry instructions in the form of action potentials
to skeletal muscle fibers. A motor neuron stimulates a muscle
fiber through a series of steps as shown in Spotlight Figure 10–9
(pp. 326–327).
Excitation–Contraction Coupling
The link between the generation of an action potential in the sarco­
lemma and the start of a muscle contraction is called e­ xcitation–
contraction coupling. This coupling occurs at the triads. On
reaching a triad, an action potential triggers the release of Ca2+
from the cisternae of the sarcoplasmic reticulum. The change
in the permeability of the SR to Ca2+ is temporary, lasting only
about 0.03 second. Yet within a millisecond, the Ca2+ concentra­
tion in and around the sarcomere reaches 100 times resting levels.
Because the terminal cisternae are l­ocated at the zones of overlap,
where the thick and thin filaments interact, the effect of calcium
ion release on the sarcomere is almost instantaneous. Troponin is
the lock that keeps the active sites inaccessible. Calcium is the key
to that lock. Recall from Figure 10–7b that troponin binds to both
actin and tropomyosin, and that the tropomyosin molecules cover
the active sites and prevent interactions between thick filaments
and thin filaments. Each troponin molecule also has a binding
rest. Calcium binding changes the shape of the troponin molecule
and weakens the bond between troponin and actin. The troponin
molecule then changes position, rolling the attached tropomyosin
strand away from the active sites (Spotlight Figure 10–10). With
this change, the contraction cycle begins.
The Contraction Cycle
The contraction cycle is a series of molecular events that en­
able muscle contraction. Spotlight Figure 10–11, pp. 330–331,
shows the interlocking steps of the contraction cycle.