1. Explain the various phases of action potentials. 2. D efine action potential and threshold potential. 3. Explain the effects of myelination on an axons ability to conduct action potentials. 4. What is the all-or-none phenomenon? 5. Describe “resting potential.”
Cell Membrane
Potential
A cell membrane’s surface is
usually electrically charged (polarized) compared with its inner contents. This
is due to unequal amounts of positive and negative ions and is important for
conduction of nerve and muscle impulses. Adequate stimulation of a neuron
causes gen-eration of an electrical impulse in response. An action potential is
a change in neuron membrane polarization and a return to its resting state. An
action potential forms a nerve impulse propagated along an axon. The human body
is electrically neutral, with the same num-ber of positive and negative electrical
charges. Some regions, however, are positively or negatively charged. Opposite
charges attract each other, requiring energy to separate them. Therefore, when
opposite charges come together, energy is liberated to perform cellular work.
The threshold
potential causes permeability to sud-denly
change. Sodium channels open and sodium diffuses freely inward. The membrane
becomes depo-larized. Nearly simultaneously, potassium channels open to allow
potassium to diffuse freely outward. The inside of the membrane becomes briefly
hyperpolar-ized and then repolarized to its resting
potential. For example, if the resting membrane potential is ‒70 mV and the
threshold is ‒60 mV, a membrane potential of ‒62 mV will not produce an action
potential. The action
potential is defined as this
rapid sequence of depolarization and repolarization, taking only about one-thousandth of a second. Only cells
with excitable membranes can generate action potentials. These cells include
muscle cells and neurons. Synaptic activity produces graded potentials in
postsynaptic cell plasma membranes.
The terms depolarization and hyperpolarization describe
membrane potential changes that are related to resting membrane potential. In
depolarization, the inside of the membrane becomes less negative (e.g., it
moves from ‒70 to ‒60 mV). In hyperpolarization, the inside of the membrane
becomes more negative. Many action potentials can occur, and resting potentials
can be reestablished before the concentrations of sodium and potassium
significantly change. Active transport inside the membranes maintains the
original concen-trations on either side. Action potentials do not decay with
greater distance traveled.
In skeletal muscle cells and
neurons, action poten-tial generation and transmission occur in the same way.
Action potentials are usually generated only in axons, with neurons generating
them only when enough stimulation occurs. Stimuli change the neuron membrane’s
permeability via the opening of certain voltage-gated channels on the axon.
Changes in the membrane potential cause these channels to open and close (FIGURE 11-8A). Graded potentials (local currents)
activate them, with these currents spreading toward axons along the dendrite
and cell body membranes. The method in which an action potential is generated is shown in FIGURE 11-8B.
Beginning with a neuron in its
polarized (resting) state, all gated sodium and potassium ion channels are
closed. Leakage channels are the only ones open, and they maintain resting
membrane potential. Depolariza-tion opens sodium channels and then inactivates
them. The axon membrane is first depolarized, followed by sodium channels
opening and the rushing in of sodium ions into the cell. These positively
charged ions depo-larize the local membrane area to a greater degree, opening
more sodium channels. The cell interior, there-fore, becomes less negative on a
continual basis. When threshold is reached at the stimulation site,
depolar-ization becomes self-generating. Threshold is usually between ‒55 mV
and ‒50 mV. Positive feedback assists the process, with depolarization being
driven by ionic currents that were created by the sodium ion influx.
In repolarization, sodium channels are inactivating, with potassium channels open. The intense rise of action potential is only about 1 msec in length, being self-limited because of the slow inactivation gates of the sodium channels closing at this time. The membrane permeability to sodium, therefore, reduces to resting levels. The net influx of sodium ions completely stops, meaning the action potential spike stops its rise. The slow potassium channels open and potassium quickly leaves the cell along its electrochemical gradient. The internal negativity of the resting neuron is, therefore, restored (repolarization). The fast decline in sodium permeability and the increased potassium permeability aid in repolarization.
In hyperpolarization, some potassium ion channels remain open and
sodium ion channels are reset. Usu-ally, the time in which increased potassium
permea-bility occurs lasts longer than is actually required to restore the
resting state. A hyperpolarization is seen on the action potential curve,
appearing as a small dip after the spike; this is the result of excessive
potassium ion efflux before the closure of the potassium channels.
Action potentials are not always
produced by depo-larization events. For depolarization to produce an action
potential, it must reach threshold values to make an axon “fire.” Threshold may
be the membrane potential at which potassium movement’s outward current is
identical to sodium movement’s inward current. When the membrane has been depolarized
by 15 mV to 20 mV from its resting value, threshold is usually reached. An
action potential is, therefore, an all-or-none
phenomenon, a principle occurring
completely or not at all.
A neuron cannot respond to any
amount of stimulus when an area of neuron membrane is generating an action
potential and its voltage-gated sodium chan-nels are opened. The absolute refractory period is the period from which sodium channels open until they begin to reset
to their resting state. This period results in each action potential being a
unique all-or-one occurrence. It also enforces the one- way transmission of
the action potential. The interval that follows the absolute refractory period
is the relative refractory period. At this time, most sodium
channels have resumed their resting
state, but some potassium channels are still open, and repolarization is
occurring.
Propagation of action potentials may occur in several different ways. In unmyelinated axons, con-tinuous propagation
is the method by which action potentials move. At the first segment of the
axon, there is a brief change of the transmembrane poten-tial when it becomes
positive instead of negative.
As sodium ions begin to move, a
local current devel-ops, spreads, and depolarizes nearby areas of the membrane.
A chain reaction occurs, with the process repeating and moving the action
potential forward but not backward. Backward movement is prevented by the
previous axonal segment still being in its abso-lute refractory period. The
furthest portions of the plasma membrane are eventually affected. The action
potential that reaches the synaptic terminal is identi-cal to the one that was
initially generated. Continuous propagation occurs at a rate of approximately 1
meter per second, which is about 2 miles per hour. A second stimulus is needed
for a second action potential to occur at the same site.
In the CNS and PNS, saltatory propagation moves
action potentials much more quickly along axons. An action potential appearing
at the first segment of a myelinated axon avoids the internodes and
depolarizes the nearest node to threshold. The action potential jumps the 1–2
mm distance between the nodes in a large, myelinated axon. This requires less
energy than continuous propagation, because there is less surface area involved
and not as many sodium ions are needed to be pumped from the cytoplasm.
Because of active transport, body
cells have more sodium ions outside of them and more potassium ions inside
them. These cells’ cytoplasm contains many negatively charged phosphate ions,
sulfate ions, and proteins. Distribution of ions is determined partly by selectively permeable channels located
in the cell mem-branes. Some are open, whereas others can open or close.
Certain channels can allow specific ions to pass through, whereas others
cannot. Potassium ions pass through cell membranes more easily than sodium
ions. Therefore, potassium ions contribute greatly to membrane polarization.
Membrane channels are large proteins with subunits. Their amino acid chains
are distributed in a back and forth pattern across the membrane. Those known as
leakage (nongated) channels remain open constantly. These are also called passive channels . Gated channels open and close based on certain signals. These are also called active channels . Every gated channel
can either be closed but able to
open, open (also called activated),
or closed and unable to open (also called inactivated).
Chemically gated channels bind to
specific chem-icals to open or close. Examples include the receptors that bind
acetylcholine (ACh) at neuromuscular junctions. These channels are most common
on dendrites and cell bodies of neurons. Voltage-gated channels respond to changes in the transmembrane potential by opening or closing, and are common on excitable membranes, which are those that can generate or conduct
action potentials. These channels are common on the sarcolemma of skeletal or
cardiac muscle fibers and the axons of unipolar and multipolar neurons. Mechanically gated channels respond to physical distortions of membrane surfaces by opening or
closing. They are important in sensory receptors involving pressure, touch, or
vibration.
Sodium and potassium ions move
from areas of high concentration to areas of low concentration, based on
permeability. Because resting cell membranes are more permeable to potassium
ions than sodium ions, the potassium ions diffuse out of cells more rapidly
than sodium ions diffuse. More positive charges leave the cell by diffusion
than enter it, making the outside of the cell membrane positive and the inside
negative. This difference in charges is called a potential differ-ence. In a resting nerve cell, this potential
difference is called a resting potential. If
undisturbed, the cell membrane remains polarized. Sodium and potas-sium
continue to be actively transported, maintaining the concentrations needed for
diffusion. Membrane voltage can be measured by using a voltmeter, with one microelectrode inserted into a neuron and the
other into its extracellular fluid. Membrane voltage is approximately ‒70 mV.
The minus sign means that the cytoplasmic (inside) portion of the membrane is
neg-atively charged compared with the outside portion. In different types of
neurons, the value of the resting membrane potential ranges from ‒40 to ‒90 mV.
The resting potential only exists across the membrane, with solutions inside
and outside the cell being elec-trically neutral. The resting potential is
generated by either differences in permeability of the plasma mem-brane to the
intracellular and extracellular fluids or differences in the ionic composition of these fluids.
A lower concentration of sodium
ions and a higher concentration of potassium ions exist in the cell cyto-sol in
comparison with the extracellular fluid. Anionic (negatively charged) proteins
aid in balancing the pos-itive charges of intracellular cations, which are
mostly potassium ions. The positive charges of sodium and other cations are
mostly balanced by chloride ions in the extracellular fluid. There are many
other solutes in both fluids, including glucose and urea. Even so, potassium
plays the chief role in generating the mem-brane potential.
When resting, the plasma membrane
is not perme-able to large anionic cytoplasmic proteins. It is slightly
permeable to sodium, but nearly 25 times more per-meable to potassium. Also, it
is highly permeable to chloride ions. These permeabilities are related to the
leakage ion channel properties. Along their concen-tration
gradient, potassium ions diffuse out of the cell very easily in comparison with how easily sodium ions can enter.
The cell becomes more negatively charged inside as potassium ions flow outward.
The slowly entering sodium ions cause the cell to become just slightly more
positive than it would be if only potas-sium was flowing. Therefore, at resting
potential, the cell’s negative interior is based much more on the abil-ity of
potassium to diffuse outward than it is on the entrance of sodium. Via the
adenosine triphosphate (ATP)-controlled sodium-potassium
pump, three sodium ions are ejected from the cell followed by two potassium
ions being transported back in. This pump stabilizes the resting potential via
maintenance of con-centration gradients for both sodium and potassium.
Nerve cells respond with
excitability to changes in the surroundings. Some can detect specific changes
such as temperature, pressure, or light from outside the body. Many neurons
respond to neurotransmit-ters from other neurons, usually affecting the resting
potential in a certain part of the nerve cell’s mem-brane. If the resting
potential decreases, it is described as being depolarized. The amount of change in resting potential is
proportional to the amount of the stim-ulus. The greater the stimulus, the
greater the depo-larization. Sufficiently depolarized neurons cause the
membrane potential to reach its threshold potential. When this happens, an
action potential is reached, which is the basis for the nerve impulse. The
primary method in which neurons send signals over long dis-tances throughout
the body is the generation and transmission of action potentials.
1. Explain
the various phases of action potentials.
2. D efine
action potential and threshold potential.
3. Explain the effects of myelination on
an axons ability to conduct action potentials.
4. What is
the all-or-none phenomenon?
5. Describe
“resting potential.”
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