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Nerve Cells = polar cells
Motorneurons are small cells in the spinal cord that sends its long projections out, which is like a
long tube, to project signals. The signals that are being sent have to travel over a large distance
relative to the sides of the cells. This is a problem b/c electrical signals diminish in amplitude with
distance.
Think about why this is the case? And how this is overcome?
Describe the changes in membrane permeability that occur when the membrane of a neuron is
depolarised to threshold, and how they produce the changes in membrane potential that we refer to as
the action potential.
What are meant by the terms “threshold for the action potential” and “the all-or-none action
potential”?
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Motorneurone from the spinal cord, it receives excitable input from the motor cortex, brainstem
and if the excitable signals are great enough they narrate  action potentials
Hence these motorneurones (i.e. a projection neurone) work by receiving excitable signals not
from one but from many excitable synapses from the input part of the cell
If the excitable signals reach a significant threshold (value)  result in nerve impulse/ an action
potential / spike generated that propagate down the axon
Where the 'spike' happens it is referred to the excitability of nerves
Nerves and muscle cells have ion channels (like every other cell) but only nerve and muscles are excitable in
this way, i.e. when they reach a certain threshold value they set of an 'all or none' nerve impulse action
potential.
Why do you need excitatory of nerves and a threshold?
1. Amplification. It has a long axon (1m+). It has a
long distance to travel, and signals diminish over
distance. There is conductive fluid in the middle
of the cell i.e. cytoplasm and return path through
the extracellular fluid. Hence need the action
potential excitability property in nerves is to
amplify the signal (since signal diminish with
distance) and allow the signal to travel further.
2. Gate flow of information. The cell is processing information, descending in the cell all the time,
motorneurone bombarded with information from the brain, periphery, pattern generators
form the spinal cord. If all the information was passed on this neuron would be active all the
time. This is the same for central neurons. They have a gated system to stop information
flowing unless it is really important information. The information comes in as analogue signals,
small depolarisations that can add together as they descend down through the dendritic to the
soma to the axon hillock. But unless they reach a certain threshold value, the signals go
nowhere, unless they are amplified. Hence, need system in the nervous system to gate the flow
of information overload. Only signals that reach a
certain threshold value will be passed on from
one cell to another in the circuit
*axon hillock is the anatomical part of a neuron
that connects the cell body (the soma) to the
axon. It is described as the location where the
summation of inhibitory postsynaptic potentials
(IPSPs) and excitatory postsynaptic potentials
(EPSPs) from numerous synaptic inputs on the
dendrites or cell body occurs.
1 |Action Potential Generation and Propagation
Depolarising signals diminish with distance from the
source
 Most central neurons are contacted by other
neurons that form excitatory synapses on their
dendrites
 When excitatory synapses are active, ligand gated
ion channels produce inward sodium currents
depolarising the membrane
 The inward current tends to raise the membrane
potential
 The spread of such graded depolarisations is limited
by intrinsic electrical
 Amplification is needed
Depolarisation initiates neuronal signalling (electrical signalling)
 Excitatory signals means that instead of the membrane being at steady resting level (e.g. -60mV)
due to the continuous flow of potassium through the leakage channels and sodium diffusing in
through the sodium leakage channels. In this steady state, there is a rise in membrane potential 
reach threshold value  result action potential
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Membrane is depolarised when there is a next inward current
Depolarisation is usually initiated by opening of ligand gated cation channels at an excitatory
synapse
Depolarisation can also be triggered artificially, by applying an electrical stimulus
Action Potentials Travel long distances without losing strength
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Action potentials aka spikes, differ from graded potentials in that they do not diminish in strength
as they travel through the neuron. The ability of a neuron respond rapidly to a stimulus and fire an
action potential is called the cell's excitability.
The strength of the graded potential that initiates an action potential has no influence on the
amplitude of the action potential. Action potentials are sometimes called all-or none phenomena
b/c they either occur as a maximal depolarization (if the stimulus reaches threshold) or do not
occur at all (if the stimulus is below threshold).
An action potential measured at the distal end of an axon is identical to the action potential that
started at the trigger zone. This property us essential for the transmission of signals over long
distances, such as from a fingertip to the spinal cord.
2 |Action Potential Generation and Propagation
Describe the functional characteristics of the voltage-gated sodium ion channels responsible for
producing the depolarisation phase of the action potential.
Describe in your own words the changes that occur in membrane permeability during the rising phase
of the action potential.
Describe the characteristic channel-gating properties of the voltage-gated sodium and voltage-gated
potassium channels that together give rise to the successive changes in membrane potential during the
action potential. Consider: ion permeability, kinetic (speed) of channel opening and channel
inactivation associated with each of these channel types.
The Action Potential
Recording the changes in membrane potential as excitatory signally comes through the cell and
triggers an action potential: (in the cytoplasm of the axon)
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Resting membrane potential
Triggering then happens where the excitatory synapses become particularly active
Membrane potential rises
Reach threshold value then result in 'all or none ' action potential
*All or none action potential. Involves the rapid rise (exponential rise) in membrane potential
reaching a peak value where it stops rising (never quite reaches the nerve potential for sodium),
repolarises back, even hyperpolarises below the resting level, and finally returns back to the resting
potential.
 Action potential sequence: triggering event rapid depolarisation rapid repolarisation
hyperpolarisation return back to the resting level
3 |Action Potential Generation and Propagation
Action Potentials Represent Movement of Na+ and K+ across the Membrane
Action potentials occur when voltage-gated ion channels open, altering membrane permeability to
Na+ and K+. The graph shows the voltage and ion permeability changes that take place in one section
of membrane during an action potential. The graph can be divided into 3 phases:
1. The rising phase of the action potential,
2. The falling phase and
3. The after-hyperpolarisation phase
Before and after the action potential, at (1) and (9), the neuron is at its resting membrane potential of
-70mV.
The rising phase of the action potential.
 Is due to a sudden temporary increase in the cell's permeability to Na+
 An action potential begins when a graded potential reaching the trigger zone (2) depolarizes the
membrane to threshold (-55mV) (3).
 As the cell depolarises, the voltage gated Na+ channels open  making the membrane much more
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permeable to Na+. B/c Na+ is more concentrated outside the cell and b/c the negative membrane potential
inside the cell attracts these positively ions, Na+ flows into the cell
The addition of positive charge to the intracellular fluid depolarizes the cell membrane, making it
progressively more positive (shown by the steep rising phase on the graph (4)). In the top 3rd of the rising
phase, the membrane potential has reversed polarity; i.e. the inside of the cell has become more positive
than the outside. This reversal is represented on the graph by the overshoot, that portion of the action
potential above 0mV.
As soon as the cell membrane potential becomes positive, the electrical driving force moving Na+ into the
cell disappears. However, the Na+ concentration gradient remains, so Na+ continues to move into the cell.
As long as Na+ permeability remains high, the membrane potential moves toward the Na+ equilibrium
potential (ENa) of +60mV. However, before the ENa is reached, the Na+ channels in the axon close. Sodium
permeability decreases dramatically, the action potential peaks at +30mV (5)
*ENa = is the membrane potential at which the movement of Na+ into the cell down its concentration
gradient is exactly opposed by the positive membrane potential
The falling phase of the action potential
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...corresponds to an increase in K+ permeability
Voltage-gated K+ channels, like Na+ channels, start to open in response to depolarisation.
The K+ channel gates are much slower to open, however, the peak K+ permeability occurs later
than peak Na+ permeability (see ion permeability graph). By the time the K+ channels are open, the
membrane potential of the cell has reached +30mV b/c of the Na+ influx through faster-opening
Na+ channels
When the Na+ channels close at the peak of the action potential, the K+ channels have just finished
opening, making the membrane very permeable to K+. At a positive membrane potential, the
concentration and electrical gradients for K+ favor movement of K+ out of the cell. As K+ moves out
of the cell, the membrane potential rapidly becomes more negative, creating the falling phase of
the action potential (6) and sending the cell toward its resting potential
When the falling membrane potential reaches -70mV the voltage-gated K+ channels have not yet
closed. Potassium continues to leave the cell through both voltage-gated and K+ leak channels, the
membrane hyperpolarises, approaching the EK of -90mV. This after hyperpolarisation (7) is also
called the undershoot. Once the slow voltage-gated K+ channels finally close, some of the outward
K+ leak stops (8). Retention of K+ and Na+ leak inward bring the membrane potential back to 70mV (9), the value that reflects the cell's resting permeability to K+, Cl- and Na+
In summary...
 The action potential is a change in membrane potential that occurs when voltage-gated ion
channels the membrane open, increasing the cell's permeability first to Na+ and then to K+. The
4 |Action Potential Generation and Propagation
influx (movement into the cell) of Na+ depolarizes the cell. This depolarisation is followed by K+
efflux (movement out of the cell), which restores the cell to the resting membrane potential
Voltage- gated sodium channels
 Closed when the membrane is polarised
 Begin to open as the membrane depolarises
 Selectively permeable just Na+
 Begin to inactivate as the membrane depolarises
 Inactivation shuts off the Na+ current flow
 'voltage gates' and ' activation gates'
Voltage gated potassium channels
 Mostly closed when the membrane is polarised
 Begin to open as the membrane depolarises
 Do not inactivate
 Fraction of channels open increases proportionately w/ depolarisation
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Voltage-gated channels are closed most of the time but has a gate so that the pore of the channel
can open or close
Voltage channels are closed at resting membrane potential (at -60mV)
Membrane permeability depends on the membrane leakage channels
As the membrane becomes depolarised
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Rapid increase of membrane permeability to Na  changing the normal balance; Resting membrane is
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20x more permeable to K than to Na
Membrane becomes much more permeable consequently (driving forces: inward chemical driving force &
inward electrical driving force) Na diffuses in at a faster rate  since there are more ion channels
permeable to Na+
The rate of movement of Na+ is measured as a current
5 |Action Potential Generation and Propagation
Model of the voltage-gated Na+ channel
Na+ Channels in the axons have 2 gates
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6 |Action Potential Generation and Propagation
Voltage gated Na channels have 2 gates to
regulate ion movement rather than a single gate
The 2 gates known as:
1. Activation
2. Inactivation
Flip-flop back and forth to open and shit the Na
channel
When a neuron is at its resting membrane
potential, the activation gate of the Na channel is
closed and no Na moves through the channel (a)
The activation gate, apparently an amino acid
sequence resembling a ball and chain on the
cytoplasmic side of the channel is open.
When the cell membrane near the channel
depolarises, the activation gate swings open (b)
This opens the channel pore and allows Na to
move into the cell down its electrochemical
gradient (c)
The addition of positive charge further
depolarises the inside of the cell and starts a
positive feedback loop.
More Na channels open, and more Na enters,
further depolarising the cell. As long as the cell
remains depolarised, activation gates in Na
channels remain open
As happens in all positive feedback loops, outside
intervention is needed to stop the escalating
depolarisation of the cell. This outside
intervention is the role of the inactivation gates in
the Na channels.
Both activation &inactivation gates move in
response to depolarisation, but the activation
gate delays its movement by 0.5msec. During that
delay the Na+ channel open, allowing enough Na+
influx to create the rising phase of the action
potential. When the slower inactivation gate
finally closes (d), Na+ influx stops and the action
potential peaks.
While the neuron repolarises during K+ efflux, the
Na+ channel gates reset to their original positions
so they can respond to the next depolarisation
(e).
Thus, voltage gated Na+ channels use a 2-step
process for opening and closing rather than a
single gate that swings back and forth.
This important property allows electrical signals
along the axon to be conducted in only one
direction.
What are the relationships among membrane potential, channel gating and transmembrane currents
during the Hodgkin Cycle?
Hodgkin Cycle
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Stimulus depolaristion opens a small fraction of voltage gated
Na+ channels
Increase in inward current through these Na+ channels further
depolarises the membrane
As membrane depolarises more, a greater fraction of the Na+
channels open leading to more depolarisation etc.
Voltage-gated Na+ channels can exist in multiple states
The Hodgkin cycle represents a positive feedback loop in
which an initial membrane depolarization leads to
uncontrolled deflection of the membrane potential to near
VNa. The initial depolarization must reach or surpass
threshold in order to activate voltage-gated Na+ channels.
Opening of Na+ channels allows Na+ inflow which, in turn,
further depolarizes the membrane. Additional
depolarization activates additional Na+ channels. This cycle
leads to a very rapid rise in Na+ conductance (gNa), which
moves the membrane potential close to VNa.
Ion movement during an action potential
The entry of Na+ into the cell creates a positive feedback loop that stops when the Na+ channel
inactivation gates close
7 |Action Potential Generation and Propagation
What are the key differences in inactivation properties of the voltage-gated Na+ and K+ channels?
Explain how these relate the structure of the channels and to the absolute refractory
period of nerves.
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The double gating of Na+ channels plays a major role in the phenomenon known as the refractory
period
The 'stubbornness'of the neuron refers to the fact that once an action potential has begin, a
second action potential cannot be triggered for about 2 msec, no matter how large the stimulus.
This period is called the absolute refractory period and represents the time required for the Na+
channel gates to reset to their resting positions. The absolute refractory period ensures that a
second action potential will not occur before the first has finished.
Action potentials cannot overlap and cannot travel backward because of their refractory periods.
A relative refractory period follows the absolute refractory period. During the relative refractory
period, a stronger-than-normal depolarising graded potential is needed to bring the cell up
threshold, the action potential will be smaller than normal. During this time, many but not all Na+
channel gates have reset to their original positions and a threshold-level depolarisation will open
them. Those Na+ channels that have not quite returned to their resting position can be opened by
a higher-than-normal graded potential.
During the relative refractory period, K+ channels are still open. Although Na+ can enter through
newly reopened Na+ channels, depolarisation due to Na+ entry will be offset by K+ loss. As a result,
any action potentials that fire will have a smaller amplitude than normal
The refractory period is a key characteristic that distinguishes action potentials from graded
potentials. If 2 stimuli reach the dendrites of a neuron within a short time, the successive graded
potentials created by those stimuli can be added to one another. If, however, 2 suprathreshold
graded potentials reach the action potential trigger zone within the absolute refractory period, the
2nd graded potential will be ignored b/c the Na+ channels are inactivated and are incapable of
being opened again so soon.
Refractory periods limit the rate at which signals can be transmitted down a neuron. The absolute
refractory period also ensures one-way travel of an action potential from cell body to axon
terminal by preventing the action potential from travelling backward
8 |Action Potential Generation and Propagation
Refractory Periods
During the refractory period, no stimulus can trigger another action potential. During the relative
refractory period, only a larger-than-normal stimulus can initiate a new action potential. A single
channel shown during a phase means that the majority of channels are in this state. Where more than
one channel of a particular type is shown, the population is split between the states.
9 |Action Potential Generation and Propagation
Describe the characteristic arrangement of the soma, axon, dendrites and axon terminal of a somatic
motor neuron and explain the roles that these structures play in the function of the neuron.
Axon.
 is the elongated fiber that extends from the cell
body to the terminal endings and transmits the
neural signal.
 The larger the axon, the faster it transmits
information.
 Some axons are covered with a fatty substance
called myelin that acts as an insulator. These
myelinated axons transmit information much faster
than other neurons.
Characteristics:
 Most neurons have only one axon.
 Transmit information away from the cell body.
 May or may not have a myelin covering.
Soma.
 Aka. Cell body
 is where the signals from the dendrites are joined and passed on.
 The soma and the nucleus do not play an active role in the transmission of the neural signal.
Instead, these two structures serve to maintain the cell and keep the neuron functional.
 The support structures of the cell include mitochondria, which provide energy for the cell, and the
Golgi apparatus, which packages products created by the cell and secretes them outside the cell
wall.
Dendrites.
 are treelike extensions at the beginning of a neuron that help increase the surface area of the cell
body and are covered with synapses.
 These tiny protrusions receive information from other neurons and transmit electrical stimulation
to the soma.
Characteristics:
 Most neurons have many dendrites.
 Short and highly branched.
 Transmits information to the cell body.
Axon terminal of a somatic motor neuron.
 Motor neuron: a nerve cell in the spinal cord, rhombencephalon, or mesencephalon characterized
by having an axon that leaves the central nervous system to establish a functional connection with
an effector (muscle or glandular) tissue
 somatic motor neuron directly synapse with striated muscle fibers by motor endplates
Neurons.
 are the basic building blocks of the nervous system.
 These specialized cells are the information-processing units of the brain responsible for receiving
and transmitting information.
 Each part of the neuron plays a role in the communication of information throughout the body.
Axon Hillock.
 is located and the end of the soma and controls the firing of the neuron. If the total strength of the
signal exceeds the threshold limit of the axon hillock, the structure will fire a signal down the axon
10 |Action Potential Generation and Propagation
Describe the differences between non-gated, ligand-gated and voltage-gated ion channels.
Non-gated channels.
 open channels, spend most of the time with their gate open, allowing ions to move back and forth
across the membrane without regulation
 these gates may occasionally flicker closed, but for most part behave as if they have no gates
Ligand-gated channels.
 Aka. ionotropic receptors, this group of channels open in response to specific ligand molecules
binding to the extracellular domain of the receptor protein.
 Ligand binding causes a conformational change in the structure of the channel protein that
ultimately leads to the opening of the channel gate and subsequent ion flux across the plasma
membrane.
 Examples of such channels include the cation-permeable "nicotinic" Acetylcholine receptor,
ionotropic glutamate-gated receptors and ATP-gated P2X receptors, and the anion-permeable γaminobutyric acid-gated GABAA receptor.
 Gated channels:
- Spend most time in closed state, allows channels to regulate the movement of ions through them
- When a gated channel opens, ions move through the channel just as they move through open
channels.
- When a gated channel is closed, it allows no ion movement b/w the intracellular and extracellular
fluid
Voltage-gated ion channels
 are a class of transmembrane ion channels that are activated by changes in electrical potential
difference near the channel; these types of ion channels are especially critical in neurons, but are common
in many types of cells.
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They have a crucial role in excitable neuronal and muscle tissues, allowing a rapid and co-ordinated
depolarisation in response to triggering voltage change. Found along the axon and at the synapse,
voltage-gated ion channels directionally propagate electrical signals.
What is meant by depolarised? Hyperpolarised? Threshold?
11 |Action Potential Generation and Propagation
Depolarised.
 A decrease in the potential difference across the cell membrane of a neuron. Most neurons
depolarize in response to stimulation.
Hyperpolarised.
 An increase in the potential difference across the cell membrane of a neuron.
 The interior become more negative or more positive--the charge is moving away from zero in one
direction or the other. This occurs after action potential.
Threshold.
Considering the role of ion-leakage channels, explain why the resting membrane potential for most
neurons is in the negative range of about -50mV to -80mV. Why isn't it positive? Why might
electrophysiologists find differences among neurons in their resting membrane potentials?
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When a neuron is at rest, the plasma membrane is far more permeable to K+ ions than to other
ions present, such as Na+ and Cl-. The electrochemical equilibrium that results from the
distribution of these ion species across the membrane, together with the relative permeabilities of
each ion, is responsible for the -60mV charge that can be measured across the membrane. i.e. the
resting membrane potential.
Many of the body's solutes, including organic compounds such as pyruvate and lactate, are ions
and therefore carry a next electrical charge. K+ is the major cation within cells, and Na+ dominates
the extracellular fluid. Cl- ions mostly remain with Na+ in the extracellular fluid, whereas
phosphate ions and negatively charged proteins are the major anions of the intracellular fluid.
However, the intracellular compartment is not electrically neutral: there are high concentration of
large, negatively charged proteins/ anions that do not have matching cations  giving the cell a
negative charge
12 |Action Potential Generation and Propagation
Outline the influence of the Na+/K+ ATPase (Na+/K+ pump) on the resting membrane potential. Does it
repolarise the membrane after each action potential? Explain its true neurophysiological role in relation
to neuronal signalling.
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Na+/K+-ATPase helps maintain resting potential, avail transport
and regulate cellular volume
The pump uses energy from ATP to exchange Na+ that enters
the cell for K+ that leaked out of it
(this exchange does not need to happen before the next action
potential fires, however, b/c the ion concentration gradient
was not significantly altered by one action potential)
A neuron without a functional Na+/K+pump may fire a
thousand or more action potentials before a significant change
in the ion gradients occurs
In the figure are two triangles that indicate concentration gradients of Na+ and K+ across the membrane.
The Na+-K+ ATPase will transport Na+ ions against its concentration gradient and K+ ions against its
concentration gradient.
1. 3 Na+ ions bind to the ATPase under conditons of low Na+ concentrations because ATP andthe
transport protein has a high affinity for Na+. This means the protein will bind Na+ ions even
when the Na+ concentration is low Mg++ bind to the protein . These are exergonic reactions
2. The transport protein cleaves ATP into ADP and Phosphate ion.The phosphate ion becomes
covalently bonded to the protein.The phosphorylation of the protein causes it to become
energetically unstable and the protein changes conformation.The shift in conformation of the
protein in some manner causes the Na+ to travel across the protein and they are released from
the protein on the other side of the membrane because the protein now has a low affinity for
Na+ .These are exergonic processes
3. K+ ions bind to the protein even it there is a low K+ concentration because in this conformation
the protein has a high affinity for K+ ions.The covalently bound phosphate group is cleaved
from the protein which causes the protein to undergo another conformational shift
4. This conformational shift causes the K+ to be in some manner transported across the protein
and released on the other side of the membrane. The K+ ion is released because now the
protein has a low affinity for K+ ions. The protein is restored to the ordinal conformation of the
protein and the process starts again .
13 |Action Potential Generation and Propagation
Motor neurons receive converging signals from interneurons, afferents and descending upper motor
neurons. What do we mean by this? Describe the way in which the activity received by these converging
inputs can activate the motor neuron.
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Motoneuron firing is the result of summed actions of many excitatory synaptic inputs
Motoneurons are contacted by the terminals of many interneurons, afferent fibres and descending
pre-motor axons
Excitatory Postsynaptic Potentials (EPSPs) are the brief depolarizations produced by inward Na+
currents at these synapses
Action potentials are generated when many such excitatory synapses are active at the same time
to produce sufficiently large EPSPs.
14 |Action Potential Generation and Propagation
The abundance of synapses on a
postsynaptic neuron.
The cell body and dendrites of a somatic
motor neuron are nearly covered by
hundreds of axon terminals from other
neurons.
Continuous Propagation
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The action potential normally starts at the axon hillock where the density of voltage-gated Na+
channels is high
In non-myelinated nerves the action potential propagates continuously along the axons by
sequentially activating populations of Na+ channels in adjoining segments of axon
15 |Action Potential Generation and Propagation
Conduction of action potentials
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The stimulus is a graded potential above threshold that enters the trigger zone (1)
The depolarisation opens voltage-gated Na+ channels, Na+ enters the axon, the initial segment of
axon depolarizes (2)
Positive charge from the depolarised trigger zone spreads to adjacent sections of membrane (3),
repelled by the Na+ that entered the cytoplasm and attracted by the negative charge of the resting
membrane potential
The flow of local current toward the axon terminal begins conduction of the action potential. When
the membrane distal to the trigger zone depolarises, its Na+ channels open, allowing Na+ into the
cell (4). This starts the positive feedback loop: depolarisation opens Na+ channels, Na+ enters,
causing more depolarisation and opening more Na+ channels in the adjacent membrane. The
continuous entry of Na+ down the axon toward the axon terminal means that the strength of the
signal does not diminish as the action potential propagates itself.
As each segment of axon reaches the peak of the action potential, its Na+ channels inactivate.
During the action potential's falling phase, K+ channels are open, allowing K+ to leave the
cytoplasm. Finally, the K+ channels close and the membrane in that segment of axon returns to its
resting potential.
16 |Action Potential Generation and Propagation
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Although positive charge from a depolarised segment of membrane may flow backward toward the
cell body (5), depolarisation in that direction has no effect. The section of axon proximal to the
active region is in the absolute refractory period, with its Na+ channels inactivated; therefore, the
action potential does not move backwards.
17 |Action Potential Generation and Propagation
Saltatory propagation in myelinated fibres
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Adaptation to permit faster propagation
Myelin internodes formed by oligodendrocytes wrapped around internode regions of axons
(~0.2mm long)
Inward current during the rising phase of the action potential creates “local circuits”
Local circuits depolarise neigbouring “Node of Ranvier” stimulating regeneration of the action
potential
18 |Action Potential Generation and Propagation
Myelination changes the passi ve el ectrical properties of the axon membrane, thus increasing the
spread of the depolarising inward curr ent, and reducing delays. Small portions of the axon membrane
(Node s of Ranvi er generate the depolarising inward current (Hodgkin Cy cle ). Whether generated
artifi cially by a stimulator as shown, or naturall y by the Hodgkin Cycle , the incr eased membrane
resistance due to the thi ck , insulating myelin sheath means that the brief depolarising inward
current can spread much further along the axon. The reduc ed t endency to store charge ( capacitance)
within the my elinated internode region means that the brief depolarisation moves mor e qui ckly from
one Node of Ranvi er to the next .
In saltatory propagation
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Voltage-gated Na+ channels are concentrated at the axon hillock and Nodes of Ranvier
The Hodgkin Cycle is triggered at one Node after another. This amplifies the signal.
The signal travels passively as an electrical current between Nodes.
The thick myelin insulation of the Internode allows the local circuit current to spread much further
and faster than in un-myelinated fibres
Loss or myelin sheath (demyelination)
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Increases permeability of membrane to ions in the demyelinated internode regions
Reduced membrane electrical resistance leads to loss of amplitude of signal
Increased membrane capacitance in the denervated internode regions
Inevitable slowing of action potential propagation through regions with high membrane
capacitance.
19 |Action Potential Generation and Propagation