It is over 60 years since Hodgkin and
Huxley1 made the first direct recording of
the electrical changes across the neuronal
membrane that mediate the action
potential. Using an electrode placed inside a
squid giant axon they were able to measure a
transmembrane potential of around 260 mV
inside relative to outside, under resting
conditions (this is called the resting membrane
potential). The action potential is a
transient (,1 millisecond) reversal in the
polarity of this transmembrane potential
which then moves from its point of initiation,
down the axon, to the axon terminals. In a
subsequent series of elegant experiments
Hodgkin and Huxley, along with Bernard
Katz, discovered that the action potential
results from transient changes in the permeability
of the axon membrane to sodium (Na+)
and potassium (K+) ions. Importantly, Na+ and
K+ cross the membrane through independent
pathways that open in response to a change
in membrane potential.
As testimony to their pioneering work, the
fundamental mechanisms described by
Hodgkin, Huxley and Katz remain applicable
to all excitable cells today. Indeed, the
predictions they made about the molecular
mechanisms that might underlie the changes
in membrane permeability showed remarkable
foresight. The molecular basis of the action
potential lies in the presence of proteins
called ion channels that form the permeation
pathways across the neuronal membrane.
Although the first electrophysiological
recordings from individual ion channels were
not made until the mid 1970s,2 Hodgkin and
Huxley predicted many of the properties now
known to be key components of their
function: ion selectivity, the electrical basis
of voltage-sensitivity and, importantly, a
mechanism for quickly closing down the
permeability pathways to ensure that the
action potential only moves along the axon in
one direction.
2. Communicate
Neurons communicate by means of an electrical
signal called the Action Potential
Action Potentials are based on movements of ions
between the outside and inside of the axon
When an Action Potential occurs, a molecular
message is sent to neighboring neurons
Action Potential is an All or Nothing Process
(like a gun firing)
6. MEMBRANE (Resting)
POTENTIAL
Potential across membrane is called as membrane
potential.
Inside cell: conc. Of potassium ions and organic
compounds is more than outside the cell ( negatively
charged)
Outside cell: concentration of chloride ions and sodium
ions is more than inside the cell (positively charged)
Sodium open/leaky channels: flow of Na+ occurs in
and out of cell
Potassium open/ leaky channels: flow of K+ occurs
in and out of cell
Sodium-potassium pump: voltage gated channel;
allow the efflux of 3 Na+ ions for influx every 2 K+ ions;
7. All the above channels and pump maintains
the resting potential (electro-chemical
gradient) across the membrane i.e. -70 mV
9. DEPOLARISATION
As potential strike -55 mV (threshold potential) , Na+
voltage gated channels open, and allow the influx of
Na+ ions into the cell.
Due to influx of sodium ions, the potential across the
membrane increases.
More increase in potential, more influx of ions
This leads to change in charge across membrane.
Inside_ +vely charged
Outside_ -vely charged
As this potential reaches +40 mV(overshoot), the ,
Na+ voltage gated channels closes, and the , K+
voltage gated channels opens
10. REPOLARISATION
As this potential reaches +40 mV, the , Na+ voltage gated
channels closes, and the , K+ voltage gated channels
opens. This leads to repolarisation
This leads to efflux of potassium ions
Thus the potential across the membrane decrease
Inside_ -vely charged
Outside_ +vely charged
As the potential reaches -70mV, the potassium voltage-
gated channels closes.
However, due to gradual closing of channel, the is some
amount of leaked ions, due to which the potential
decreases below -70mV. This leads to
HYPERPOLARISATION
12. HYPERPOLARISATION AND
REFRACTORY PERIOD
Due to gradual closing of channel, the is some
amount of leaked ions, due to which the potential
decreases below -70mV. This leads to
HYPERPOLARISATION
the refractory period and the axon cannot fire again
until it returns to resting potential (negative polarized
state).
Thus, the membrane undergoes the refractory period.
In the refractory period ,the axon cannot fire again
until it returns to resting potential (negative
polarized state). It lasts for 3-5msec
As the resting potential is restored via open
channels and Na+/K+ pump, new action potential
is fired.
13. • Each spike is followed by a refractory
period.
• An absolute refractory period - it is
impossible to evoke another action potential –
during spike and right after it (Na channels
are open and after that inactivated)
• A relative refractory period - a stronger than
usual stimulus is required to evoke an action
potential (hyperpolarization; part of Na
channels recovered)
14.
15.
16. All-or-None Principle
Throughout depolarisation,
the Na+ continues to rush
inside until the action
potential reaches its peak
and the sodium gates
close.
If the potential cross -55mV ,
then the action potential
will reach to its fate, via
repolarisation and
hyperpolarisation.
If the depolarisation is not
great enough to reach
threshold, then an action
potential and hence an
impulse are not produced.
This is called the All-or-
None Principle.
21. - without the depression (an energy comes from the cell) along
nerve or muscle fibers
- a wave (a spot) of electrical negativity on the surface (electrical
positivity on the internal site of membrane) due to openning
and closing of voltage gated ion channels
Propagation of action potential – local currents
refractoriness
22.
23.
24. 1. Threshold is reached
2. +Na ions enter beginning of
axon
3. this triggers the next Na
gates to open.
4. As they open & allow in Na+,
5. previous gates begin
pumping the Na+ out.
6. Before the action potential
has reached the end, the
beginning of the axon is back
at resting potential & ready for
another firing.