The document discusses the resting potential, graded potential, and action potential in neurons. It provides details on:
1) The resting potential of neurons is normally between -60 to -80 mV due to concentrations of potassium and sodium ions inside and outside the cell. The sodium-potassium pump helps maintain this gradient.
2) A graded potential is an intermediate voltage change before an action potential. It involves the opening of voltage-gated potassium and sodium ion channels, making the intracellular voltage more negative or less negative.
3) An action potential is a brief, all-or-nothing increase in voltage caused by the rapid influx of sodium ions through opened voltage-gated channels, followed by the efflux
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.
Action potential By Dr. Mrs. Padmaja R Desai Physiology Dept
To study the Concept of Action Potential and describe the stages of action potential.
Ionic basis of Action Potential & its Propogation.
Properties of Action Potential.
Types action Potential
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.
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.
Action potential By Dr. Mrs. Padmaja R Desai Physiology Dept
To study the Concept of Action Potential and describe the stages of action potential.
Ionic basis of Action Potential & its Propogation.
Properties of Action Potential.
Types action Potential
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.
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3. • Membrane potential of a resting neuron.
• State of neuron at rest which is not sending
signals.
• Volts : -60 - -80 mV
• -ve sign means that inside of a neuron has –ve
charge to the outside.
4. Formation of resting potential
• Involve changing of the charge of plasma
membrane of nerve cell.
• Resting potential is driven by changing of
chemical potential energy to electrical
potential energy.
5. • Importance of substance involve in this
process are :
* potassium ion
* sodium ion
• Each of the ion has concentration gradient
within the plasma membrane of the cell.
6.
7. • Concentration gradient of potassium and
sodium within the plasma membrane
represent the chemical form of potential
energy.
• During formation of resting potential,
chemical energy is convert into electrical
energy.
8. • This conversion involves sodium - potassium
pumps to be used.
• Sodium – potassium pumps generates and
maintain the ionic gradient of Na+ and K+ into
the cell.
• ATP also is used to transport Na+ and K+ in
opposite direction.
9. Step by step
protein pore is formed by clusters of specialized
protein that span the membrane. it is also
carried out selective permeability (specific ion
can bind to).
1
10. • Ions diffuse through ion channel.
• Each ion carry the units of electrical charge.
• Diffusion of ions will result net movement of
positive or negative charge.
• Produce voltage across membrane.
2
11. • During resting potential, a lot of potassium
channels open and few sodium channel open.
• Diffusion of K+ occurred
• From inside to outside of the cell.
• [K+ inside] higher than [K+ outside].
3
4
12. • [Cl-] will present inside of the cell.
• Cl- cannot diffuse out of the cell because there
are very few Cl- channels open.
• Leaving high negative charge inside the cell
thus build up -ve charge inside membrane.
5
13. • The separation of charge cause voltage to be
produced.
• This in turn cause the electrical gradient to
counterbalance the [K+].
6
14. Limitation of diffusion of [K+]
1. The building up of negative charge inside the
cell indefinitely is prevented by excess of
negative charge.
2. Excess negative charge exerts attractive force
that oppose the flow of additional positively
charge K+ out of the cell.
16. • Intermediate potential before action potential
take place.
• Involves ion channels which are potassium
and sodium gated channels.
• Gated channels can open and closed in
response to one of three kinds of stimuli.
17. Gated
channel
Stretch – gated ion
channels
Voltage – gated
ion channels
Ligand – gated
ion channels
• Sense stretch cells
• Open when membrane is
mechanically deformed.
• Found at synapses.
• Open and closed
when a specific
chemical
(neurotransmitter)
binds to the channel.
• Found in axon.
• Open or closed when
the membrane
potential changes.
18. • Sodium and potassium gated channels are
therefore voltage – gated ion channel.
20. • Increase the magnitude of membrane
potential.
• Inside of the membrane becomes more
negative.
• More K+ ions channels open.
• Movement of more K+ to the outside of cell.
• Inside becomes more negative thus more
negative value of potential is produced.
21. • Reduction in the magnitude of membrane
potential.
• Inside of the membrane becomes less
negative.
• More Na+ ions channels open.
• More movement of Na+ into the cell. Inside of
the cell becomes less negative.
• Less negative value of potential is produced.
23. Nerve impulse
Nerve impulse of signals that carry information
along the axon.
The transport of information can occur at great
distances, for example, from toes to spinal cord.
24. Action potential is very brief.
• 1-2 millisecond in duration
• Enable a neuron to produce the voltage at
high frequency
• This feature is important as neuron encode
information in their action potential
frequency. For example, knee-jerk reflex
2
28. Resting potential
• On Na+ ion channel, activation gate is closed.
Meanwhile, inactivation gate is open in most
channel.
• On K+ ion channel, activation gate is closed.
1
29. Depolarization
• Occur when stimulus is present and
depolarizes membrane.
• On Na+ ion channel, both gates open. Na+
diffuse into the cell. Then Na+ influx causes
further depolarization. More Na+ diffuse into
the cell, so on.
• Inside membrane become less negative.
• On K+ ion channel, activation gate remain
close.
2
30. Rising phase of
the action potential
• Threshold crossed, membrane potential close
to ENa (62 mV) .
• On Na+ ion channel, activation gate is open
and inactivation gate open too.
• On K+ ion channel, activation gate is closed.
3
31. Falling phase of action potential
• On Na+ ion channel, activation gate is open.
Inactivation gate is closed. Which block the
Na+ influx.
• On K+ ion channel, activation gate is open.
Which permit K+ reflux. This caused the inside
of the membrane becomes negative and
membrane potential close to EK, -72 mV.
4
32. Undershoot
• Membrane’s permeability of K+ is higher than at
rest. Membrane potential close to EK.
• On Na+ ion channel, both activation and
inactivation gates are closed.
• On K+ ion channel, the activation gate is open
initially, soon it will closed and increase the
membrane potential to rest potential.
• Second depolarising stimulus occurs during this
period, but it will not able to trigger an action
potential, refractory period.
5
34. • Action potential is along distance signal
without diminishing from the cell body to the
synaptic terminals.
• Long distance signals does regenerating.
35.
36. 1
• At the site where action potential is initiated,
the Na+ influx during rising phase creates
electric current that depolarised axon the
neighbouring membrane.
• Depolarisation in neighbouring region is large
enough to reach threshold. This is the point
where action potential is reinitiated.
• This process is repeated many times as action
potential travels the length of axon.
37. 2
• Behind travelling zone of depolarization due to
Na+ influx, this region is known as zone of
repolarization due to K+ efflux.
• At this zone, inactivation gate Na+ channel
closed.
• Inward current that depolarises the axon
membrane ahead of the action potential cannot
produce action potential behind it.
• This prevents action potential from travelling
back toward the cell body.
• Action potential moves in only one direction.
38. 3
• Depolarisation – repolarisation process is
repeated in the next region of the membrane.
• Local current of ions across the membrane
caused action potential to be propagated
along the length of the axon.