these slides contain a brief introduction of neurons and its classification as well as details of generation of action potential, resting potential and eletrotonic potential.
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
these slides contain a brief introduction of neurons and its classification as well as details of generation of action potential, resting potential and eletrotonic potential.
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
this presentation explains what is action potential, how it is initiated.
it deals with short notes and brief description on the various processes that undergoes in the action potential
this presentation will help you out to summarize and conclude important points.
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.
Membrane potential (also transmembrane potential or membrane voltage) is the difference in electric potential between the interior and the exterior of a biological cell. ... Almost all plasma membranes have an electrical potential across them, with the inside usually negative with respect to the outside.
this presentation explains what is action potential, how it is initiated.
it deals with short notes and brief description on the various processes that undergoes in the action potential
this presentation will help you out to summarize and conclude important points.
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.
Membrane potential (also transmembrane potential or membrane voltage) is the difference in electric potential between the interior and the exterior of a biological cell. ... Almost all plasma membranes have an electrical potential across them, with the inside usually negative with respect to the outside.
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Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
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2. • Excitable cells have an inside negative voltage or electric potential gradient across their plasma
membranes, membrane potential.
• In excitable cells this potential can become zero or even reversed.
• The membrane voltage in typical neuron called, resting potential because of state when no signal is
in transit. This is established by Na+ and K+ ions pumps in the plasma membrane.
• Subsequent movement of K+ channels outside cell through resting K+ channel results in net
negative charge inside the cell compared with outside.
• Typical membrane potential of neuron is about -60 mv.
• The signals take a form of brief voltage changes from inside negative to inside positive designated
as depolarisation.
• A powerful surge of depolarising voltage change, moving from one end of neuron to another is
called action potential.
• After action potential passes a sector of neuron, channel proteins and pumps restore the inside
negative channel proteins and pumps restore the inside negative resting potential called
repolarisation.
• The restoration process chases the action potential down the axon to terminus, leaving neuron to
signal again.
3. • Action potential follows all or none law.
- Once the threshold to start one is reached,, the full firing occurs.
• Resting Membrane potential
---- Generated by outward movement of K+
---- Hydrolysis of phosphoanhydride bonds in ATP to pump Na+ outward
---- Na channels closed in resting cells.
• During action potential, Na channels open, allowing inward movement of Na charge, depolarise the membrane. Resulting
influx of positive charged Na ions into cytosol will compensate for efflux of K ions through K channels.
• Cycle of changes in membrane potential and return to the resting value that constitutes an action potential lasts 1-2
milliseconds.
• Repolarisation of the membrane that occurs during refractory period is due largely to opening of voltage gated K+ channels.
The subsequent increased efflux of K channels from cytosol removes the excess positive charge from cytosolic face, thereby
restoring the inside negative resting potential.
• For brief instant, the membrane actually becomes hyperpolarised at the peak of this hyperpolarisation, the potential approaches
Ek, which is more negative than resting potential.
• The inability of Na channel to reopen during refractory period ensures that action potential propagate in single direction.
4. • Action potential jumps from one node of ranvier to another in myelinated fibres called saltatory
conduction. Oligondendrocytes and schwann cells make myelin sheath for CNS and PNS.
• Damage to protein produced by oligondendrocytes produce Multiple sclerosis. Mutation in mice that
eliminate Schwann cells cause death of neurons.
• Arrival of action potential at axon terminus cause rise in Calcium triggering fusion of vesicles with
plasma membrane of presynaptic neurons, releasing neurotransmitters.
• Neurotransmitter can be excitatory and inhibitory. Neurotransmitter binding to GPCR induce opening
and closing of separate ion channels.
• Electric synapses are direct, gap junctions connections between neurons. Electrical synapses employ
neurotransmitters for fast signal transmission and are bidirectional.