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Action Potential
By Ajay Prakash Uniyal
• 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.
• 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.
• 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.
Action potential

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Action potential

  • 1. Action Potential By Ajay Prakash Uniyal
  • 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.