The document explains the action potential in excitable cells, detailing the processes of membrane potential, depolarization, repolarization, and the all-or-none law governing action potential generation. It describes the role of ion channels, neurotransmitters, and the structure of myelinated fibers in signal transmission. Additionally, it touches on conditions such as multiple sclerosis that affect neuronal function.

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.