Neurons communicate with each other through their dendrites and axon. Generally, incoming
signals are received at dendrites, while outgoing signal travels along the axon to the nerve
terminal. In order to achieve rapid communication over its long axon, the neuron sends electrical
signals, from the cell’s body to the nerve terminal, along the axon. These are known
as nerve impulses, or action potentials. An action potential is essentially a brief reversal
of electric polarity across the cell membrane. Cells are polarized, meaning there is an electrical
voltage across the cell membrane. In a resting neuron, the typical voltage, known as the
resting membrane potential, is about -70mV. The negative value means the
cell is more negative on the inside. At this resting state, there are concentration gradients
of sodium and potassium across the cell membrane: more sodium outside the cell and more potassium
inside the cell. These gradients are maintained by the sodium-potassium pump which constantly
brings potassium IN and pumps sodium OUT of the cell.
A neuron is typically stimulated at dendrites and the signals spread through the soma. Excitatory
signals at dendrites open ligand-gated sodium channels and allow sodium to flow into the
cell. This neutralizes some of the negative charge inside the cell and makes the membrane
voltage LESS negative. This is known as depolarization as the cell membrane becomes LESS polarized.
The influx of sodium diffuses inside the neuron and produces a current that travels toward
the axon hillock. If the summation of all input signals is excitatory and is strong
enough when it reaches the axon hillock, an action potential is generated and travels
down the axon to the nerve terminal. The axon hillock is also known as the cell’s “trigger
zone” as this is where action potentials usually start. This is because action potentials
are produced by voltage-gated ion channels that are most concentrated at the axon hillock.
Voltage-gated ion channels are passageways for ions in and out of the cell, and as their
names suggest, are regulated by membrane voltage. They open at some values of the membrane potential
and close at others. For an action potential to be generated, the
signal must be strong enough to bring the membrane voltage to a critical value called
the threshold, typically about -55mV. This is the minimum required to open voltage-gated
ion channels. At threshold, sodium channels open quickly. Potassium channels also open
but do so more slowly. The initial effect is therefore due to sodium influx. As sodium
ions rush into the cell, the inside of the cell becomes more positive and this further
depolarizes the cell membrane. The increasing voltage in turn causes even more sodium channels
to open. This positive feedback continues until all the sodium channels are open and
corresponds to the rising phase of the action potential. Note that the polarity across the
cell membrane is now reversed. As the action potential nears its peak, sodium
channels begin to close. By this time, the slow potassium channels are fully open. Potassium
ions rush out of the cell and the voltage quickly returns to its original resting value.
This corresponds to the falling phase of the action potential. Note that sodium and potassium
have now switched places across the membrane. As the potassium gates are also slow to close,
potassium continues to leave the cell a little longer resulting in a negative overshoot called
hyper-polarization. The resting membrane potential is then slowly restored thanks to diffusion
and the sodium-potassium pump. During and shortly after an action potential
is generated, it is impossible or very difficult to stimulate that part of the membrane to
fire again. This is known as the refractory period. The refractory period is divided into
absolute refractory and relative refractory. The absolute refractory period lasts from
the start of an action potential to the point the voltage first returns to the resting membrane
value. During this time, the sodium channels are open and subsequently inactivated while
closing and thus unable to respond to any new stimulation. The relative refractory period
lasts until the end of hyper-polarization. During this time, some of the potassium channels
are still open, making it difficult for the membrane to depolarize, and a much stronger
signal is required to induce a new response. During an action potential, the sodium influx
at a point on the axon spreads along the axon, depolarizing the adjacent patch of the membrane,
generating a similar action potential in it. The sodium currents diffuse in both directions
on the axon, but the refractory properties of ion channels ensure that action potential
propagates ONLY in ONE direction. This is because ONLY the unfired patch of the axon
can respond with an action potential; the part that has just fired is unresponsive until
the action potential is safely out of range. An action potential generated at the axon
hillock usually travels down the axon to the nerve terminal and not back to the cell body.
This is because the concentrations of voltage-gated ions channels are higher in the axon than
in the cell body.