Notes
Communication within a Neuron (Action Potential)
Neurons are the cells that make up our nervous system, and they’re made up of three
main parts.
o The dendrites, which are little branches off of the neuron that receive signals from
other neurons,
o the soma, or cell body, which has all of the neuron’s main organelles like the
nucleus,
o And the axon which is intermittently wrapped in fatty myelin.
Those dendrites receive signals from other neurons via neurotransmitters, which when
they bind to receptors on the dendrite act as a chemical signal. That binding opens ion
channels that allow charged ions to flow in and out of the cell, converting the chemical
signal into an electrical signal.
Since a single neuron can have a ton of dendrites receiving input, if the combined effect
of multiple dendrites changes the overall charge of the cell enough, then it triggers an
action potential- which is an electrical signal that races down the axon up to 100 meters
per second, triggering the release of neurotransmitter on the other end and further
relaying the signal.
So neurons use neurotransmitters as a signal to communicate with each other, but they
use the action potential to propagate that signal within the cell.
Some of these neurons can be very long, especially ones that go from the spinal cord to
the toes, so the movement of this electrical signal is super important!
The cell has an electric charge because there are more Na+ or sodium ions, Cl- or
chloride ions, and Ca2+ or calcium ions on the outside, and more K+ or potassium ion
and A- (negatively charged anions), on the inside.
Overall, the distribution of these ions gives the cell a net negative charge of close to -70
millivolts relative to the outside environment - this is called the neuron’s resting
membrane potential.
When a neurotransmitter binds to a receptor on the dendrite, a ligand-gated ion channel
opens up to allow certain ions to flow in, depending on the channel. (Ligand-gated
literally means that the gate responds to a ligand, which in this case is a
neurotransmitter.)
So if we take the example of a ligand-gated Na+ ion channel, which, when it opens, lets
Na+ flow into the cell. The extra positive charge that flows in makes the cell less
negative (resting potential is -70mV), and therefore less “polar” - so that’s why gaining
positive charge is called depolarization.
Neurotransmitters typically open various ligand-gated ion channels all at once, so ions
like sodium and calcium, may flow in, while other ions like potassium, may flow out,
which would actually mean some positive charge leaves the cell.
If there is a net influx of positive charge, then it’s called an excitatory postsynaptic
potential (EPSP).
In contrast, a net influx of negative charge, creating an inhibitory postsynaptic potential
(IPSP), making the cell potential more negative or repolarizing it. (happens when opening
of only ligand-gated Cl- ion channels)
Now, a single EPSP or IPSP causes only a small change on the resting membrane
potential, but, if there are enough EPSPs across multiple sites on the dendrites then
collectively they can push the membrane potential to a specific threshold value. (-55mV,
although this can vary by tissue)
When this occurs, it triggers the opening of voltage-gated Na+ channels at the start of the
axon - the axon hillock, voltage-gated channels open in response to a change in voltage,
and when these open, it causes sodium ions to rush into the cell. The influx of sodium
ions and the resulting change in membrane potential causes nearby voltage-gated sodium
channels to open up as well - setting off a chain reaction that continues down the entire
length of the axon—which is our action potential, and when this happens, we say that the
neuron has ‘fired.’
Once a lot of sodium has rushed across the neuronal membrane, the cell actually becomes
positively charged relative to the external environment (up to about +40mV). The
depolarization process ends when the sodium channel stops allowing sodium to flow into
the cells- a process known as inactivation.
o This inactivated state is different than when the channel’s closed or open. The
voltage-gated sodium channel has an inactivation gate, which blocks sodium
influx shortly after depolarization, and stays in that state until the cell repolarizes
and the channel enters the closed state again.
o The open state therefore is the only state where sodium gets let into the cell
through the channel, and this is a very short window of time.
There are potassium voltage-gated channels, which are slow to respond and don’t open
until the sodium channels have already opened and become inactivated.
o The result is that after the initial sodium rush into the cell, potassium flows out of
the cell down its own electrochemical gradient-removing some positive charge
and blunting the effect of the sodium depolarization.
o The potassium channels, do not have a separate inactivation gate and therefore
remain open for slightly longer, which means that there is a period of time when
there is a net movement of positive ions out of the cell, causing the membrane
potential to become more negative, or repolarize.
During this repolarization phase, the cell also relies on the sodium-
potassium pump, an active transporter that moves 3 sodium ions out of the
cell and 2 potassium ions into it.
It’s during this repolarization phase that the cell’s in its absolute
refractory period, since the sodium channels are inactivated and
won’t respond to any amount of stimuli.
This absolute refractory period keeps the action potentials from
happening too close together in time,
It also keeps the action potential moving in one direction.
The combined efforts of this pump and the extended opening of the
potassium channels results in a small period of overcorrection where the
neuron becomes hyperpolarized relative to the resting potential, and at this
point the sodium channels go back to their initial closed state, and for a
short period the potassium channels stay open.
This is the relative refractory period since the sodium channels are
closed but can be activated, but because the potassium channels are
still open and we’re in a hyperpolarized state, so it’s takes a strong
stimulus to depolarize.
o Finally, as the potassium channels close, the neuron returns to its resting
membrane potential.
Graphical recap, with membrane potential on the y and time on the x.
o First we start at resting potential of around -70 mV and voltage-gated sodium and
potassium channels are closed,
o We receive EPSPs enough to hit threshold at about -55 mV, voltage-gated sodium
channels open and
o We reach a peak of about +40 mV, at which point the sodium channels become
inactivated and we’re in the absolute refractory period.
o Voltage-gated potassium channels open, and along with the sodium-potassium
pump, start to repolarize the cell, so much so that it overshoots and hyperpolarizes
the cell.
o Next the sodium channels enter their closed resting state as potassium channels
start to close we’re in the relative refractory period,
o Until finally they all close and we reach our resting membrane potential.
This process of positive sodium ions moving in and depolarizing the cell transmits the
electrical signal down the length of the axon. This process isn’t fast.
So that’s where the fatty myelin comes in, which comes from glial cells like Schwann
cells or oligodendrocytes.
These myelinated areas don’t have voltage-gated ion channels spanning the membrane,
so ions can’t simply flow into the cell; that only happens in the spots between the myelin,
called nodes of Ranvier.
So instead of propagating via channels, the charge essentially jumps from node to node.
But the ions aren’t just diffusing down the length of the myelin to the other side; the
sodium ions rushing in bumps other positive sodium ions already inside the cell, which
bumps another one, and so on until it reaches the next node.
The charge moving in this way with the myelinated areas moves really fast, and is called
salutatory conduction, which makes it look like the action potential “jumps” from one
node to the next.
Summary: neuron action potentials happen when dendrites receive enough EPSPs to open
voltage-gated sodium channels, which cause rapid depolarization of the neuronal membrane and
propagation of an electrical charge from node to node down the length of the axon.
SUMMARY of communication within a neuron
Resting membrane potential
The lipid bilayer membrane that surrounds a neuron is impermeable to charged molecules
or ions.
To enter or exit the neuron, ions must pass through special proteins called ion channels
that span the membrane.
Ion channels have different configurations: open, closed, and inactive.
Ion channels that change their structure in response to voltage changes are called voltage-
gated ion channels. Voltage-gated ion channels regulate the relative concentrations of
different ions inside and outside the cell.
The difference in total charge between the inside and outside of the cell is called
the membrane potential.
A neuron at rest is negatively charged: the inside of a cell is approximately 70 millivolts
more negative than the outside.
This voltage is called the resting membrane potential; it is caused by differences in the
concentrations of ions inside and outside the cell.
Action potential
Transmission of a signal within a neuron (from dendrite to axon terminal) is carried by a
brief reversal of the resting membrane potential called an action potential.
When neurotransmitter molecules bind to receptors located on a neuron’s dendrites, ion
channels open.
At excitatory synapses, this opening allows positive ions to enter the neuron and results
in depolarization of the membrane—a decrease in the difference in voltage between the
inside and outside of the neuron.
A stimulus from a sensory cell or another neuron depolarizes the target neuron to its
threshold potential (-55 mV).
o Na+channels in the axon hillock open, allowing positive ions to enter the cell.
o Once the sodium channels open, the neuron completely depolarizes to a
membrane potential of about +40 mV.
Action potentials are considered an “all-or nothing” event, in that, once the threshold
potential is reached, the neuron always completely depolarizes.
Once depolarization is complete, the cell must now “reset” its membrane voltage back to
the resting potential.
o To accomplish this, the Na+ channels close and cannot be opened.
o This begins the neuron’s refractory period, in which it cannot produce another
action potential because its sodium channels will not open.
o At the same time, voltage-gated K+channels open, allowing K+ to leave the cell.
o As K+ ions leave the cell, the membrane potential once again becomes negative.
The diffusion of K+ out of the cell actually hyperpolarizes the cell, in that the membrane
potential becomes more negative than the cell’s normal resting potential.
At this point, the sodium channels will return to their resting state, meaning they are
ready to open again if the membrane potential again exceeds the threshold potential.
Eventually the extra K+ ions diffuse out of the cell through the potassium leakage
channels, bringing the cell from its hyperpolarized state, back to its resting membrane
potential.
Propagation of Action Potential
The process of depolarization just through movement of ions is not fast enough. The
axons have fatty Myelin Sheath which speeds up the process.
As these myelinated areas don’t have voltage-gated ion channels ions can’t simply flow
into the cell; that only happens in the spots between the myelin, called nodes of Ranvier.
So instead of propagating via channels, the charge essentially jumps from node to node.
But the ions aren’t just diffusing down the length of the myelin to the other side; the
sodium ions rushing in bumps other positive sodium ions already inside the cell, which
bumps another one, and so on until it reaches the next node.
The charge moving in this way with the myelinated areas moves really fast, and is called
salutatory conduction, which makes it look like the action potential “jumps” from one
node to the next.
AN EVEN SMALLER SUMMARY
The formation of an action potential can be divided into five steps:
(1) A stimulus from a sensory cell or another neuron causes the target cell to depolarize toward the
threshold potential.
(2) If the threshold of excitation is reached, all Na+ channels open and the membrane depolarizes.
(3) At the peak action potential, K+ channels open and K+ begins to leave the cell. At the same time,
Na+ channels close.
(4) The membrane becomes hyperpolarized as K+ ions continue to leave the cell. The hyperpolarized
membrane is in a refractory period and cannot fire.
(5) The K+ channels close and the Na+/K+ transporter restores the resting potential.
The presence of myelin sheath causes salutatory conduction which allows faster propagation of the
signal as the channels are only in nodes of Ranvier, so the charge jumps from one node to the other.
