Understanding the tiniest parts of your body

The three primary components of neurons, the cells that comprise our nervous system, are as follows. The soma, or cell body, contains the nucleus and all other major components of the neuron, as well as the axon, which is sporadically covered in fatty myelin. Dendrites are little branches of the neuron that receive signals from other neurons.

Neurotransmitters, which attach to receptors on the dendrite to produce a chemical signal, are the means by which those dendrites receive signals from other neurons. The chemical signal is changed into an electrical signal by this binding, which opens ion channels and permits charged ions to enter and exit the cell.

Since a single neuron can have a large number of dendrites receiving input, an action potential—an electrical signal that travels down an axon at up to 100 meters per second and causes the release of neurotransmitter on the other end to further relay the signal—is produced if the combined effect of several dendrites changes the overall charge of the cell sufficiently.

To interact with each other, neurons employ neurotransmitters as a signal, and the action potential is how they spread that signal throughout the cell. The movement of this electrical signal is quite significant since some of these neurons can be very lengthy, especially the ones that extend from the spinal cord to the toes!

However, why does the cell initially have an electric charge?

That depends on the variations in ion concentrations inside and outside of the cell. On the outside, there are typically more Na+ (sodium ions), Cl- (chloride ions), and Ca2+ (calcium ions), while on the inside, there are generally more K+ (potassium ions) and A- (which we only use for negatively charged anions).

The cell has a net negative charge of about 65 millivolts compared to the external environment as a result of the distribution of these ions; this is known as the neuron's resting membrane potential. Depending on the channel, a ligand-gated ion channel opens to let specific ions pass through when a neurotransmitter attaches to a receptor on the dendrite. Ligand-gated refers, quite literally, to a gate that reacts to a ligand—in this example, a neurotransmitter.

Using a ligand-gated Na+ ion channel as an example, we can see that when it opens, Na+ can enter the cell.

Gaining positive charge is known as depolarization because the additional positive charge that enters the cell reduces its negative potential (remember, it's normally -65 mV) and makes it less "polar." Usually, neurotransmitters open many ligand-gated ion channels simultaneously. This results in the entry of certain ions, such as calcium and sodium, and the exit of other ions, such as potassium, which actually causes some positive charge to leave the cell.

When everything is said and done, however, an excitatory postsynaptic potential (EPSP) results from a net input of positive charge. The cell potential would become more negative or repolarize if solely ligand-gated Cl-ion channels were to open, as this would result in a net influx of negative charge and an inhibitory postsynaptic potential (IPSP).

A single IPSP or EPSP, however, only slightly alters the resting membrane potential. However, when enough EPSPs are present at various dendritic sites, the membrane potential can be raised to a threshold value, usually -55 mV, though this can vary depending on the tissue.

This causes voltage-gated Na+ channels near the axon's beginning, known as the axon hillock, to open in response to a voltage change. When these channels open, sodium rushes into the cell.

When this happens, we say that the neuron has "fired." The influx of sodium ions and the ensuing change in membrane potential cause nearby voltage-gated sodium channels to open up as well, starting a chain reaction that continues down the entire length of the axon—which is our action potential.

Up to roughly +40 mV, the call really becomes positively charged in relation to the outside world once a significant amount of sodium has surged across the neuronal membrane.

When the sodium channel becomes inactivated, or stops allowing sodium to enter the cells, the depolarization process comes to an end. However, this condition is not the same as what the majority of other channels have whether they are closed or open, respectively.

The voltage-gated sodium channel is distinct, though, because it has an inactivation gate that, soon after depolarization, stops sodium influx. This process continues until the cell repolarizes, at which point the channel enters the closed state once more and the inactivation gate ceases to block influx. Despite this, the channel remains closed, meaning that no sodium can enter the cell.

Consequently, sodium can only enter the cell through the channel during this halfway open state, and this window of opportunity is very brief.

Potassium voltage-gated channels are also present, but they respond slowly and don't open until the sodium channels have previously opened and become inactivated. These are the voltage-gated potassium channels. As a result, potassium flows out of the cell along its own electrochemical gradient following the initial sodium rush into the cell, reducing part of the positive charge and lessening the impact of the soPotassium exits the cell via its own electrochemical gradient as a result of the initial sodium rush, which lessens the impact of the sodium depolarization by eliminating some positive charge.

As the potassium channels lack a distinct inactivation gate, they are able to stay open for a little while longer. This results in a net outflow of positive ions from the cell, which causes the membrane potential to repolarize, or become more negative.

Potassium voltage-gated channels are also present, but they respond slowly and don't open until the sodium channels have previously opened and become inactivated. These are the voltage-gated potassium channels. As a result, potassium flows out of the cell along its own electrochemical gradient following the initial sodium rush into the cell, reducing part of the positive charge and lessening the impact of the soAdditionally, the cell depends on the sodium-potassium pump, an active transporter that pumps two potassiums into and three sodiums out of the cell during this repolarization phase.

Since the sodium channels have been deactivated and are not responsive to any stimuli, the cell is in its absolute refractory period throughout this repolarization phase. The action potential is preserved in one direction and is prevented from occurring too soon apart by this absolute r

efractory period.

The sodium channels return to their initial closed state at this point, and the potassium channels remain open for a brief while due to the combined actions of this pump and the prolonged opening of the potassium channels, causing a brief period of overcorrection during which the neuron becomes hyperpolarized in relation to the resting potential.

Since the potassium channels are still open and we are in a hyperpolarized state, it requires a significant stimulus to activate the sodium channels, which means we are currently in the relative refractory period. Finally, the neuron reaches its resting membrane potential when the potassium channels close.

Now for a quick graphic recap: time is shown on the x-axis, and membrane potential is shown on the y-axis. Voltage-gated sodium and potassium channels are closed at the initial resting potential of approximately -65 mV. When we receive enough EPSPs to reach the threshold at approximately -55 mV, voltage-gated sodium channels open and reach a peak of approximately +40 mV. At this point, the sodium channels become inactivated, and we enter the absolute refractory period.

When voltage-gated potassium channels open, the sodium-potassium pump and other factors begin to repolarize the cell to the point where the cell overshoots and becomes hyperpolarized. We then enter the relative refractory period, during which potassium channels begin to close and sodium channels eventually close completely, bringing us to our resting membrane potential.

Alright, so the electrical signal is transmitted down the length of the axon by means of positive sodium ions entering the cell and depolarizing it.

Fantastic.

However, this process isn't actually that quick.

This is the reason fatty myelin, which is derived from glial cells such as oligodendrocytes and Schwann cells, is important.

Ions cannot just flow into the cell in these myelinated regions because there are no voltage-gated ion channels spanning the membrane; instead, ion flow occurs only at the nodes of Ranvier, which are the spaces between the myelin.

So instead of propagating via channels, the charge essentially jumps from node to node. That said though, these ions aren’t just diffusing down the length of the myelin to the other side...that’d be way to slow.

What actually happens is more like 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.

Therefore, the charge essentially jumps from node to node rather than traveling via channels.

However, these ions aren't merely spreading along the myelin's length to the opposite side—that would be far too slow.

In reality, what occurs is something like this: as the sodium ions enter the cell, they bump into other positive sodium ions already present, which in turn bumps into still another, and so on, until they reach the nodes.

The charge moving in this way with the myelinated areas moves really fast, and is called saltatory conduction, which makes it look like the action potential “jumps” from one one node to the next. Okay extremely quick recap - 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.