Video Transcript
In this video, we’ll learn how to explain the resting potential of neurons, how the resting potential is maintained, and how to describe the electrical and chemical changes that occur during an action potential. We’ll also learn about the main stages of an action potential and what factors can affect the speed of transmission of an action potential.
The human body contains over seven trillion nerve cells, or neurons as they are more frequently called. Each of the seven trillion nerve cells communicates with other nerve cells by sending signals that can travel at speeds up to 120 meters per second. These high speeds are possible because the main function of a neuron is to transmit information in the form of an electrical signal. The electrical signal transmitted from neuron to neuron is called the nerve impulse.
A nerve impulse is initiated by a stimulus, which is a change in the internal or external environment. Here, our stimulus is a lit candle. This change in environment stimulates a receptor. The receptor sends a nerve impulse to the central nervous system for processing. After processing, the central nervous system will send a nerve impulse to different organs, which will allow us to react to the stimulus appropriately.
At this point, you may be wondering how exactly does a neuron initiate and propagate these nerve impulses. To understand the details of initiation and propagation of the nerve impulse, we’ll need to take a closer look at the neuron, so let’s zoom in. At the level of the neuron, the stimulus information is received by the dendrites in the form of a chemical signal. The nerve impulse is converted back into an electrical signal and sent to the cell body for integration and processing. From the cell body, the nerve impulse may be transmitted down the axon. The axon is the threadlike part of the neuron that conducts the nerve impulse.
Some neurons, like this one, have an insulating layer that surrounds the axon called the myelin sheath. The myelin sheath is shown here in blue. You may notice that the myelin sheath is not continuous. These small gaps in the myelin sheath are called the nodes of Ranvier. They play an important role in increasing the speed of the nerve impulse. However, before the nerve impulse is sent down the axon, it must be initiated. Neurons are able to initiate nerve impulses because they’re electrically excitable, a property of the neuron’s membrane.
If we were to zoom in on the neuron’s membrane, we would see that it separates two specific fluids, the fluid on the inside called the cytoplasm and the fluid on the outside called the extracellular space. Both of these fluids have a different chemical composition, which means they contain different amounts of charged ions. For example, the extracellular space typically has an excess of positive charges. The difference in the amount of charged ions on either side of the membrane creates what is called the membrane potential, which is measured in volts.
The membrane potential is important because changes in the membrane potential are how nerve impulses are initiated and propagated. When a neuron is not transmitting a nerve impulse, it is said to be at rest. And when the neurons are at rest, the membrane potential is called the resting membrane potential. In neurons, the resting membrane potential is about negative 70 millivolts. Let’s take a look at how the resting membrane potential is maintained by the neuron. The resting membrane potential of negative 70 millivolts is maintained through the transport of ions across the membrane. Active transport of ions happens through proteins embedded in the neuron’s membrane called sodium–potassium pumps.
When a neuron is at rest, there are more potassium ions that are found within the cytoplasm than there are found within the extracellular space. Similarly, there are more sodium ions found within the extracellular space than there are to be found within the cytoplasm of the neuron. The sodium–potassium pump moves three sodium ions from the cytoplasm to the extracellular space. Since the sodium ions are moving from an area of low concentration to high concentration, ATP is needed to power the pump. As the sodium is pumped out, two potassium ions are able to be transported from the extracellular space into the cytoplasm.
With the action of the sodium–potassium pump, the voltage in the extracellular space becomes more positive than in the cytoplasm. The constant activity of the sodium–potassium pump helps to make neurons excitable. Activity of the sodium–potassium pump also creates an imbalance in the distribution of sodium and potassium ions. Now, within the cytoplasm, there’s a higher concentration of potassium ions. However, the neuron’s membrane allows for a minimal flow of potassium ions out of the cell. Potassium passively diffuses out of the cell through pores called leak channels. Leak channels are always open and selectively allow for potassium to move from the cytoplasm to the extracellular space. This net flow of ions ultimately lowers the membrane’s potential as the outside of the cell becomes more positively charged.
The action of the sodium–potassium pump and the leak channels contributes to maintaining a resting membrane potential of around negative 70 millivolts. It also helps the neurons to be excitable. Excitability of the neuron means when it is not at rest, it is able to conduct a nerve impulse, which is called an action potential. Action potentials are the change in the electrical potential caused by the movement of charged ions as the impulse passes along the membrane of a neuron. There’re several main stages of an action potential. They are depolarization, repolarization, hyperpolarization, and finally a brief refractory period during which another action potential cannot be generated.
Let’s take a closer look at depolarization. Depolarization is the change in membrane potential from negative to positive. This temporary change in the membrane’s potential is largely due to the movement of sodium ions through voltage-gated sodium channels. When receptors at the dendrites are stimulated, it triggers an opening of the voltage-gated sodium channels. This makes the neuron’s membrane more permeable to sodium ions. Thanks to the action of the sodium–potassium pump, which has been actively moving three sodium ions out of the cell, sodium ions diffuse into the cytoplasm where they are less concentrated.
As sodium diffuses into the cell, the neuron’s cytoplasm becomes more positively charged. The increased positivity of the membrane potential causes more voltage-gated sodium channels to open. This allows sodium to diffuse into the cytoplasm at an even faster rate. This rapid influx of sodium ions causes the membrane potential to increase from negative 70 millivolts to around positive 40 millivolts.
After depolarization is repolarization. Repolarization is the change in membrane potential from positive back to negative. This change from positive to negative is due to the movement of potassium ions through the voltage-gated potassium ion channels. When membrane potentials reach a positive 40 millivolts, the voltage-gated sodium ion channels close and the voltage-gated potassium channels open. When this happens, sodium can no longer enter the cell. Potassium is now more concentrated in the cytoplasm of the neuron due to the action of the sodium–potassium pump.
So now, potassium ions can flow out of the cytoplasm through the voltage-gated potassium ion channels along its concentration gradient. Movement of the potassium to the extracellular space lowers the membrane potential back towards the negative resting potential.
Next is hyperpolarization. Hyperpolarization is the change in membrane potential to more negative than the resting membrane potential. Since so much potassium diffuses out of the cytoplasm when the voltage-gated channels open, the membrane potential temporarily becomes more negative than the resting potential. After a short delay, the voltage-gated potassium channels close. This signals a brief period of time called the refractory period. In the refractory period, the membrane is unresponsive to further stimulation and therefore cannot generate another action potential. This makes it possible for the sodium–potassium pump to reset the membrane back to resting potential. While the refractory period only lasts one to three milliseconds, it is important as it helps to keep the action potential traveling in one direction towards the axon terminal.
If we were to graph the change in membrane potential during an action potential, it would look something like this with several distinct stages. In stage one, the negative 70-millivolt resting potential is maintained by the sodium–potassium pump and the potassium leak channels. In stage two, a stimulus causes voltage-gated sodium channels to open. This influx of sodium ions causes the membrane to depolarize to positive 40 millivolts. At positive 40 millivolts, the voltage-gated sodium channels close and the voltage-gated potassium channels open. As potassium ions diffuse out of the axon, the membrane repolarizes. In stage four, the slow closing of potassium ion channels causes the membrane to hyperpolarize and overshoot the resting membrane potential.
After hyperpolarization is the refractory period. Here, the sodium-potassium pump works to reset the resting membrane potential to negative 70 millivolts. This cycle describes the action potential in just one patch of the membrane. As the action potential is propagated down the axon, these changes in the membrane potential are repeated. Generation of an action potential is determined by stimulus strength. In order to generate an action potential, the stimulus strength must pass a threshold value. If the stimulus does not pass this value, then no action potential will be generated. If the stimulus strength passes the threshold value, then an action potential will be generated.
This binary decision-making process is why action potentials are called all-or-nothing responses. Importantly, if the stimulus passes the threshold, the action potential that is generated will always be the same size. There are three factors that affect the speed of transmission of an action potential. They are temperature, axon size, and myelination. At low temperatures, ions diffuse slowly out of the cell. This is because they have less kinetic energy. At higher temperatures, ions have more kinetic energy and can diffuse out of the cell faster. With more kinetic energy and faster diffusion, the speed of the action potential increases. The diameter of the axon can also affect the speed of transmission.
In small-diameter axons, diffusing ions encounter resistance against their movement in the form of large proteins also found in the cytoplasm of the axon. You can think of this resistance as heavy traffic on a narrow roadway. This resistance slows the speed of transmission. In larger-diameter axons, there’s less resistance against ion movement since there’s more space in the cytoplasm. With less resistance in the cytoplasm, the speed of transmission for the action potential is faster. Finally, whether or not the axon is myelinated also affects the speed of transmission. Only unmyelinated portions of the axon can conduct the action potential as this is where the voltage-gated ion channels are found.
This means in axons without myelination, the entire length of the axon must open and close ion channels to conduct the action potential down the axon to the axon terminals. This slows the speed of transmission for the action potential. In axons with myelination, the action potential must jump from one unmyelinated node of Ranvier to the next. Since only a small portion of the membrane can conduct the action potential, less time is taken in opening and closing the ion channels. This speeds up the transmission of the action potential.
Let’s wrap up by taking a moment to review some key points we learned in this video. We learned that the membrane potential is determined by the movement of sodium and potassium ions across the neuron’s membrane and that the resting membrane potential is maintained by the sodium–potassium pump and potassium leak channels. We also learned that action potentials transmit electrical information and consist of the following stages: depolarization, repolarization, hyperpolarization, and a refractory period.
We also reviewed the all-or-nothing principle of action potentials, which states if a stimulus passes a threshold value, an action potential will always be generated. And finally, the speed of transmission of an action potential is affected by temperature, axon size, and myelination.
