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Action potential velocity

Brain cells called neurons send information and instructions throughout the brain and body. The information is sent via electro-chemical signals known as action potentials that travel down the length of the neuron. These neurons are then triggered to release chemical messengers called neurotransmitters which help trigger action potentials in nearby cells, and so help spread the signal all over.
However, not all information is equally important or urgent. Especially when it comes to sensations such as touch and position sense, there are some signals that your body needs to tell your brain about right now, and some that can wait a little while to be processed. For example, pain from a shallow cut travels faster than pain originating in your liver. This means that different types of information will be sent on different types of neurons.

Some Signals Are Very Fast

Imagine you are walking along and suddenly you trip and begin to fall. Luckily, your body senses that your limbs are in the wrong place and instead of falling to the ground, you just stumble a little. This sense of knowing where you are in space is known as proprioception, and the nerves that transmit this information are among the fastest in your body! This is because they have two special characteristics that allow them send information very quickly – a large diameter, and a myelin sheath.
Diagram of neuron with dendrites, cell body, axon and action potential


Action potentials travel down neuronal axons in an ion cascade. Positive ions (mostly sodium ions) flow into the cell body, which triggers transmembrane channels at the start of the axon to open and to let in more positive ions. These new positive ions trigger the channels next to them, which let in even more positive ions. This continues down the axon and creates the action potential.
Larger diameter axons have a higher conduction velocity, which means they are able to send signals faster. This is because there is less resistance facing the ion flow. We have a lot of ions flooding into the axon, so the more space they have to travel, the more likely they will be able to keep going in the right direction. An axon is still part of the cell, so it’s full of cytoplasmic proteins, vesicles, etc. The larger the diameter of the axon, the less likely the incoming ions will run into something that could bounce them back.
The action potential depends on positive ions continually traveling away from the cell body, and that is much easier in a larger axon. A smaller axon, like the ones found in nerves that conduct pain, would make it much harder for ions to move down the cell because they would keep bumping into other molecules.
Diagram of large-diameter axon vs small diameter axon


The second way to speed up a signal in an axon is to insulate it with myelin, a fatty substance. In the peripheral nervous system, myelin is found in Schwann cell membranes. In the central nervous system, oligodendrocytes are responsible for insulation. These cells wrap around the axon, creating several layers insulation. As our action potential travels down the membrane, sometimes ions are lost as they cross the membrane and exit the cell. The presence of myelin makes this escape pretty much impossible, and so helps to preserve the action potential.
A myelin sheath also decreases the capacitance of the neuron in the area it covers. Since the neuron is at a negative membrane potential, it’s got a lot of agitated negative ions that don’t have a positive ion nearby to balance them out. Like charges repel, so the negative ions spread out as far from each other as they can, to the very outer edges of the axon, near the membrane. This then attracts positive ions outside the cell to the membrane as well, and helps the ions in a way, calm down. We then end up with thin layers of negative ions inside of the cell membrane and positive ions outside the cell membrane. However, where myelin wraps around the cell, it provides a thick layer between the inside and the outside of the cell. Fewer negative ions gather at those points because it is further away from the positive charges. Now there are parts of the axon that are still negative, but contain proportionally far fewer negative ions. This means that as the action potential comes rushing by, it is easier to depolarize the areas that are sheathed, because there are fewer negative ions to counteract.
Diagram of myelinated axon and saltatory spread; unmyelinated axon and slow spread
The spaces between the myelin sheaths are known as the nodes of Ranvier. These areas are brimming with voltage-gated ion channels to help push the signal along. Since these areas are unsheathed, it is also where the positive ions gather, to help balance out the negative ions. When the channels open, there are plenty of positive ions waiting to swarm inside. It almost looks like the signal jumps from node to node, in a process known as saltatory conduction. To saltate means to move by leaps or jumps, like the action potential seems to do down the axon. In reality, the internal current of flowing positive ions is activating the opening of the gates down the axon.
Diagram of saltatory conduction

Consider the Following:

  • Pain is actually one of the slowest sensations our bodies can send. Smaller fibers without myelin, like the ones carrying pain information, carry signals at about 0.5-2.0 m/s (1.1-4.5 miles per hour). The fastest signals in our bodies are sent by larger, myelinated axons found in neurons that transmit the sense of touch or proprioception – 80-120 m/s (179-268 miles per hour). Scientists believe that this reflects the evolution of these senses - pain was among the most important things to sense, and so was the first to develop through small, simple nerves. More nuanced senses like vibration and light touch evolved later, in larger, more complex structures.
  • Demyelination diseases that degrade the myelin coating on cells include Guillain-Barre syndrome and Multiple Sclerosis. Guillain-Barre syndrome is the destruction of Schwann cells (in the peripheral nervous system), while MS is caused by a loss of oligodendrocytes (in the brain and spinal column). These disorders have different causes and presentations, but both involve muscle weakness and numbness or tingling. These symptoms occur because the nerves aren’t sending information the right way. When the myelin coating of nerves degenerates, the signals are either diminished or completely destroyed. If the nerves are afferent (sensory) fibers, the destruction of myelin leads to numbness or tingling, because sensations aren’t traveling the way they should. When efferent (motor) nerves are demyelinated, this can lead to weakness because the brain is expending a lot of energy but is still unable to actually move the affected limbs. Limbs are especially affected, because they have the longest nerves, and the longer the nerve, the more myelin it has that can potentially be destroyed.

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