Download LESSON 2.3 WORKBOOK How fast do our neurons signal?

LESSON 2.3 WORKBOOK
How fast do our neurons signal?
DEFINITIONS OF TERMS
Glial cell – several classes
of non-neuronal cells of the
nervous system.
For a complete list of defined
terms, see the Glossary.
Remember that winning goal you scored, that snowball you
dodged or the cup of coffee you managed to catch before
the cat knocked it all over your computer? Hundreds of
times a day our quick reactions improve our performance or
save us from disaster. Take a minute to think of something
that happened to you this week. Often we react so quickly
that we’ve reacted before we even know what has happened.
How can your neurons signal so quickly? In this lesson we
will find out, and to do so we need to learn about the other
important type of cell in our nervous systems – the glial cell.
Glial Cells
There are actually far more glial cells (usually referred to as glia) than neurons in the CNS of vertebrates
— between 10 to 50 times more in fact. Nerve cell bodies and axons are surrounded by them and because of this they were named from the Greek word for glue. For a long time neuroscientists thought glial
cells did behave like glue, and pretty much ignored them. Over the last few years though they have been
found to be far more active than we thought, conducting their own signals and acting more as partners
for neurons than the boring old structural cells we originally thought. Glia in fact have several vital roles
in neuronal function:
Wo r k b o o k
Lesson 2.3
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They provide firmness and structure to the brain. This isn’t trivial. Remember from the
lesson on neural imaging that the brain has very low density. Glia beef up the density
and make the neurons more resistant to trauma. That’s important because remember
that if a brain neuron is damaged and dies it can’t be replaced.
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Two different types of glial cells act as insulation, which as we shall see, allows the action potential to travel faster – important if we want to move a signal quickly.
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When the brain is developing in the embryo, some glia act as guides so that the neural
network forms its connections in the right place.
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Other glial cells help form an impermeable lining around the capillaries and venules of
the brain that prevents toxic substances in the blood from entering the brain. This lining
is called the blood-brain barrier.
What are glia cells, and what are some of
their functions?
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LESSON READING
Myelination increases the conduction speed of the action potential
In the last lesson we saw that if only one action potential occurred at the beginning of the axon, the depolarizing current wouldn’t reach the axon terminal. This happens because as it travels down the axon some
of the current leaks out of the axon across the membrane, and also because the materials in the axon
(chiefly protein) offer resistance to the current. We also learned that some axons solve this problem by lining up their voltage-gated Na+ channels along the axon membrane, so multiple action potentials can occur
in rapid succession, ensuring that the signal is transmitted all the way down the axon.
DEFINITIONS OF TERMS
Nodes of Ranvier – gaps
between adjacent myelin
segments on an axon.
Demyelination – the loss of
myelin insulating neurons.
For a complete list of defined
terms, see the Glossary.
Wo r k b o o k
Lesson 2.3
This is not a great solution because the energy required to keep the Na+/K+ pump working to repolarize
the axon membrane is huge. So axons have come up with another strategy, which is to have the action
potential jump along the axon rather than progress down it (think of the action potential pogo-sticking down
the axon rather than walking down). This how it works.
Remember that the problem with a single action potential was that the current would decay.
To prevent that decay glial cells wrap around the
axon like beads on a necklace covering the axon
tightly except for the areas in between the beads
called nodes of Ranvier which remain naked
axon (Figure 17). Two things make this strategy
work. First the glia make a substance called myFigure 17: Nodes of Ranvier. Myelin is formed
elin, which acts as an insulator. Now the parts of
from membranes of glial cells wrapping tightly
the axon that are wrapped around by the myelin
around the axon, like beads on a necklace.
are insulated and the depolarizing current can’t
Between the beads of myelin are spaces of naked
leak out. Second the sodium channels are conaxon, called the nodes of Ranvier.
centrated in the small areas of naked axon in
between each myelin ‘bead’ so the action potential can hop down the axon like a pogo stick. Let’s have a
look in a bit more detail:
Figure 18: Cross
section of myelinated axons. The glial
cell membranes
wrap so tightly
around the axon
that the cytoplasm
is squeezed out of
the glial cells.
The glial cells wrap around the axon like paper wrapping around a pencil. The glial cell membrane attaches so tightly to the axon, and to itself that there is no
extracellular fluid in contact with the axon in that area
(Figure 18). The only place where the axon comes
into contact with extracellular fluid is at a node of Ranvier, where the axon is naked. In the myelinated areas
therefore, there can be no inward flow of Na+ into the
axon because the myelin insulates the axon from the
extracellular fluid.
How does myelination increase the conduction velocity of the action potential?
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LESSON READING
DEFINITIONS OF TERMS
Saltatory conduction –
conduction of the action potential
from one node of Ranvier to the
next along a myelinated axon.
How then does the action potential travel along the area
of an axon covered by a myelin sheath? The answer
to this is by behaving like an electrical cable. Since the
axon is covered in myelin, there is minimal leakage of
depolarizing charge out of the axon so the depolarizing
current is able to travel passively between the nodes
of Ranvier. When the depolarizing current reaches the
next node of Ranvier, it encounters both Na+ ions and
Na+ channels, and so it can trigger another action potential at the node. The action potential gets retriggered,
or repeated, at each node of Ranvier and the depolarizing current moves passively along the myelinated portions of the axon to the next node. This type of conduction, which appears to hop from node to node, is called
saltatory conduction, from the Latin saltare, “to leap,
to dance” (Figure 19).
Figure 19: Saltatory conduction. Action
potentials are conducted down the myelinated axon via saltatory conduction. The
depolarization “jumps” from one node to the
next without decaying.
Why is myelination an advantage for the axon?
For a complete list of defined
terms, see the Glossary.
Wo r k b o o k
Lesson 2.3
What are the advantages of myelination?
We can immediately see two advantages of saltatory conduction. The first is it saves energy. Sodium ions that enter axons
during the action potential must eventually be removed. You’ll
remember that the Na+ ions are removed by Na+/K+ pumps,
which use significant amounts of energy. As we mentioned
before, in axons that aren’t myelinated, these pumps must be
located along the entire length of the axon, because Na+ ions
can enter everywhere. However, in a myelinated axon, where
Na+ ions can only enter at the nodes of Ranvier, much less Na+
gets in, and consequently, much less needs to be pumped out.
Therefore, in myelinated axons much less energy is needed to
remove Na+ ions and maintain the high extracellular Na+ concentration.
Figure 20: Comparing action potential conduction in unmyelinated and
myelinated axons. The black arrows
represent current flowing down an
unmyelinated axon and the red arrows represent current flowing down
a myelinated axon. Notice how
much faster the myelinated current
travels.
The second advantage of myelin is speed. The action potential is conducted much faster in a myelinated axon because
transmission between the nodes, which occurs by means of
the axon’s cable properties, is very fast (Figure 20). Increased
speed enables us to react faster and undoubtedly to think faster. In fact, the fastest myelinated axon, 20 micrometers (µm) in
diameter, can conduct action potentials at speeds of 150 m/s,
or 335 mph!
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Think about your big toe neuron. Imagine the
axon starts under your armpit. How long will
an action potential take to travel down to your
big toe if is myelinated?
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55
LESSON READING
Under what circumstances would it be beneficial not to have myelinated axons?
Why aren’t all neurons myelinated?
Since myelin provides such important benefits – decreasing energy consumption and increasing speed –
why aren’t all of our axons myelinated? In fact, most of our axons are myelinated, but later we’ll argue that
having some unmyelinated axons is important.
DEFINITIONS OF TERMS
Demyelination – the loss of
myelin insulating neurons.
Saltatory conduction –
conduction of the action potential
from one node of Ranvier to the
next along a myelinated axon
Demyelination – the loss of
myelin insulating neurons
Take for example the so-called C fibers (fibers is just another name for nerve). C fibers are sensory neurons located in the PNS and involved in the pain response. They are not myelinated and their conduction
velocities are slow 2 m/s (or only 4.5 mph). But conducting pain information slowly, gives us an advantage
because we can respond to the source of the pain before the pain sensation becomes intense. Sometimes
it is actually beneficial for a signal to reach our brains more slowly.
What happens when myelin gets damaged?
Demyelination is the loss of the myelin sheath insulating neurons. As you might imagine, losing even a
part of the myelin sheath disrupts action potential conduction. When myelin is disrupted, conduction along
an axon may become desynchronized or even fail completely.
Demyelination is the hallmark of some neurodegenerative diseases including multiple sclerosis, (MS) and
Charcot-Marie-Tooth disease. Demyelination results in a set of symptoms that will depend on which neurons are affected.
We’ll talk more about demyelinating diseases in the last lesson of this unit, but for now remember that the
myelin sheath insulates the axon increasing the conduction velocity of the action potential, as well conserving the axon’s energy.
For a complete list of defined
terms, see the Glossary.
When does myelination occur?
Recently, research has shown that our brains
gradually add myelin as we mature. Figure 21 is
taken from one of the studies on which that statement is based. Remember, grey matter is where
neurons connect with each other and white matter is where the myelinated axons are. The study
Figure 21: Loss of grey matter and gain of white
analyzed changes in grey matter relative to white
matter from 5 – 20 years. Notice that our frontal
matter, so another way to look at the data is that
lobes are the last areas to become heavily myelinnot only does grey matter decrease, but white
ated and thus be represented as mostly white
matter also increases as we mature. Take a look
matter.
specifically our frontal lobes, which do not become fully myelinated until we are about 20. Some scientists have taken this further to argue that teenagers show poor judgment because their frontal lobes aren’t fully myelinated. This conclusion has been hotly
debated in the field, and might be one you’d like to take a minute to think about.
Mostly grey ma-er Mostly white ma-er Wo r k b o o k
Lesson 2.3
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What if your big toe neuron wasn’t myelinated? How long would it take the action potantial to reach your toe then? Would this be
an advantage or not?
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At what age does our frontal lobe become
myelinated?
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STUDENT RESPONSES
You just read about research that shows that the human brain, specifically the frontal lobe, is not heavily myelinated until the
age of 20. Some scientists argue that teenagers show poor judgment because their brains aren’t fully myelinated. What do you
think? Do you agree with the scientists’ arguments? Do you think there could be another explanation?
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Lesson 2.3
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