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The nerve cell or neuron is certainly one of the most elaborate and fascinating cells
in the body, and they are nearly universal in eumetazoans—that’s all animals with
the exception of sponges. As we noted in the previous video, the nerve cell’s function
of carrying a signal quickly from one point in the body to another part of the body is
an important element of how the animal is able to respond to stimuli.
A “classic” neuron like the one you would find in a textbook looks like this. There’s
the nerve cell body—that’s where the nucleus is—and this cell body typically has several
extensions called dendrites. The nerve cell receives “input” from many different sources—typically
other nerve cells—on its cell body and dendrites. In your nervous system, each nerve cell has
between a thousand and ten thousand of these connections—called synapses—with its input
sources. Then there’s the axon, which is a long, tubular extension of the cell that
carries a signal from the cell body to the terminal end of the axon, where it will relay
its signal to similarly numerous other nerve cells that are at the axon’s terminus.
The signal that the axon carries is not “detailed information”—not in the least. It’s
basically a little “blast” of cellular activity called an action potential that originates
at the nerve cell body and travels the length of the axon. The effect the action potential
has upon reaching the synapse-connection with the dendrites of the next neuron may be either
excitatory—that is, causing the next neuron to be more likely to fire its own action potential—or
it may be inhibitory—making it less likely to fire.
The way the nerve cell works is that it sums up all of the excitatory and inhibitory signals
that it receives from other cells, and when the excitatory signals outweigh the inhibitory
by a sufficiently large margin the nerve cell will “fire” its own action potential down
its axon. While this is simple enough thinking about it at the cellular level, the potential
of the nervous system to produce complex behavior grows with the number of neurons comprising
the nervous system and the ability of the nerve cells to connect in new ways, creating
different patterns of activity. Your ability to listen and watch and to understand what
I’m saying and to generate memory of meaning and later to respond to test questions based
on your learning—all of this is occurring as the result of the massively complex connectivity
of the nervous system within your brain.
The axon represents the majority of the nerve cell’s length, which can be quite long.
A motor neuron that carries a signal to your big toe has its cell body in the spinal cord,
which ends about two-thirds of the way down your back. The axon terminus, of course, is
near your big toe, so this would have to be a very long cell and practically all of it
would be axon. A much bigger animal like an elephant or a T. rex would have an even longer
toe motor neuron.
As you might imagine, larger body size requires greater distance over which the action potential
must travel, and this also means that it takes somewhat greater amounts of time for the signals
to get to and from the extremities of a larger animal relative to a smaller one. If animals
evolve larger body size while needing to maintain their ability to respond quickly, there is
strong selection for mechanisms to compensate for the slowness that is caused simply by
the longer distances that action potentials must travel in a larger-bodied organism.
One such adaptation—seen in vertebrates which as a group represent a big chunk of
the more successful “larger” animals—is the myelin sheath, which forms from specialized
cells called Schwann cells that wrap themselves around the axon, and this dramatically increases
the speed of the action potential. Instead of the axon’s big blast of a signal sort
of chugging its way down its length as it is in this unmyelinated nerve cell of an invertebrate
like a cockroach or a squid, the action potential in a vertebrate neuron—a myelinated neuron—once
it gets to a Schwann cell, will zoom through the axon where it has been wrapped by the
Schwann cell—until it gets to the end of that Schwann cell, or to the node of Ranvier
or little blank spot between the Schwann cells. Then the action potential gets re-propagated
and it zooms through the next Schwann cell to the next node.
From here, the importance of myelination of axons could be taken in two directions—one
would be the way it relieved what would have been a serious constraint to the evolution
of larger body size in vertebrates, and the second would be its role in some rather serious
and common human neuropathies, such as multiple sclerosis. But we’re going to focus next
on what happens at the end of the axon terminus. This is where a nerve cell “passes information
along” to the next nerve cell, and it does so via chemicals we call neurotransmitters.
So at the end of the axon there is usually a little branching going on—this allows
our neuron to communicate to several recipient cells. At the tips of the branches are the
little spots where the axon connects with the dendrites or cell bodies of the next neuron.
These are called synapses, and anatomically the important aspect here is the very tiny
space between the cell membranes of the two nerve cells and this is called the synaptic
cleft.
The end-of-the-axon side of the cleft is called the pre-synaptic surface while the dendrite
or cell body side is called the post-synaptic surface. Now the communication between the
two cells occurs with the release of neurotransmitters from the presynaptic side which then diffuse
across the tiny gap of the synaptic cleft and are received by the postsynaptic surface.
From there, the surface receptors of the neurotransmitter will create excitatory or inhibitory signals
that will be summed up as the receiving cell decides when it’s time to fire off its own
action potential.
That’s basically how nerve cells interact, and it’s through this mechanism of cell-to-cell
communication via neurotransmitter chemicals that an animal’s nervous system causes all
sorts of things to happen: sensing, motor, homeostatic, and behavioral. A mouse behaves
timidly—especially around cats—when all of its neurons are properly placed and firing
with the right balance of neurotransmitter chemicals. If you’re a mouse, being timid
around cats is generally a pretty good idea.
But if the mouse happens to be infected by the sporozoan parasite Toxoplasma, the mouse
becomes bolder—for example, less cautious about running along the walls of a room and
preferring to move about in the middle of the room, and these infected mice are also
more likely to call out a cat. “You want a piece of me, cat?” –this is basically
suicidal behavior in mice, and this aberrant behavior is indeed induced by the parasite.
Now if you’re thinking like a zoologist, there’s a perfectly logical explanation
for this. Earlier we talked about intermediate and definitive hosts of parasites, and here
the mouse is the intermediate host of Toxoplasma, which needs to get into the cat which is the
parasite’s definitive host. By making its intermediate host more likely to be eaten
by the cat, Toxoplasma gains in fitness. Great story, right? Well, I’m not done.
The mechanism employed by Toxoplasma to alter the behavior of the mouse is—you guessed
it—a neurotransmitter. In this case it seems that dopamine is both the natural neurotransmitter
used in the behavioral centers of the mouse’s brain and it is also a substance that is produced
by the parasite while in the mouse. Its effect is a very specific behavioral change in the
mouse, making it considerably less fearful of cats.
But now thinking about it further, Toxoplasma is not just a parasite of mice and cats—many
other mammal species can be infected—including humans. In fact it’s estimated that one
third of all people have contracted and are harboring the parasite. This is not typically
considered worrisome—the effect of Toxoplasmosis is very mild in humans (with the exception
of *** patients and pregnant women let’s assume here that we’re talking about ***-negative,
non-pregnant persons). But if the dopamine released by Toxoplasma in the brains of mice
is causing them to become suicidal, isn’t it possible that there could be some behavior
alteration occurring in human carriers as well?
A study published in July 2012 compared suicide rates in Toxoplasma-infected vs. uninfected
women. The use of women and not men in this study is because screening for Toxoplasma
in expectant mothers is a standard practice in some countries— remember that toxoplasmosis
is serious during pregnancy. The researchers found that infected women were 54% more likely
to attempt suicide and twice as likely to succeed.
Is this surprising? Well, I’m sure this sort of thing had been suspected for a while—this
is just the first study that I’m aware of that provides evidence for an effect of Toxoplasma
on human behavior. Note that the parasite’s ability to alter human behavior is not really
a part of the evolutionary equation for the Toxoplasma. Cats don’t eat infected humans,
so no parasite living in a human is ever going to make it into the next generation anyways.
The neurotransmitter release is an adaptation of Toxoplasma that strictly results from its
coevolution with mice and cats. The impact on humans is a random (and unfortunate) cross-species
effect that happens because of our physiological similarity with mice!
This phenomenon of behavior alteration in intermediate hosts is something that is well-documented
in several species, and it’s a great demonstration not only of the chemical basis of animal behavior
but also of the coevolution of parasites with their various hosts. How did Toxoplasma “know”
that dopamine would make the mice behave in a way that would make them fall prey to cats?
Well, they didn’t—of course—microbes don’t think or reason things out or understand
the neuroanatomy of their vertebrate hosts. It was natural selection that favored those
variants of Toxoplasma’s ancestors that were most successful in completing their life
cycles, and dopamine production was simply one of the mechanisms involved in their success.