On the other hand, most mammals have it worse than we do. They have only two types of cones. While a dog or a cat can see with clarity, it can’t see in color. The dog’s or cat’s world looks luminous, perhaps, but also lacks the energetic “red” that a fish blessed with special types of cones gets to experience. In a dog’s world, there are no beautiful shades of red at all.
What humans do share with cephalopods (and with many other animals, including dogs), rather than cones, are rods—light-sensitive structures in the back of the eye that are stimulated by shapes and lines rather than by color. So, when we find the color changes in cephalopods so fascinating, it’s even more fascinating to keep in mind that the animals making those colors don’t directly perceive them. This strikes me as sadly ironic.
But the cephalopods do receive compensation for their loss via their probable ability to see various levels of brightness, or degrees of luminosity. It’s worth pausing to think about: Cephalopods make these colors because of the ongoing oceanic arms race and not because they themselves can see them. For survival, it’s apparently more important that other animals see the cephalopod colors than that the cephalopods themselves see those colors.
The comparative study of the human and cephalopod eye calls into question “convergent” evolution, the theory that two very different species with very different ancestries might evolve similar solutions to the same problem. The classic example of convergent evolution is the wing of the bat and the wing of the bird. Birds evolved from dinosaurs and bats evolved from the proto-mammals that survived the extinction of the dinosaurs. Yet their wings are similar. Evolutionary theorists used to say that the two wings converged on the same solution. The image is one of two different roads meeting at an intersection.
The human eye and the cephalopod eye were said to be another such example. Those who doubt the theory of evolution have often said that such a thing is impossible and that the similarity of the two eyes is proof of a divine creator. The concept of random mutation resulting in two similar eyes, they suggest, is simply absurd. In that one issue, creationists and Charles Darwin were agreed.
But it turns out that neither eye evolved by accident. The genes to create both eyes, scientists now believe, were probably present from the early days of animal evolution. The cephalopod eye has shown scientists a continuity in evolution that’s more organized than we suspected even a few short decades ago.
Indeed, evolution is a much simpler mechanism than anyone guessed. All eyes in the animal kingdom start with the same basic genetic building blocks. These building blocks, certain specific genes, are simply juggled in different ways to make different styles of eyes. Imagine a small set of Legos. From that set, you can build all sorts of things—cars, houses, furniture, railroads. All these seemingly different items evolve out of the same set of building blocks.
This is the surprise: To evolve different styles of eyes, it was not necessary for brand-new genes to appear. All that was necessary was the juggling of genes already present. Eyes throughout the animal kingdom have evolved different styles as a result of complex interactions between this basic eons-old genetic tool kit and the world in which the animal lives. The eye of the nautilus, cousin to the squid, is a simple pinhole eye. It is much less complex, requires much less energy to make and to operate, and is all the animal, protected by a shell, needs to survive. The squid and the octopus, on the other hand, need much better eyes in order to hunt and to hide from predators. You can think of the camera eye as the squid’s equivalent of a protective shell: As they lack a shell, the camera eye provides them with a substantial advantage.
All of this might seem a bit far-fetched, but researchers in the past several years have shown that the journey from a simple eye to one like ours is comparatively short—perhaps less than a half million years.
Scientist and author Neil Shubin believes that most animals possess what he calls a “master switch in eye evolution.” Because of this, he and others suggest, the concept of “convergent” evolution might be outdated. In a paper in Nature, they wrote that the more accurate term might be “parallel” evolution.
If it’s sad to us that cephalopods can’t see the full range of the bewildering beauty they create, their ability to control all these chromatophores with the numerous supporting cells nevertheless requires a great deal of brainpower. The basis of that power is another kind of cell—the neuron—that’s apparently also been present for quite a while on the evolutionary timeline. These squid neurons with their tree-trunk-like axons have helped us answer one of the beachgoer’s most pressing questions: Why, when a crab bites your toe, does your mouth scream “Ouch!”?
CHAPTER SEVEN
DIAPHANOUS AND DELICATE
The biology of the mind will be to the twenty-first century what the
biology of the gene was to the twentieth century.
—ERIC KANDEL
or more than a century, the summertime village of Woods Hole, Massachusetts, has been a world-renowned center of intellectual excitement as well as a fashionable watering hole for the scientific elite. Some of the world’s best biologists, including a liberal salting of Nobel Prize winners, have come to sit on the beach and play tennis, to work in the research facilities of the Marine Biological Laboratory, to give and attend lectures, and to exchange ideas. The village’s sidewalks overflow with scientists, students, and tourists. There’s rarely a place to park your car, even on Albatross Street, and you can count on the Water Street drawbridge, which lets boats leave their Eel Pond moorings for destinations like Martha’s Vineyard or Nantucket, being raised and lowered many times throughout the day.
But in the winter, the village can be awfully forlorn. Water Street has a distinctly dowdy look, as though it’s down on its luck. Slate-gray skies hang heavy over the silent, institutional buildings. The renowned science library, where you can hold in your own hands scientific journals from the mid-1800s, is almost deserted. If you walk down the main street on the wrong November day, you could easily think that the village is on the skids.
But if you’re there on the right November day, there’s an intellectual Indian summer. That’s when the neurosurgeons arrive, ready to bone up on the latest discoveries in their field. Among the many skills they learn is how to dissect a live axon from a decapitated squid. Or, at least, they try to learn that skill.
On the particular day I went to observe, it was chilly and wet. Sheets of rain flooded the streets. Farther north in New England, it was snowing. The first crew of confident neurosurgeons made their way, heads down against the downpour, to the research building where so many Nobel scientists have worked and where squid and other marine life-forms have been studied for nearly a century.
Course teacher Bruce Andersen, a neurosurgeon from Idaho, picked up an eight-inch squid, a common Loligo pealei, in one hand. He held a pair of scissors in the other. The animal’s chromatophores were showing. It flushed a deep, rich red.
Andersen held on to the squid body. The animal’s one head, eight arms, and two tentacles writhed.
“We’ll start with the gross dissection,” he said.
Then he snipped off the head.
A deep, anguished groan came from the thirty mostly male surgery residents.
“Neurosurgeons are surprisingly squeamish,” Andersen told me later.
“And it’s all for the good of science,” he told them.
“This is all the guts ’n’ stuff,” he said as he cleaned the body out.
Next, he demonstrated how to lay out the squid’s body, find the giant axon that allowed the animal to swim, and gently remove it.
Andersen gave each student a squid and ordered the students to begin their own fine dissection—the removal of the squid axon from the animal’s flesh. Properly handled, an axon can continue to function for hours after the animal is dead, even when completely removed from the specimen. The point of the exercise was to remove the axon without harming it.
Loligo’s giant axon
This turned out to be more difficult than the neurosurgeons expected. Loligo’s axon is large and easily visible, but it’s also diaphanous, like a beautiful bridal veil or a thin sheet of water cascading over rocks. It’s as delicate as gossamer and as easily destroyed as the filament spun by a small spider.
Nick the axon cell membrane and you’re toast.
All the surgeons tried. All failed.
Their axons died on the operating table.
“You’ll all have to go talk to the families now,” Andersen instructed. “Luckily, few squid have good lawyers.”
It may seem strange that medical doctors practice their neuroscience skills on squid, but it turns out that the squid’s neuron with its axon, so diaphanous and delicate, behaves quite like a neuron in our own brains. These nerve cells, or neurons, are “the workhorse of the nervous system,” in the words of one particularly articulate neuroscientist, Robert Sapolsky. Without the neuron, we wouldn’t function. It allows us to move our muscles, to meditate on the meaning of life, to read books and talk about what we’ve read. Yet in humans, neurons are ineffably tiny. “Few things in clinical neurosurgery approach the scale and delicacy of dissecting a 300-micron human axon,” Andersen said.
We humans have very roughly 100 billion such cells. And as unlovely and nonmammalian as Dosidicus and Architeuthis and other squid may be, we share this important cell with them. Because of this, scientists suspect that the neuron in one form or another has been around on our planet for quite a while, possibly since the days of urbilateria.
For us, neurons are not easy to come by. In general, we get all the neurons we’ll ever have soon after birth, although under the right circumstances the human brain may be able to grow a few absolutely spanking new neurons in a few locations in the brain during adulthood. This process is called “neurogenesis,” and it remains poorly understood and somewhat controversial. We certainly can’t generate new neurons on a large scale, though.
Human neurogenesis pales next to the ability of the cephalopod to continue to create neurons throughout much of its life. In many cephalopod species, if an arm or tentacle is lost, the animal is able to grow a new one. No one understands exactly how this happens, but scientists consider it a fertile avenue for future study.
But there is one overarching and somewhat astonishing truth, a marvelous fact of evolutionary history: A neuron is a neuron is a neuron. The neuron is a near-universal phenomenon, existing throughout much of the animal world. Because life is flexible, there are some differences in neurons among various species, but the basic idea has been around for hundreds of millions of years.
I find this thrilling. Comforting, really. Sharing our neuron—the cell that gives us our individuality and our particular personality—with so many other species makes our planet a little less lonely. The foundation of our ability to think is the same foundation that allows the cuttlefish to change color and shape instantly, or the Humboldt to swim in the ocean or fly through the air at super-high speeds. (Yes, Humboldt and some other squid species can “fly” by shooting out of the water at very high speeds, although they don’t flap their fins the way birds flap their wings.) The neuron allows the giant squid to live in the deepest parts of our ocean and the colossal squid to hunt by using its “headlights.” It allows birds to navigate our skies. There were neurons in dinosaurs that allowed them to eat, and neurons in the first tiny proto-mammals that allowed them to survive the destruction that killed the dinosaurs and eventually to become—us. As evolution continues and we disappear from the universe, as we certainly will sooner or later, the neuron will probably go on, blossoming in some other intelligent being’s brain and, hopefully, creating a life-form that finally figures out how to stop fighting and just enjoy being alive.
The neuron is the main cell in the cephalopod’s brain, and in my brain, and in your brain. As you read these words, your neurons are hard at work, assembling the black ink on the page into very large concepts, like the universality of life.
A typical human neuron
The neuron has three basic parts that you need to know about: the cell body, the dendrites, and the axon.
The first is the cell body, a kind of a torso, in a sense. Like your own torso, the cell body contains most of the parts necessary to keep the cell alive. The body of a neuron, an extremely busy place, is like the manufacturing hub of a large city. The nucleus, where most of the neuron’s DNA resides, performs a kind of executive function, directing the building of all kinds of molecules the neuron needs in order to thrive and help you accomplish goals like moving muscles, reading a book, and thinking about science.
The second major part of a neuron is the network of dendrites leading into the cell body. Dendrites extend from the cell body like little hairs and are there to absorb information from the world outside the neuron and take it into the cell body for consideration. Dendrites are roughly the equivalent of e-mail in-boxes. Some scientists call dendrites the “antenna systems” of the neuron, because they absorb signals and then send those signals to the cell body. The absorbed information might come from another neuron, or it might come from the world outside. There are special neurons, called “sensory neurons,” with unique types of dendrites that allow you to see, to hear, to smell, to touch, and to taste. The number of sensory neurons differs greatly from species to species. A dog does not see the array of colors that we see, but has many, many more neurons and dendrites devoted to smell than we humans do. We are limited to roughly 5 million such smell receptors, while some dogs may have more than 200 million. While the dog misses the glorious world of color that we see, we enjoy only a fraction of the odiferous universe that the dog gets high on when it rides in the back of the car. There are even sometimes immense differences in breeds. German shepherds have twice as many neurons devoted to smell than do dachshunds.
Sometimes the dendrites leading into a nonsensory neuron are so plentiful that, under a microscope, they look very much like a richly branched coral, or perhaps like a piece of finely tatted lace. This is a good thing. In the case of dendrites, complexity is what you want. The more dendrites a neuron has, the better connected that neuron is with other neurons in the brain. Dendrites are constantly growing and changing. The more reading, thinking, information gathering, and just plain experiencing a person enjoys, the richer his or her dendritic connections.
Human infants are born with some, but not a lot, of dendrites. There is, however, plenty of space for dendrites to develop, and if the infancy is normal, that’s exactly what happens. The process of growing up is the process of developing more and more dendrites. This is why kids shouldn’t spend all their time playing with their electronic toys: They’re missing out on building all the other dendritic connections they will need to live a full life as an adult. Experience-deprived kids have many fewer dendrites (and the consequent interconnections with other neurons) than do humans who were fortunate enough to enjoy a highly enriched childhood.
Nurture—experience—intertwines with nature. As important as our DNA is, our lives are not genetically predetermined, because the genes we are born with interact constantly with the world we live in.
The third main part of the neuron is the axon, which performs its main function after the neuron’s cell body assembles all the information brought in by the dendrites; if conditions are correct, the information is sent down the axon to another cell. The axon is huge compared to the rest of the neuron. It’s often more than 99 percent of the whole cell. Each axon is essential to your body because you don’t constantly grow new ones. Moreover, many neurons have only one axon, only one pathway through which they can send information or instructions out of the cell. And that’s pretty much it. For life. If you damage that axon, forget about the cell. Eventually the axon will die back all the way to the cell body, and the cell itself will die. Nerve injuries are actually destroyed axons, and researchers have learned that the cause of many neurological diseases is a slowly disintegrating axon.
Neural axons v
ary greatly in length. The axon may carry information to other neurons located right next door in the brain. In that case, the axon may be very short, perhaps only a little more than a hair’s width. Or it may send instructions, like “run away from the crab that just bit you,” to muscles all the way down your torso and then connect with other neurons in your spinal cord that pass the message on to your leg and, ultimately, to your toe.
Human axons like these may be several feet in length. A giraffe may have an axon that’s as long as 15 feet, while the blue whale, currently the planet’s largest animal, may have an axon as long as 60 feet. The blue whale’s axon extends from its brain down much of the length of its body. The final result: the flexing of its tail muscles. It takes a blue whale a longer time to send a message to its tail than it takes your brain to send a message to your toe. But the time difference is not one that we’d notice easily, since responses to our environmental surroundings happen, often, much more quickly than we are able to consciously think about them. In other words, we are likely to have already run away from the crab by the time we get around to thinking, Stupid crab!
Just as all neural axons are not the same length, neither are they the same diameter. The thickness of an axon is species-dependent. Humans have axons that are too thin to see without a microscope. Instead, what we see are bundles of axons, what we commonly call “nerves.” The nerve bundle that leads from our eye to our brain, called the optic nerve, has about one million axons. Neurosurgeons rarely operate on individual axons, but instead often work on these bundles when they try to repair nerves. Individual human axons are too small and too delicate to work with under normal circumstances.
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