Your Beautiful Brain

Dispatches from the frontiers of neuroscience.

by Bill Retherford '14JRN Published Winter 2016
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“Nothing changed,” he says. Turns out the deep layers weren’t relying on the upper cortex at all; they still received the incoming sensory information. The two cortex regions, Bruno discovered, can operate independently of each other. Independent yet intertwined: “They do work together,” he says. “But they also look like they have different jobs. What’s the job of this half of the cortex versus the other half? I don’t know.”

But he already has a hypothesis. Perhaps, Bruno says, the upper layers mediate “context-dependent” behaviors, and make sense of intermingling and often conflicting situations. (A rabbit is hungry. It sees wildflowers nearby. But a hawk hovers overhead. Does the rabbit chance it and go for the wildflowers? Or take off and go hungry?) The computations performed in the upper layers, suggests Bruno, are good at evaluating conflicting data in context. They decide what to do.

"Evolution is smart. Clean, clear, and simple. This is what innate hardwired circuits are all about."

If that’s so, then another theory, even more provocative, surfaces. Psychiatric patients often have problems making decisions that involve context. “Schizophrenics are an example,” says Bruno. “Interpreting sensory signals in context is difficult for them. They really struggle with it. They can’t deal with it.” Which raises the question: could the malfunctioning neuronal networks that cause schizophrenia and other psychiatric disorders reside somewhere in the upper layers?

Determining that — the approximate vicinity of the faulty networks — is huge. “We would know where to start looking,” says Bruno. “We could narrow down the places where the actual biological defect is occurring.” If researchers could then pinpoint those dysfunctional neurons and target them with drugs, effective treatments for psychological disease could eventually result.

Lots of ifs. “Until we finish the science, that part is still science fiction,” Bruno says. “But that’s the hope, right?”

Nearly no one knows this about the nose,
but “most odors,” says Richard Axel, “do not elicit any behavioral responses without learning or experience.” That means your reaction to smell is tightly twined to memory. Whether garlic or gasoline, cologne or coffee, just-cut grass or just-smoked grass, your brain, not your nose, determines if you like or loathe the smell. Aromas transport you to memories that your brain has catalogued as pleasant or unpleasant; you respond accordingly. This is the core of Axel’s current research. “We are interested in how meaning is imposed on odor,” he says.

Already, at literally a neuronal level of detail, Axel has essentially explained why we can smell; he has identified more than one thousand receptor cells in the nose that talk to the olfactory bulb, the brain’s first relay station for smell. There, the odors are fine-tuned, processed, and propelled to other parts of the brain (“to at least five higher olfactory centers,” he says). For his seminal mapping of the smell system’s molecular bedrock, Axel won the 2004 Nobel Prize in Physiology or Medicine.

Richard Axel has identified more than one thousand receptor cells in the nose that convey data to the brain. / Photograph by Columbia News

“A given odor will call forth different experiences and produce different emotional responses for different individuals,” he says. Those flexible behavioral responses — fashioned between the olfactory bulb and the hippocampus, where we collect memories — are more robust with smell than with any of the other four senses. Even the fragrance of jasmine, supposedly the most sensual of scents, is contingent on context, says Axel. Breathe it in while spending an evening with someone you love. “Then jasmine would elicit a very pleasant response,” he says. But that could change, based on new experience: “Suppose that same person turned around and hurt you seriously. Then jasmine no longer will have the same effect on you.”

In simpler brains, many aromas provoke an instinctive and unalterable response. When mice get a whiff of fox urine, their hardwired neural pathway sends them running. “That’s because mice, for a long time, have been prey to foxes,” says Axel. Only a few scents, however, are hardwired in humans. Smoke, probably, is one. Anything rotting is another (the stench of sulfur, akin to rotten eggs, is revolting to most everybody). But that’s about it. Says Axel: “It’s very hard to conjure up odors that elicit innate responses in people.”

After four decades of foundational work, Axel recognizes the connection between his fundamental research and the furthermost cures. Discovering what’s under the hood could help clarify the latest curiosity about Alzheimer’s: for many patients, an early symptom is losing their sense of smell. “What can emerge from an experiment designed to understand one aspect of science can open up something more profound,” he says. “You go in, not knowing what is going to come out.”

In 1962, Eric Kandel commenced research on Aplysia
— the sea hare — a blobby mollusk with protruding feelers that resemble rabbit ears. Studying sea hares, friends and colleagues warned, was a calamitous blunder; fifty-four years later, Kandel remembers their disapproval. “Everyone thought I was throwing my career away,” he says. But Aplysia, with only twenty thousand neurons in its central nervous system, became Kandel’s odd little portal into the human brain: “It has the largest nerve cells in the animal kingdom. You can see them with the naked eye. They’re gigantic. They’re beautiful.” Four decades later, Kandel won the 2000 Nobel Prize for Physiology or Medicine. He had discovered how those neurons in Aplysia’s brain constructed and catalogued memories.

Today, as neuroscientists worldwide pursue remedies for Alzheimer’s and age-related memory loss, Kandel’s half century of findings are considered indispensable. Substantive therapies for Alzheimer’s in particular are “poised for success,” says Jessell, a colleague of Kandel’s for thirty-five years. “We’re on the cusp of making a difference.” But accompanying that claim is a caveat; the fledgling remedies are not panaceas. “We’re not necessarily talking about curing the disease,” he says. “But we are talking about slowing the symptomatic progression of the disease so significantly that lifestyles are improved in a dramatic way. If in ten years we have not made significant progress, if we are not slowing the progression of Alzheimer’s, then we have to look very seriously at ourselves and ask, ‘What went wrong?’”

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