Build a Better Brain

Learning, the process by which we acquire information about our world, may actually change our brains for the better.

By Beth Livermore, published on September 01, 1992 - last reviewed on October 02, 2009

Picture a nerve cell. Extending out from the cell body in one direction is the axon, or output arm. Shorter receiving cables, or dendrites, stem from other parts of the cell. The ultra-thin fibers of axon and dendrite terminate in tiny branches. Between the axonal branches of one cell and the dendrite ends of the next is an infinitesimal space—the synapse—which is the site of communication between two neurons.

When an electric charge is sent from one cell to the next, it is ferried across the synaptic gap with the help of specialized chemicals knows as neurotransmitters. The neurotransmitter influences the electrical conditions at the synapse, and the receiving neuron fires if it collects enough charge, carrying the starting stimulus to the next cell down the line.

A single neuron can send and receive thousands of signals a second. All this brain noise produces a biological translation of the words that you just read. How this message is eventually stored, or retained, is less clear. Most neurobiologists suggest that memory involves some kind of sustained changes in the neurons and their connections—perhaps similar to those that occur during information acquisition. The cells that respond when you recall Hamlet's Act III soliloquy, for instance, may be the same ones that were throbbing when you were taking it in originally.

It is now widely accepted that memory is not stored in a single cell but is spread out over an extensive neuronal network. Each cell provides a tiny piece of a complex mosaic. "Even the simplest memory is spread out over millions of neurons," Stevens says.

Along the same lines, memory recall appears to involve multiple parts of the brain. The most convincing evidence comes from a study by neuroscientists Marcus Raichle, Ph.D., of Washington University in St. Louis, and San Diego's Larry Squire. The two peered by PET scan into the brains of a group of subjects asked to remember specific words. As the subjects reached back into their memory, their brain images flashed all over with light, a sign many sites were participating in the process. "Memory," says Raichle, "is like a piece of music—it has lots of different parts that come together to create the whole."

Further, "we appear to have specialized processing centers that act in different combinations when we recognize something. We know that the hippocampus plays a critical role in laying down new memories and recalling the recent past." Raichle and others think that memory formed in the hippocampus gets stored in the neighboring neocortex, a setup that frees the hippocampus for new tasks. No one, however, knows for sure how a short-term memory, which lasts for a couple of days at best, turns into long-term memory that can last a lifetime.

It is a problem Columbia University's Eric Kandel has been working on for three decades. In his painstaking investigations into how experience changes the nervous system, or the cellular and molecular mechanisms of learning and memory, he has focused on the simple nervous system of the sea snail Aplysia. Its 20,000 neurons are the largest in the animal kingdom. For this Kandel is considered by some to be the most reductive scientist of our times.

Along with magnificently accessible nerve cells, Aplysia also has an easily observable behavior, the "gill withdrawal" reflex. Tap on Aplysia's spout, or siphon, and the snail withdraws its gill. Kandel found that if he shocked the snail's tail, the creature became "sensitized." It learned to overreact, to instantly withdraw its gill upon the slightest touch. (A basic form of learning, sensitization takes place in humans as well.)

Once Kandel identified the key cells that contribute to this type of learned behavior, he then looked for changes that, with training, occurred within the cells. He and his colleagues found that a single tail shock—which produces short-term memory for sensitization—activates a cascade of cellular events in which the sensory neuron releases more neurotransmitter so that the neural connections are strengthened between the sensory neuron from the siphon and the motor neuron for the gill. As a result, the communication between the sensory and motor cells becomes more efficient.

If not reinforced, this activity is transient, and the increase in strength of the connections lasts only minutes. However, when the tail shocks are repeated at least four or five times, long-term memory forms as a result of prodding the synthesis of new proteins within the nerve cells. Under these conditions, Kandel finds, the sensory neuron actually undergoes an anatomical change. The neurotransmitter acts as a growth factor; there is a doubling of the number of synaptic connections the sensory cells make onto the motor cells. Now the cell is altered for a period of weeks so that it can send messages more effectively than before, thereby enhancing information processing within the brain.

That this phenomenon applies to you and me is becoming increasingly clear. What Kandel has observed of Aplysia, others have espied in mammals, including rats. University of Illinois neuroscientist William Greenough, Ph.D., for one, has found that neocortex neurons of rats reared in complex environments, and trained in a maze every day, had more extensive dendrites than did comparison animals. Their dendrites also sprouted more synapses. So experience seems to change the brains of rats much as it does those of sea snails.

Other researchers have recently focused increasing attention on another phenomenon, called long-term potentiation (LTP), that also seems to be a component of associative memory formation. To elicit the LTP response, researchers stick a probe into one section of hippocampal tissue and stimulate it briefly but intensely with electricity.