The Teenage Brain: A neuroscientist’s survival guide to raising adolescents and young adults. Frances Jensen E.

estate.) If, on the other hand, the information is new, then it is farmed out to one of several locations in the brain that store long-term memories. Although nearly instantaneous, the transmission of sensory information is not perfect. In the same way that the otherwise seamless signal coming from your TV is occasionally interrupted, briefly distorting the picture, so, too, does degradation occur as information races up and down the axons of your brain’s neurons. This explains why our memories are never perfect, but have holes or discontinuities, which we occasionally fill in, albeit unconsciously, with false information.

      The brain is programmed to pay special attention to the acquisition of novel information, which is what learning really is. The more activity or excitation between a specific set of neurons, the stronger the synapse. Thus, brain growth is a result of activity. In fact, the young brain has more excitatory synapses than inhibitory synapses.

      The more a piece of information is repeated or relearned, the stronger the neurons become, and the connection becomes like a well-worn path through the woods. “Frequency” and “recency” are the key words here—the more frequently and the more recently we learn something and then recall it or use it again, the more entrenched the knowledge, whether it’s remembering the route between home and work or how to add a contact to your smartphone’s directory. In both cases, the mental machinery of learning is dependent on the synapse, that minuscule space where packets of information are passed from one neuron to another by electrical or chemical messengers. For these neural connections to be made, both sides of a synapse need to be “on,” that is, in a state of excitation. When an excitatory input exceeds a certain level, the receiving neuron fires and begins the molecular process, called long-term potentiation, by which synapses and neuronal connections are strengthened. The process of long-term potentiation, or LTP, is a complex cascade of events involving molecules, proteins, and enzymes that starts and ends at the synapse.

      FIGURE 10. Long-Term Potentiation (LTP) Is a Widely Used Model of the “Practice Effect” of Learning and Memory: A. The hippocampus is located inside the temporal lobe. B. Brain cell activity recorded in hippocampal slices from rodents shows changes in cell signals after a burst of stimulation. C. LTP experiments commonly record repeated small responses to stimuli until a burst is given (akin to the “practice effect”), after which point responses from the neuron to the original stimulus become much larger, as if “memorized” or “practiced.”

      The process of LTP begins with the main excitatory neurotransmitter, glutamate, being released at the axon terminal of one neuron across the synapse to the receptor on the dendrite of the receiving neuron. Glutamate is directly involved in building stronger synapses. How does it do this? Glutamate acts as a catalyst and sets off a chain reaction that eventually builds a bigger and stronger synapse, or connection in a brain pathway. When glutamate “unlocks” the receptor, it triggers calcium ions to zip around the synapse. The calcium, in turn, activates many molecules and enzymes and interacts with certain proteins to change their shape and behavior, which in turn can change the structure of synapse and neuron to make them more or less active. Calcium can alter existing proteins very rapidly, within seconds to hours, and it can also activate genes to make new proteins, a process that can take hours to days. The end result is a synapse that is bigger and stronger and that can cause a bigger response in the activated cell. In experiments, this increased response can be measured electrically as a bigger signal. Compared with the response before the “training” and the consequent building of a stronger synapse, the response in the cell after this strengthening, or potentiation, is much larger, and these measurements are the typical ones used in LTP experiments. In fact, if you are learning any of this at all, you are building new synapses as you read. Only minutes after you learn a new thing, your synapses start to grow bigger. In a few hours they are virtually cemented into a stronger form.

      John Eccles, who would go on to win a Nobel Prize for his early work in the study of synapses, was perplexed by how much stimulation was needed to produce a synaptic change. “Perhaps the most unsatisfactory feature of the attempt to explain the phenomena of learning,” he wrote, “is that long periods of excess use or disuse are required in order to produce detectable synaptic change.” What Eccles failed to realize is that the repetitions he observed so frustratingly—those “long periods of excess use”—were the brain at work, learning and acquiring knowledge. After repeated stimulation, a brain cell will respond much more strongly to a stimulus than it initially did. Hence, the brain circuit “learns.” And the more ingrained the knowledge, the easier it is to recall and use. As when skiers race through a slalom course, the quickest route down becomes worn by use. Ruts develop. By the time the last competitors race through the gates, the route is so deeply entrenched in the snow that they can’t ski out of it, nor do they need or want to. The deeply imprinted line, in fact, guides them down without their having to search for it.