The human body is complexity built from simplicity. Our amazing internal communication system is formed by basic building blocks: neurons, or nerve cells. Throughout life, new neurons are born and unused ones wither away (Shors, 2014).

Neurons differ, but each consists of a cell body and its branching fibers (FIGURE 2.1). The neuron’s often-bushy dendrite fibers receive messages and conduct them toward the cell body. From there, the cell’s single axon fiber sends out messages to other neurons or to muscles or glands (FIGURE 2.2). Dendrites listen. Axons speak.

The messages neurons carry are electrical signals, or nerve impulses, called action potentials. These impulses travel down axons at different speeds. Supporting our billions of nerve cells are nine times as many spidery glial cells (“glue cells”). Neurons are like queen bees—on their own, they cannot feed or sheathe themselves. Glial cells are worker bees. They provide nutrients and myelin—the layer of fatty tissue that insulates some neurons. They also guide neural connections and clean up after neurons send messages to one another. Glia play a role in information processing—learning, thinking, and memory (Fields, 2011; Martín et al., 2015).

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Some action potentials trudge along at a sluggish 2 miles per hour, and others race along at 200 or more miles per hour. Can you guess which reacts faster, a human brain or a high-speed computer? The computer wins every time. Even our brain’s top speed is 3 million times slower than electricity zipping through a wire. Thus, unlike the nearly instant reactions of a computer, your “quick” reaction to a sudden event, such as a child darting in front of your car, may take a quarter-second or more. Your brain is vastly more complex than a computer, but slower at executing simple responses. And your reflexes would be slower yet if you were an elephant. The round-trip time for a message that begins with a yank on an elephant’s tail and then travels to its brain and back to the tail is 100 times longer than in the body of a tiny shrew (More et al., 2010).

Neurons interweave so tightly that even with a microscope, you would have trouble seeing where one ends and another begins. But end they do, at meeting places called synapses. At these points, two neurons are separated by a tiny synaptic gap less than a millionth of an inch wide. “Like elegant ladies air-kissing so as not to muss their makeup, dendrites and axons don’t quite touch,” noted poet Diane Ackerman (2004). How, then, does a neuron send information across the tiny gap? The answer is one of the important scientific discoveries of our age.

Each neuron is itself a miniature decision-making device, reacting to signals it receives from hundreds, even thousands, of other neurons. Most of these signals are excitatory, somewhat like pushing a neuron’s gas pedal. Others are inhibitory, more like pushing its brake.

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If the excitatory signals exceed the inhibitory signals by a minimum intensity, or threshold, the combined signals trigger an action potential. (Think of it this way: If the excitatory party animals outvote the inhibitory party poopers, the party’s on.) The neuron fires, sending an impulse down its axon, carrying information to another cell. Neurons then need a tiny break before they can fire again. This resting pause, called a refractory period, lasts fractions of a second.

A neuron’s firing doesn’t vary in intensity. The neuron’s reaction is an all-or-none response. Like guns, neurons either fire or they don’t. How, then, do we distinguish a big hug from a gentle touch? A strong stimulus (the hug) can trigger more neurons to fire, and to fire more often. But it does not affect the action potential’s strength or speed. Squeezing a trigger harder won’t make a bullet bigger or faster.

When the action potential reaches the axon’s end, your body performs an amazing trick. Your neural system converts an electrical impulse into a chemical message. At the synapse, the impulse triggers the release of neurotransmitter molecules, chemical messengers that can cross the synaptic gap (FIGURE 2.3). Within one 10,000th of a second, these molecules bind to receptor sites on the receiving neuron, as neatly as keys fitting into locks. They then act as excitatory or inhibitory signals, and the process begins again in this new cell. The excess neurotransmitters finally drift away, are broken down by enzymes, or are reabsorbed by the sending neuron—a process called reuptake. Some antidepressant medications work by partially blocking the reuptake of mood-enhancing neurotransmitters (FIGURE 2.4).

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Dozens of different neurotransmitters have their own pathways in the brain. As they travel along these paths, they carry specific but different messages that influence our motions and emotions. Dopamine levels, for example, influence our movement, learning, attention, and feelings of pleasure and reward. Serotonin levels can make us more or less moody, hungry, sleepy, or aroused. TABLE 2.1 outlines the effects of these and other neurotransmitters.

In Chapter 1, we promised to show you how psychologists play their game. Here’s an example. An exciting neurotransmitter discovery emerged when researchers attached a radioactive tracer to morphine, an opiate drug that elevates mood and eases pain (Pert & Snyder, 1973). (Radioactive tracers send out harmless but detectable energy as they pass through the body.) As researchers tracked the morphine, they noticed it was binding to receptors in brain areas linked with mood and pain sensations. Why, they wondered, would these natural “opiate receptors” exist? Might the brain have these chemical locks because our body produces a natural key—some built-in painkiller—to open them?

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Further work revealed the answer. When we are in pain or exercising vigorously, the brain does, indeed, produce several types of neurotransmitter molecules similar to morphine. These natural opiates, now known as endorphins (short for endogenous [produced within] morphine), help explain why we can be unaware of pain after an extreme injury. They also explain the painkilling effects of acupuncture, and the good feeling known as “runner’s high” (Boecker et al., 2008).

If our natural endorphins lessen pain and boost mood, why not amplify this effect by flooding the brain with artificial opiates, such as heroin and morphine? Because the brain does a chemical balancing act. When flooded with artificial opiates, it may shut down its own “feel-good” chemistry. If the artificial opiates are then withdrawn, the brain will be deprived of any form of relief. Nature charges a price for suppressing the body’s own neurotransmitter production.

Throughout this book, you’ll hear more about the many roles neurotransmitters play in our daily lives. But let’s first continue our journey into the brain.