For scientists, it is a happy fact of nature that the information systems of humans and other animals operate similarly—so much so that you could not distinguish between small samples of brain tissue from a human and a monkey. This similarity allows researchers to study relatively simple animals to discover how our neural systems operate. Cars differ, but all have engines, accelerators, steering wheels, and brakes. A space alien could study any one of them and grasp the operating principles. Likewise, animals differ, yet their nervous systems operate similarly. Though the human brain is more complex than a rat’s, both follow the same principles.

3-2 What are neurons, and how do they transmit information?

Our body’s neural information system is complexity built from simplicity. Its building blocks are neurons, or nerve cells. Throughout life, new neurons are born and unused neurons wither away (Shors, 2014). To fathom our thoughts and actions, our memories and moods, we must first understand how neurons work and communicate.

Neurons differ, but all are variations on the same theme (FIGURE 3.1). Each consists of a cell body and its branching fibers. The often bushy dendrite fibers receive information and conduct it toward the cell body. From there, the cell’s single lengthy axon fiber passes the message through its terminal branches to other neurons or to muscles or glands. (See FIGURE 3.2.) Dendrites listen. Axons speak.

Unlike the short dendrites, axons may be very long, projecting several feet through the body. A human neuron carrying orders to a leg muscle, for example, has a cell body and axon roughly on the scale of a basketball attached to a 4-mile-long rope. Much as home electrical wire is insulated, some axons are encased in a myelin sheath, a layer of fatty tissue that insulates them and speeds their impulses. As myelin is laid down up to about age 25, neural efficiency, judgment, and self-control grow (Fields, 2008). If the myelin sheath degenerates, multiple sclerosis results: Communication to muscles slows, with eventual loss of muscle control.

Supporting our billions of nerve cells are 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 insulating myelin, guide neural connections, and clean up after neurons send messages to one another. Glia also play a role in learning and thinking. By “chatting” with neurons they participate in information transmission and memory (Fields, 2011, 2013; Miller, 2005).

In more complex animal brains, the proportion of glia to neurons increases. A postmortem analysis of Albert Einstein’s brain did not find more or larger-than-usual neurons, but it did reveal a much greater concentration of glial cells than found in an average Albert’s head (Fields, 2004).

Neurons transmit messages when stimulated by signals from our senses or when triggered by chemical signals from neighboring neurons. A neuron sends a message by firing an impulse, called the action potential—a brief electrical charge that travels down its axon.

Depending on the type of fiber, a neural impulse travels at speeds ranging from a sluggish 2 miles per hour to more than 200 miles per hour. But even its top speed is 3 million times slower than that of electricity through a wire. We measure brain activity in milliseconds (thousandths of a second) and computer activity in nanoseconds (billionths of a second). Thus, unlike the nearly instantaneous reactions of a computer, your 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 if you were an elephant—whose round-trip message travel time from a yank on the tail to the brain and back to the tail is 100 times longer than that of a tiny shrew—your reflexes would be slower yet (More et al., 2010).

Like batteries, neurons generate electricity from chemical events. In the neuron’s chemistry-to-electricity process, ions (electrically charged atoms) are exchanged. The fluid outside an axon’s membrane has mostly positively charged sodium ions. A resting axon’s fluid interior (which includes both large, negatively charged protein ions and smaller, positively charged potassium ions) has a mostly negative charge. Like a tightly guarded facility, the axon’s surface is selective about what it allows through its doors. We say the axon’s surface is selectively permeable. This positive-outside/negative-inside state is called the resting potential (measured at about −70 mV [millivolts]; see FIGURE 3.3 below).

When a neuron fires, the first section of the axon opens its gates, rather like a sewer cover flipping open, and positively charged sodium ions (attracted to the negative interior) flood in through the now-open channels (FIGURE 3.3 above). The loss of the inside/outside charge difference, called depolarization, causes the next section of axon channels to open, and then the next, like a line of falling dominos. This temporary inflow of positive ions is the neural impulse—the action potential (measured at about +40 mV). Each neuron is itself a miniature decision-making device performing complex calculations as it receives signals from hundreds, even thousands, of other neurons. The mind boggles when imagining this electrochemical process repeating up to 100 or even 1000 times a second. But this is just the first of many astonishments.

Most neural signals are excitatory, somewhat like pushing a neuron’s accelerator. Some are inhibitory, more like pushing its brake. If excitatory signals exceed the inhibitory signals by a minimum intensity, or threshold (about −55 mV; see FIGURE 3.3), 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 action potential then travels down the axon, which branches into junctions with hundreds or thousands of other neurons or with the body’s muscles and glands.

Neurons need tiny breaks between action potentials. During a resting pause called the refractory period, subsequent action potentials cannot occur until the axon returns to its resting state. Then the neuron can fire again.

Increasing the level of stimulation above the threshold will not increase the neural impulse’s intensity. The neuron’s reaction is an all-or-none response: Like guns, neurons either fire or they don’t. How, then, do we detect the intensity of a stimulus? How do we distinguish a gentle touch from a big hug? A strong stimulus 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 go faster.

3-3 How do nerve cells communicate with other nerve cells?

Neurons interweave so intricately that even with a microscope you would have trouble seeing where one neuron ends and another begins. Scientists once believed that the axon of one cell fused with the dendrites of another in an uninterrupted fabric. Then British physiologist Sir Charles Sherrington (1857–1952) noticed that neural impulses were taking an unexpectedly long time to travel a neural pathway. Inferring that there must be a brief interruption in the transmission, Sherrington called the meeting point between neurons a synapse.

We now know that the axon terminal of one neuron is in fact separated from the receiving neuron by a synaptic gap (or synaptic cleft) less than a millionth of an inch wide. Spanish anatomist Santiago Ramón y Cajal (1852-1934) marveled at these near-unions of neurons, calling them “protoplasmic kisses.” “Like elegant ladies air-kissing so as not to muss their makeup, dendrites and axons don’t quite touch,” noted poet Diane Ackerman (2004, p. 37). How do the neurons execute this protoplasmic kiss, sending information across the tiny synaptic gap? The answer is one of the important scientific discoveries of our age.

When an action potential reaches the knob-like terminals at an axon’s end, it triggers the release of chemical messengers, called neurotransmitters (FIGURE 3.4). Within 1/10,000th of a second, the neurotransmitter molecules cross the synaptic gap and bind to receptor sites on the receiving neuron—as precisely as a key fits a lock. For an instant, the neurotransmitter unlocks tiny channels at the receiving site, and electrically charged atoms flow in, exciting or inhibiting the receiving neuron’s readiness to fire. The excess neurotransmitters then drift away, are broken down by enzymes, or are reabsorbed by the sending neuron—a process called reuptake.

3-4 How do neurotransmitters influence behavior, and how do drugs and other chemicals affect neurotransmission?

In their quest to understand neural communication, researchers have discovered several dozen neurotransmitters and almost as many new questions: Are certain neurotransmitters found only in specific places? How do neurotransmitters affect our moods, memories, and mental abilities? Can we boost or diminish these effects through drugs or diet?

Other modules explore neurotransmitter influences on hunger and thinking, depression and euphoria, addictions and therapy. For now, let’s glimpse how neurotransmitters influence our motions and emotions. Particular neurotransmitters affect specific behaviors and emotions (TABLE 3.1).

One of the best-understood neurotransmitters, acetylcholine (ACh), plays a role in learning and memory. In addition, it is the messenger at every junction between motor neurons (which carry information from the brain and spinal cord to the body’s tissues) and skeletal muscles. When ACh is released to our muscle cell receptors, the muscle contracts. If ACh transmission is blocked, as happens during some kinds of anesthesia and with some poisons, the muscles cannot contract and we are paralyzed.

Candace Pert and Solomon Snyder (1973) made an exciting discovery about neurotransmitters when they attached a radioactive tracer to morphine, showing where it was taken up in an animal’s brain. The morphine, an opiate drug that elevates mood and eases pain, bound to receptors in areas linked with mood and pain sensations. But why would the brain have these “opiate receptors”? Why would it have a chemical lock, unless it also had a natural key to open it?

Researchers soon confirmed that the brain does indeed produce its own naturally occurring opiates. Our body releases several types of neurotransmitter molecules similar to morphine in response to pain and vigorous exercise. These endorphins (short for endogenous [produced within] morphine) help explain good feelings such as the “runner’s high” (Boecker et al., 2008), the painkilling effects of acupuncture, and the indifference to pain in some severely injured people. But once again, new knowledge led to new questions.

HOW DRUGS AND OTHER CHEMICALS ALTER NEUROTRANSMISSION If indeed the endorphins lessen pain and boost mood, why not flood the brain with artificial opiates, thereby intensifying the brain’s own “feel-good” chemistry? But there is a problem: When flooded with opiate drugs such as heroin and morphine, the brain, to maintain its chemical balance, may stop producing its own natural opiates. When the drug is withdrawn, the brain may then be deprived of any form of opiate, causing intense discomfort. For suppressing the body’s own neurotransmitter production, nature charges a price.

Drugs and other chemicals affect brain chemistry, often by either exciting or inhibiting neurons’ firing. Agonist molecules increase a neurotransmitter’s action. Agonists may increase the production or release of neurotransmitters, or block reuptake in the synapse. Other agonists may be similar enough to a neurotransmitter to bind to its receptor and mimic its excitatory or inhibitory effects. Some opiate drugs are agonists and produce a temporary “high” by amplifying normal sensations of arousal or pleasure.

Antagonists decrease a neurotransmitter’s action by blocking production or release. Botulin, a poison that can form in improperly canned food, causes paralysis by blocking ACh release. (Small injections of botulin—Botox—smooth wrinkles by paralyzing the underlying facial muscles.) These antagonists are enough like the natural neurotransmitter to occupy its receptor site and block its effect, but are not similar enough to stimulate the receptor (rather like foreign coins that fit into, but won’t operate, a candy machine). Curare, a poison some South American Indians have applied to hunting-dart tips, occupies and blocks ACh receptor sites on muscles, producing paralysis in their prey.