Our thoughts, feelings, and actions depend on neural communication, but how does it happen? The communication of information within and between neurons proceeds in two stages. First, information has to travel inside the neuron via an electrical signal that travels from the dendrite to the cell body to the axon—a process called conduction. Then, the signal has to be passed from one neuron to another, usually via chemical messengers traveling across the synapse—a process called transmission. Let’s look at both processes in more detail.

The neuron’s cell membrane has small pores that act as channels to allow small electrically charged molecules, called ions, to flow in and out of the cell. It is this flow of ions across the neuron’s cell membrane that creates the conduction of an electric signal within the neuron. How does it happen?

The Resting Potential: The Origin of the Neuron’s Electrical Properties

Neurons have a natural electric charge called the resting potential, the difference in electric charge between the inside and outside of a neuron’s cell membrane (Kandel, 2000). The resting potential arises from the difference in concentrations of ions inside and outside the neuron’s cell membrane (see FIGURE 3.3a). Ions can carry a positive (+) or a negative (-) charge. In the resting state, there is a high concentration of a positively charged ion, potassium (K⁺), as well as negatively charged protein ions (A^–), inside the neuron’s cell membrane compared to outside it. By contrast, there is a high concentration of positively charged sodium ions (Na⁺) and negatively charged chloride ions (Cl^–) outside the neuron’s cell membrane.

The concentration of K⁺ inside and outside a neuron is controlled by channels in the cell membrane that allow K⁺ molecules to flow in and out of the neuron. In the resting state, the channels that allow K⁺ molecules to flow freely across the cell membrane are open, while channels that allow the flow of Na⁺ and the other ions are generally closed. Because of the naturally higher concentration of K⁺ molecules inside the neuron, some K⁺ molecules move out of the neuron through the open channels, leaving the inside of the neuron with a charge of about -70 millivolts relative to the outside. Like the Hoover Dam that holds back the Colorado River until the floodgates are released, resting potential is potential energy, because it creates the environment for a possible electrical impulse.

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The Action Potential: Sending Signals across the Neuron

The neuron maintains its resting potential most of the time. However, in the 1930s, biologists Alan Hodgkin and Andrew Huxley noticed that they could produce a signal by stimulating the axon with a brief electric shock, which resulted in the conduction of an electric impulse down the length of the axon (Hausser, 2000; Hodgkin & Huxley, 1939). This electric impulse is called an action potential, an electric signal that is conducted along the length of a neuron’s axon to a synapse.

The action potential occurs only when the electric shock reaches a certain level, or threshold. The action potential is all or none: Electric stimulation below the threshold fails to produce an action potential, whereas electric stimulation at or above the threshold always produces the action potential. The action potential always occurs with exactly the same characteristics and at the same magnitude regardless of whether the stimulus is at or above the threshold.

The action potential occurs when there is a change in the state of the axon’s membrane channels. Remember, during the resting potential, the channels that allow K⁺ to flow out are open, resulting in a net negative charge (–70 millivolts) relative to the outside. However, during an action potential, these channels briefly shut down, and channels that allow the flow of positively charged sodium ions (Na⁺) are opened (see FIGURE 3.3b). We’ve seen already that Na⁺ is typically much more concentrated outside the axon than inside. When the channels open, those positively charged ions (Na⁺) flow inside, increasing the positive charge inside the axon relative to the outside. This flow of Na⁺ into the axon pushes the action potential from negative (–70 millivolts) to positive (+40 millivolts).

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After the action potential reaches its maximum, the membrane channels return to their original state, and K⁺ flows out until the axon returns to its resting potential. This leaves a lot of extra Na⁺ ions inside the axon and a lot of extra K⁺ ions outside the axon. During this period when the ions are imbalanced, the neuron cannot initiate another action potential, so it is said to be in a refractory period, the time following an action potential during which a new action potential cannot be initiated. The imbalance in ions is eventually reversed by an active chemical “pump” in the cell membrane that moves Na⁺ outside the axon and moves K⁺ inside the axon (the pump does not operate during the action potential; see FIGURE 3.3c).

So far, we’ve described how the action potential occurs at one point in the neuron. But how does this electric charge move down the axon? It’s a domino effect. When an action potential is generated at the beginning of the axon, it spreads a short distance, which generates an action potential at a nearby location on the axon, and so on, thus conducting the charge down the length of the axon.

The myelin sheath facilitates the conduction of the action potential. Myelin doesn’t cover the entire axon; rather, it clumps around the axon with little break points between clumps, looking kind of like sausage links. These break points are called the nodes of Ranvier, after French pathologist Louis-Antoine Ranvier, who discovered them (see FIGURE 3.4). When an electric current passes down the length of a myelinated axon, the charge seems to “jump” from node to node rather than traverse the entire axon (Poliak & Peles, 2003). This process is called saltatory conduction, and it helps speed the flow of information down the axon.

When the action potential reaches the end of an axon, you might think that the action potential stops there. After all, the synaptic space between neurons means that the axon of one neuron and the neighboring neuron’s dendrites do not actually touch one another. However, the electric charge of the action potential takes a form that can cross the relatively small synaptic gap by relying on a bit of chemistry.

Axons usually end in terminal buttons, knob-like structures that branch out from an axon. A terminal button is filled with tiny vesicles, or “bags,” that contain neurotransmitters, chemicals that transmit information across the synapse to a receiving neuron’s dendrites. The dendrites of the receiving neuron contain receptors, parts of the cell membrane that receive neurotransmitters and either initiate or prevent a new electric signal.

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The action potential travels down the length of the axon of the sending neuron, or presynaptic neuron, to the terminal buttons, where it stimulates the release of neurotransmitters from vesicles into the synapse. These neurotransmitters float across the synapse and bind to receptor sites on a nearby dendrite of the receiving neuron, or postsynaptic neuron. A new electric signal is initiated in that neuron, which may in turn generate an action potential in that neuron. This electrochemical action, called synaptic transmission (see FIGURE 3.5), allows neurons to communicate with one another.

Neurotransmitters and receptor sites act like a lock-and-key system. Just as a particular key will only fit in a particular lock, so, too, some neurotransmitters will only bind to specific receptor sites on a dendrite. The molecular structure of the neurotransmitter must “fit” the molecular structure of the receptor site.

What happens to the neurotransmitters left in the synapse after the chemical message is relayed to the postsynaptic neuron? Something must make neurotransmitters stop acting on neurons; otherwise, there’d be no end to the signals that they send. Neurotransmitters leave the synapse through three processes (see FIGURE 3.5). First, neurotransmitters can be reabsorbed by the terminal buttons of the presynaptic neuron’s axon, a process called reuptake. Second, neurotransmitters can be destroyed by enzymes in the synapse, in a process called enzyme deactivation. Third, neurotransmitters can bind to receptor sites called autoreceptors on the presynaptic neuron. Autoreceptors detect how much of a neurotransmitter has been released into a synapse and signal the presynaptic neuron to stop releasing the neurotransmitter when an excess is present.

Types and Functions of Neurotransmitters

You might wonder how many types of neurotransmitters are floating across synapses in your brain right now. Today, we know that some 60 chemicals play a role in transmitting information throughout the brain and body and differentially affect thought, feeling, and behavior, but a few major classes seem particularly important. We’ll summarize those here, and you’ll meet some of these neurotransmitters again in later chapters.

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How Drugs Mimic Neurotransmitters

Each of these neurotransmitters affects thought, feeling, and behavior in different ways, so normal functioning involves a delicate balance of each. Even a slight imbalance—too much of one neurotransmitter or not enough of another—can dramatically affect behavior. People who smoke, drink alcohol, or take drugs, legal or not, are altering the balance of neurotransmitters in their brains.

Many drugs that affect the nervous system operate by increasing, interfering with, or mimicking the manufacture or function of neurotransmitters (Cooper, Bloom, & Roth, 2003; Sarter, 2006). Agonists are drugs that increase the action of a neurotransmitter. Antagonists are drugs that block the function of a neurotransmitter (see FIGURE 3.6).

For example, the drug L-dopa was developed to treat Parkinson’s disease, a movement disorder characterized by tremors and difficulty initiating movement and caused by the loss of neurons that use the neurotransmitter dopamine. Dopamine is created in neurons by a modification of a common molecule called L-dopa. Ingesting L-dopa will spur the surviving neurons to produce more dopamine. In other words, L-dopa acts as an agonist for dopamine. The use of L-dopa has been reasonably successful in the alleviation of Parkinson’s disease symptoms (Muenter & Tyce, 1971; Schapira et al., 2009).

As another example, amphetamine is a popular drug that stimulates the release of norepinephrine and dopamine. In addition, both amphetamine and cocaine prevent the reuptake of norepinephrine and dopamine. The combination of increased release of norepinephrine and dopamine and the prevention of their reuptake floods the synapse with those neurotransmitters, resulting in increased activation of their receptors. Both of these drugs, therefore, are strong agonists, although the psychological effects of the two drugs differ somewhat because of subtle distinctions in where and how they act on the brain. Norepinephrine and dopamine play a critical role in mood control, such that increases in either neurotransmitter result in euphoria, wakefulness, and a burst of energy. However, norepinephrine also increases heart rate. An overdose of amphetamine or cocaine can cause the heart to contract so rapidly that heartbeats do not last long enough to pump blood effectively, leading to fainting and sometimes death.

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Other drugs that mimic neurotransmitters, such as antianxiety and antidepression drugs, will be discussed later, in the Treatment of Psychological Disorders chapter.

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