Communication within the nervous system underlies all of our cognitions, emotions, and behaviors. The basis of neuronal communication involves the electrical activity of nerve cells — neurons (Figure 1) — and the transmission of this electrical activity from one neuron to others. Electrical activity of the neurons in your motor cortex, for example, travels down through the brain to neurons in your spinal cord, activating them; and the electrical activity of the spinal-cord neurons travels to the muscles of your body, causing them to contract. In short, each neuron sends "messages" to other neurons, which cause these other neurons to either become active or stay quiet. The activated neurons then send messages to still other neurons that communicate similar messages; and on and on. Eventually, these messages cause a bodily response: the movement of a muscle, secretion from a gland, etc. If patterns of communication among your neurons are changed (by drinking a caffeinated beverage, for instance), mental events and/or behaviors will change in some manner.

Figure 1. A neuron, consisting of dendrites, a cell body (soma), and an axon
(the link for this picture is here)

Although neurons come in different shapes and sizes, the neuron presented in Figure 1 shows the three structures that make up most neurons: the dendrites, the cell body (also called the soma, as in Figure 1), and the axon. The dendrites are branches of the neuron that receive messages sent by other neurons. The cell body is the part of the neuron that contains the nucleus and other important cell structures. The messages sent by other neurons are "summed" within the cell body, and at this point, a "decision" is made about whether or not the neuron will send its own messages to other neurons. If the decision is yes, then a change in the neuron's electrical activity occurs, which results in an "electrical impulse" being sent down the axon, the long extension traveling away from the cell body. When the electrical impulse reaches the end of the axon, changes occur that result in the release of biochemicals from the axon. These biochemicals — the actual "messages" sent by the neuron (see below) — travel to other neurons and bind to them, starting the whole process over. Thus, communication between one neuron and another involves four steps:

1. Biochemical "messages" released by neurons travel to the dendrites of a neuron and bind to it.
2. These biochemical messages cause an electrical impulse to develop in the neuron's cell body.
3. The electrical impulse travels down the neuron's axon, which causes the release of biochemicals.
4. These biochemical messages travel to the dendrites of other neurons and bind to them.

In the remainder of this section, I will talk about some of the details of this four-step communication process. But first, you may be wondering why you need to learn about neuronal communication. Learning about neuronal communication will help you to understand possible causes of mental disorders, why drugs have the effects they do, and so on. With respect to the causes of mental disorders, it is thought that many mental disorders are caused most proximally by communication problems among brain neurons. Obsessive-compulsive disorder (OCD), for example, is thought to be caused by a disturbance in neuronal communication. People with OCD suffer from very disturbing intrusive thoughts (obsessions) and repetitive behaviors (compulsions) that are very difficult to inhibit or control. In the following passage, a person with OCD describes an episode of obsessive thinking and compulsive behavior:

I’m driving down the highway doing 55 MPH. I’m on my way to take a final exam. My seat belt is buckled and I’m vigilantly following all the rules of the road. No one is on the highway—not a living soul.... While in reality no one is on the road, I’m [suddenly] intruded with the heinous thought that I might have hit someone.... I think about this for a second and then say to myself, “That’s ridiculous. I didn’t hit anybody.” Nonetheless, a gnawing anxiety is born.... I start ruminating, “Maybe I did hit someone and didn’t realize it.... I have to go back and check.” Checking is the only way to calm the anxiety.... I pray this outrageous act of negligence never happened. My fantasies run wild. I desperately hope the jury will be merciful. I’m particularly concerned about whether my parents will be understanding. After all, I’m now a criminal.... I turn the car around and head back to the scene of the mythical mishap. I return to the spot on the road where I “think” it “might” have occurred. Naturally, nothing is there. No police car and no bloodied body. Relieved, I turn around again to get to my exam on time. (Rapoport, 1989; pp. 23-25)

Nevertheless, his irrational thoughts about having run over someone and his attempts to make sure that he hadn’t were not over yet. They quickly returned and he spent a great deal of time going back down the road to check for a body that he knew was not there, but which he felt compelled to check for anyway. What is the evidence that a problem in neuronal communication is the cause of such symptoms? Some of this evidence consists of the fact that medications taken to control obsessions are known to influence communication among neurons in particular parts of the brain. The medications, it is thought, correct the patterns of neuronal communication, making them more normal, and thereby reducing or eliminating obsessive thinking.

Resting Potentials

Neurons are somewhat like weak batteries: each neuron has a very small voltage associated with it. We know this because, when an electrode is placed inside a neuron and another one is placed outside of it, a very small “electrical potential” (another name for voltage) — much smaller than that of the smallest battery — can be measured across the cell membrane. The cell membrane is a structure that forms the outer boundary of the cell, somewhat like the cell's "skin." And like a car battery, a neuron has a “positive terminal,” which exists on the external surface of its cell membrane, and a “negative terminal” which exists on the internal surface of its cell membrane. When a neuron is not being affected by outside influences, its electrical potential is about -70 mV (mV stands for millivolt — a thousandth of a volt). This very small voltage is known as the neuron’s resting potential.

What causes a neuron to have a resting potential? The resting potential results from the distribution of electrically charged atoms, called ions, on the inside and outside surfaces of the cell membrane (see Figure 2). An ion is an atom (or molecule) that has either a positive or negative electrical charge. The electrical charge is caused by the subtraction or addition of electrons. Positively charged ions are more common on the outside surface of the cell membrane and negatively charged ions are more common on the inside surface of the cell membrane. This uneven distribution of positively and negatively charged ions causes the resting potential.

Figure 2. A neuron with negatively charged ions on the internal surface of the cell membrane (blue circles) and positively charged ions on the external surface of the cell membrane (red circles)
(from Seamon & Kenrick, 1994, p. 45)

Cell membranes are permeable in that ions, proteins, and other substances may pass through it. But not just any substance can do so. Cell membranes are selectively permeable: only certain substances are able to pass through the membrane. The selective permeability of cell membranes is one mechanism for keeping neurons at their resting potentials. Those ions most important for maintaining the resting potential typically do not pass easily through cell membranes, and some cannot pass through at all.

There are several different kinds of ion involved in creating the resting potential of a neuron, but you will learn about only two — postively charged sodium ions (abbreviated Na+) and negatively charged chloride ions (abbreviated Cl-). When the neuron is "at rest," the concentration of sodium ions is higher on the external surface of the cell membrane and the concentration of chloride ions is higher on the internal surface of the cell membrane, thereby causing the overall electrical charge on the inside of the cell to be more negative than the overall electrical charge on the outside.

The electrical activity generated by neurons (and measured by the EEG and other devices) is caused by changes in the permeability of cell membranes. These changes allow sodium ions to more easily pass through a membrane and into the neuron's interior, which changes the neuron's electrical potential so that the inside of the cell is less negative with respect to its outside than it was before. For example, the electrical potential might change from -70 mV (the resting potential) to -65 mV at the point where sodium ions enter. Changes in membrane permeability are caused by chemicals — neurotransmitters — released by other neurons, that travel to a neuron's dendrites and bind to receptor sites embedded in the cell membrane, thereby changing its permeability, which allows sodium ions to enter the cell. In short, the main function of neurotransmitters is to change the electrical potential of the neurons to which they bind. Let's look more closely at this process.

Postsynaptic Potentials

Neurotransmitters sometimes are referred to as “chemical messengers” since they represent a type of “message” sent from one neuron to another during neuronal communication. There are many different kinds of neurotransmitter in the nervous system (dopamine is one neurotransmitter that you've learned about already), but each neuron typically produces only one and places it into “sacs” called vesicles (small pouch-like structures) stored at the end of the neuron's axon, which is called the axon terminal (see Figure 3). Communication occurs when neurotransmitters are released from the axon terminal and travel across a small gap between that neuron and another, where they attach to binding sites on the dendrites of the second neuron. The "junction" where the axon of one neuron meets the dendrite of another neuron is called the synapse. The gap between the two neurons is called the synaptic gap (or synaptic cleft, as in Figure 3). The neurotransmitter-binding sites on the dendrites are called receptors. (You may ignore the other terms in Figure 3.)

Figure 3. The end of an axonal branch (yellow) with vesicles containing neurotransmitter molecules and the dendrite of a "receiving neuron" (green) with receptors sites for neurotransmitters (the link for this picture is here)

As already stated, neurotransmitter molecules bind to special receptor sites on the dendrites. When a neurotransmitter binds to a receptor site, it changes the electrical potential of the neuron only around that site by allowing a small number of sodium ions to enter the cell. As stated above, the change is small (perhaps 5 mV or less). These small changes in electrical potential occurring in the dendrites are called postsynaptic potentials because they occur "after (post) the synapse." Although a postsynaptic potential occurs only around a single receptor site, it's important to remember that neurotransmitters are binding to many receptor sites scattered throughout the dendrites, causing a large number of postsynaptic potentials. Each of these small changes in electrical potential then "flows into" the cell body.

Action Potentials and Neural Impulses

The cell body is the part of the neuron that contains the nucleus and other important cell structures. At a spot in the cell body near the beginning of the axon, the individually small postsynaptic potentials caused by the binding of neurotransmitters are "summed together." If the summed value of these individual potentials reaches a particular value (the "threshold") — perhaps causing the voltage of the cell at this point to go from -70 mV to -55 mV, for example — a large change in the electrical potential will occur because of a large change in the permeability of the cell membrane at this point —a change that allows a large influx (flowing in) of sodium ions. The change in electrical potential may be so large that the inside of the cell briefly becomes positive with respect to the outside of the cell (that is, the electrical potential may go, for example, from -70 mV to +20 mV). The large change in electrical potential that occurs when the summed postsynaptic potentials pass a particular threshold value for a neuron (-55 mV, in this example) is called an action potential. It is important to remember that, if the summed postsynaptic potentials do not reach the threshold value for an action potential, nothing happens and the cell quickly returns to its normal resting potential.

If the threshold value is passed, an action potential begins in the cell body that then quickly enters the axon. We will refer to the moving action potential as a neural impulse. When a neural impulse is generated, we say that the neuron has "fired." Neural impulses occur because the influx of sodium ions at one point of the axon causes a large change in membrane permeability at the point next to it, and the influx of sodium ions at that point causes a large change in membrane permeability at the point next to it, and so on. When the neural impulse finally reaches the axon terminals, it causes changes that result in the movement of vesicles containing neurotransmitter molecules to the cell membrane at the ends of the terminals. The vesicles attach to the cell membrane and release their neurotransmitter molecules into the synaptic gap. The released neurotransmitters travel to the dendrites of other neurons and start the whole process all over again (see Figures 3 & 4). It is the electrical impulse generated in a neuron, the release of neurotransmitters from the end of the neuron, and the binding of these neurotransmitters to other neurons, which represents the act of communication between neurons.

Figure 4. A synapse showing the release of neurotransmitters and their binding to receptor site (from Wallace & Goldstein, 1997, p. 43)

The process leading to action potentials is somewhat like the control of an air conditioner by a thermostat. You control the threshold value of an air conditioner by setting the thermostat to, say, 75° F. Heat from the outside is seeping through cracks, walls, and windows throughout the house (which is analogous to the generation of postsynaptic potentials throughout the dendrites). At the spot where the heat enters, the temperature rises a bit (just as the electrical potential changes around the receptor site at which a neurotransmitter binds). All of these individual changes in air temperature travel into the house toward the thermostat (just as the individual postsynaptic potentials travel into the cell body towards a particular point). The thermostat is the place where all of these individual changes in air temperature are "summed together." If the overall change in air temperature passes the threshold value (75° F), the air conditioner turns on. If the threshold value is not reached, nothing happens: there is an “all-or-none response” of the air conditioner to changes in air temperature. The same is true with an action potential. The individual postsynaptic potentials travel into the cell body. At a certain spot in the cell body (perhaps we could call it the “neuronal thermostat”), these changes are summed together. If the overall change in electrical potential passes the threshold value for this neuron (usually about -55 mV), an action potential is initiated. If the threshold value is not reached, nothing happens. Thus, there is an “all-or-none response” of the cell body to changes in electrical potential.

Because each neuron in the brain may be affected by hundreds or even thousands of other neurons, and that neuron may affect hundreds or even thousands of other neurons, neuronal "networks" in the brain can quickly become very complex. Hundreds, thousands, or millions of neurons may communicate in this way in the production of a single mental event or behavior.

Study Questions for Section 4-12

1. What are the three parts of a neuron and what are their roles in neuronal communication?
2. What are the four steps of neuronal communication?
3. What is the resting potential of a neuron and what is(are) its cause(s)?
4. What is the role of the cell membrane in maintaining the resting potential?
5. What are the roles of sodium and chloride ions in maintaining the resting potential?
6. What is the role of the cell membrane in generating electrical activity in neurons?
7. What is the role of neurotransmitters in generating electrical activity in neurons?
8. How would you define the following terms?
   (a) vesicle
   (b) axon terminal
   (c) synapse
   (d) synaptic gap (also called "synaptic cleft")
   (e) receptor site
9. What is a postsynaptic potential and what is(are) its cause(s)?
10. What is an action potential and what is(are) its cause(s)?
11. What is a neural impulse?
12. What dow we mean when we say that a neuron has "fired"?
13. What happens when a neural impulse reaches an axon terminal?
14. What affects the complexity of neuronal networks in the brain?

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