Nerve Cells: Communication Portals 115
• Neurons: The Brain’s Communicators
• Glial Cells
• Electrifying Thought
• Chemical Communication: Neurotransmission
• Neural Plasticity: How and When the Brain Changes
ἀe B rain–Behavior Network 123
• The Central Nervous System: The Command Center
• The Peripheral Nervous System
from inquiry to understanding How Do We Recognize Faces? 128
ἀe E ndocrine System 134
• The Pituitary Gland and Pituitary Hormones
• The Adrenal Glands and Adrenaline
• Sexual Reproductive Glands and Sex Hormones
Mapping the Mind: ἀe B rain in Action 136
• A Tour of Brain-Mapping Methods
• How Much of Our Brain Do We Use?
• Which Parts of Our Brain Do We Use for What?
• Which Side of Our Brain Do We Use for What?
psychomythology Are Some People Left-Brained and Others Right-Brained? 142 evaluating claims Diagnosing Your Brain Orientation 143
Nature and Nurture: Did Your Genes—or Parents—Make You Do It? 144
• How We Come to Be Who We Are
• Behavioral Genetics: How We Study Heritability
Your Complete Review System 150
Chapter
3
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do specific regions on the brain’s surface correspond to different personality traits?
do we use only about 10 percent of our brain’s capacity?
Can we trace complex psychological functions, like religious belief, to specific brain regions?
are there left- and right-brained people?
is the heritability of a trait fixed within populations, or can it change from one year to another?
July 31, 2001 started normally for Howard Engel, a well-known Canadian author of detec- tive novels. As he did every other morning, Engel made himself breakfast and opened his front door to grab his newspaper. When he did, he noticed something exceedingly odd (Sacks, 2010).
Engel could see the newspaper just fine, and he could tell that it contained words.
Yet the words that he had read effortlessly for most of the 70 years of his life suddenly looked like gibberish. They seemed to be written in a bizarre language, much like Egyptian hieroglyphics. He initially wondered whether this was all a prank pulled on newspaper readers by the editors, but when he looked at one of the books in his collection, he found to his horror that the words were written in the same nonsensical language.
Engel soon learned that he had experienced a serious stroke. A stroke is in essence a “brain attack,” a loss of neural tissue stemming from a sudden cut-off of blood supply to the brain. Engel’s stroke, it turns out, damaged the area of his brain that allows us to read by sight, producing a rare condition called “word blindness.”
Yet over time, Engel learned to compensate for the deficits caused by his stroke, and regained his ability to read. Remarkably, he found that he could trace the shape of words using his tongue. By quickly tracing the shapes of letters with his tongue and trans- ferring these shapes to his front teeth, Engel discovered a different way to read. Moreover, his brain had learned to reorganize itself, delegating the functions that allow us to read from its visual areas to its touch areas.
Today, none of us is surprised to learn that Howard Engel’s striking deficits stemmed from damage to his brain. In the early twenty-first century, we take for granted the fact that the brain is the seat of psychological activity, including reading, memorizing, and thinking. When we struggle with a difficult homework problem, we say that “our brains hurt”; when we consult friends for advice about a complicated question, we “pick their brains”; and when we compliment others’ intelligence, we call them “brainiacs.” Yet throughout much of human history, it seemed self-evident that the brain wasn’t the prime location for our memories, thoughts, and emotions.
For example, the ancient Egyptians believed that the heart was the seat of the human soul and the brain was irrelevant to mental life (Finger, 2000; Raulin, 2003).
Egyptians often prepared corpses for mummification by scooping their brains out through the nostrils using an iron hook (you’ll be pleased to know that no drawings of this practice survive today) (Leek, 1969). Although some ancient Greeks correctly pinpointed the brain as the source of the psyche, others, like the great philosopher Aristotle, were convinced that the brain functions merely as a radiator, cooling the heart when it becomes overheated.
Even today, we can find holdovers of this way of thinking in our everyday language. When we memorize something, we come to know it “by heart” (Finger, 2000), and when we’re devastated by the loss of a romantic relationship, we feel “heartbroken.”
Why were so many of the ancients certain that the heart, not the brain, was the source of mental activity? It’s probably because they trusted their “common sense,” which as we’ve learned is often a poor signpost of scientific truth (Chapter 1). They noticed that when people become excited, angry, scared, or passionate, their hearts pound quickly, whereas their brains seem to be doing little or nothing. Therefore, they reasoned, the heart must be causing these emotional reactions. By confusing correlation with causation, the ancients’ intuitions probably misled them.
Today, we recognize that the mushy pinkish organ lying between our two ears is by far the most complicated structure in the known universe. Our brain has the consistency of gelatin, and it weighs a mere 3 pounds. Despite its rather unimpressive appearance, it’s capable of astonishing feats. As poet Robert Frost wrote, “The brain is a wonderful organ. It starts work- ing the moment you get up in the morning and does not stop until you get into the office.”
In recent decades, scientists have made huge technological strides that have taught us a great deal about how our brains work and helped them to correct age-old misconceptions (Aamodt & Wang, 2008). Researchers who study the relationship between the nervous system—a vast communication network consisting of nerve cells, both inside and outside of the brain and spinal cord—and behavior go by the names of biological psychologists or correlATIon vs. cAusATIon ▶
Can we be sure that a causes b?
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nerve cells: communication Portals 115
neuroscientists. By linking brain to behavior, these scientists often bridge multiple levels of analysis within psychology (see Chapter 1). The history of our evolving understanding of the brain provides a wonderful example of the self-correcting nature of science. Over time, accurate knowledge has slowly but surely taken the place of mistaken beliefs about the brain (Finger, 2000).
nerve cells: communication Portals
3.1 Distinguish the parts of neurons and what they do.
3.2 Describe electrical responses of neurons and what makes them possible.
3.3 Explain how neurons use neurotransmitters to communicate with each other.
3.4 Describe how the brain changes as a result of development, learning, and injury.
If we wanted to understand how a car works, we’d open it up and identify its parts, like its engine, carburetor, and transmission, and figure out how they operate in tandem. Similarly, to understand how our brain works, we first need to get a handle on its key components and find out how they cooperate. To do so, we’ll start with the brain’s most basic unit of communication: its cells, and then examine how they work in concert to generate our thoughts, feelings, and behaviors.
Neurons: The Brain’s Communicators
The functioning of our brain depends on cross-talk among neurons—nerve cells specialized for communication with each other (see fIGure 3.1 on page 116). Our brains contain about 85 billion neurons. To give you a sense of how enormous this number is, there are more than 10 times as many neurons in each of our brains as there are people on Earth. If we lined up all the neurons in our brain side to side, they would reach back and forth from New York to California five times.
In turn, neurons make tens of thousands of connections with other neurons, permitting a stag- gering amount of inter-cellular communication. In total, there are probably about 160 trillion connections in the human brain, a number too large for any of us to grasp (Tang et al., 2001).
Moreover, although our brains are much slower than our desktop computers or iPhones, they are still unmatched in many crucial psychological abilities. For example, no computer comes close to the human brain in its capacities for face or voice recognition (Li & Jain, 2011). You’ve probably discovered this if you’ve ever tried speaking to a computerized voice recognition system over the telephone and discovered that it couldn’t understand what you were saying.
Although many cells have simple and regular shapes, neurons are markedly different. They have long extensions that help them respond to stimulation from other neurons and communicate with them. To understand how the neuron works, let’s first look at the components that make it up.
THE CELL BODY. The cell body, also called the soma, is the central region of the neuron.
It manufactures new cell components, which consist of small and large molecules (refer to Figure 3.1). Because the cell body contains the nucleus, where proteins are manufactured, damage to this part of the neuron is fatal. The cell body also provides continual renewal of cell components.
DENDRITES. Neurons contain multiple branchlike extensions for receiving information from other neurons. Like the receivers on our cell phones, these numerous dendrites spread out to “listen in” on conversations from neighboring neurons and pass them on to the cell body (refer to Figure 3.1).
AXONS AND AXON TERMINALS. If dendrites are like cell phone receivers, axons are the transmitters. They’re specialized for sending messages to other neurons. These long tail-like extensions are usually very thin near the cell body. This narrowness creates an area that’s easily activated by incoming signals. Tiny spheres called synaptic vesicles travel the length
neuron
nerve cell specialized for communication dendrite
portion of neuron that receives signals axon
portion of neuron that sends signals
Factoid
Despite what many people believe, alcohol doesn’t actually kill brain cells.
But that doesn’t mean it’s a safe to drink heavily, because alcohol may damage or destroy some of the dendrites of nerve cells (Aamodt & Wang, 2007; O’Connor, 2007). This finding may explain the origin of this false belief, because prolonged heavy drinking does shrink brain volume.
Neurons and their dendrites (shown stained blue) with their nuclei (shown stained pink).
Explore in MyPsychLab the Concept:
the Structure of a Neuron
synaptic vesicle
spherical sac containing neurotransmitters
Neuron
Action potential
Action potential
Synapse
Nucleus
Cell body
Materials needed by the neuron are made here
Synapse Terminal point of axon branch, which releases neurotransmitters Dendrite
Projection that picks up impulses from other neurons
Myelin sheath
Fatty coat that insulates the axons of some nerve cells, speeding transmission of impulses Axon
Nerve fiber projecting from the cell body that carries nerve impulses Node
Gap in the myelin sheath of an axon, which helps the conduction of nerve impulses
Axon terminal (Synaptic knob)
FIGURE 3.1 A Neuron with a Myelin Sheath. Neurons receive chemical messages from other neurons by way of synaptic contacts with dendrites. Next, neurons send action potentials down along their axons, some of which are coated with myelin to make the electrical signal travel faster. (Source: Modified from Dorling Kindersley)
of the axon on their way to a knoblike structure at its far end called the axon terminal (see FIGURE 3.2). When the synaptic vesicle reaches the end of its little journey at the axon terminal, it bursts, releasing neurotransmitters, chemical messengers that neurons use to communicate with each other. We can think of the synaptic vesicles as similar to gel capsules filled with cold medicine. When we swallow a capsule, its exterior dissolves and the medicine inside it moves down our digestive tracts.
SYNAPSES. Once released from the synaptic vesicle, neurotransmitters enter the synapse, a tiny fluid-filled space between neurons through which neurotransmitters travel. The synapse consists of a synaptic cleft, a gap into which neurotransmitters are released from the axon terminal. This gap is surrounded by small patches of membrane on each side, neurotransmitter
chemical messenger specialized for communication from neuron to neuron synapse
space between two connecting neurons through which messages are transmitted chemically
synaptic cleft
a gap into which neurotransmitters are released from the axon terminal
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nerve cells: communication Portals 117
one on the sending axon of the first neuron and the other on the receiving dendrite of the second neuron. As neurotransmitters are released from the axon of a cell into the synapse, they’re picked up quickly by the dendrites of nearby neurons, just as cell phone receivers quickly pick up signals from other cell phones.
Glial Cells
Neurons aren’t the only players in our nervous systems: Glial cells (“glial” means glue) are also remarkably plentiful. Although researchers once thought that glial cells greatly outnumbered neurons, by as much as 10:1, recent research suggests that the ratio is much lower, and closer to 1:1 (Azevedo et al., 2009). Glial cells perform a variety of functions. Scientists once regarded them as nothing more than a sort of protective scaf- folding for the neurons held by synapses. Nevertheless, over the past 20 years or so, researchers have realized that glial cells do much more (Fields, 2009).
The most abundant of glial cells are astrocytes. A single astrocyte interacts with as many as 300,000–1,000,000 neurons. Astrocytes communicate closely with neurons, increase the reliability of their transmission, control blood flow in the brain, and play a vital role in the development of the embryo (Metea & Newman, 2006). Astrocytes, in con- cert with other glial cells, are intimately involved in thought, memory, and the immune system (Gibbs & Bowser, 2009; Koob, 2009).
We can find astrocytes in abundant supply in the blood–brain barrier, a protective shield that insulates the brain from infection by bacteria and other intruders. Tiny blood vessels are wrapped with a fatty coating, blocking large molecules, highly charged particles, and molecules that dissolve in water but not fat from entering the brain.
Another type of glial cell, an oligodendrocyte, promotes new connections among nerve cells and releases chemicals to aid in healing. In addition, this cell produces an insulating wrapper around axons called the myelin sheath. This sheath contains numerous gaps all the way along the axon called nodes, which help the neuron conduct electricity more efficiently (refer again to Figure 3.1). Much like a person playing hopscotch, the neural signal jumps from node to node, speeding up its transmission.
The importance of the myelin sheath is illustrated in sufferers of multiple sclerosis. In this autoimmune disease, the myelin sheaths surrounding neurons are progressively
“eaten away,” resulting in a loss of insulation of neural messages. As a consequence, these messages become hopelessly scrambled, resulting in a wide variety of physical and emotional symptoms.
Glial cells also clear away debris, acting as the brain’s cellular garbage disposals.
Treatments that target glial cells may one day assist in treating a variety of conditions related to the number and activity of these cells, including depression and schizophrenia (Cotter, Pariant, & Everall, 2001; Schroeter et al., 2009), as well as inflammation, chronic pain, and Alzheimer’s disease (Suter et al., 2007).
Electrifying Thought
Neurons respond to neurotransmitters by generating electrical activity (see FIGURE 3.3 on page 118). We know this to be true because scientists have recorded electrical activity from neurons using electrodes, small devices made from wire or fine glass tubes. These electrodes allow researchers to measure the potential difference in electrical charge inside versus outside the neuron. The basis of all electrical responses in neurons depends on an uneven distribution of charged particles across the membrane surrounding the neuron (see Figure 3.3). Some particles are positively charged, others negatively charged. When there are no neurotransmitters acting on the neuron, the membrane is at the resting potential.
In this baseline state, when the neuron isn’t doing much of anything, there are more negative particles inside than outside the neuron. In some large neurons, the voltage of the resting potential is about one-twentieth that of a flashlight battery, or about –60 millivolts (the negative sign means the inside charge is more negative than outside). While at rest,
glial cell
cell in nervous system that plays a role in the formation of myelin and the blood–brain barrier, responds to injury, removes debris, and enhances learning and memory myelin sheath
glial cells wrapped around axons that act as insulators of the neuron’s signal
Axon Neural impulse
Axon terminal Synapse
Receptor site
Neurotransmitter fitting into receptor site Receiving neuron Synaptic vesicles (with
neurotransmitter molecules inside)
Neurotransmitter molecules
FIGURE 3.2 The Axon Terminal. The axon terminal contains synaptic vesicles filled with neurotransmitter molecules.
Factoid
Recent research reveals that Albert Einstein’s brain contained twice as many glial cells as do typical brains (Fields, 2009). Although we’ve learned in Chapter 2 that we must be cautious in drawing conclusions from case study evidence, this intriguing finding may fit with evidence that glial cells play key roles in neural transmission.
resting potential
electrical charge difference (–60 millivolts) across the neuronal membrane, when the neuron is not being stimulated or inhibited
FIGURE 3.3 The Action Potential. When a neuron is at rest there are positive and negative ions on both sides of the membrane.
During an action potential, positive ions rush in and then out of the axon. This process recurs along the axon until the axon terminal releases neurotransmitters.
particles of both types are flowing in and out of the membrane. When the electrical charge inside the neuron reaches a high enough level relative to the outside, called the threshold, an electrical impulse called an action potential is triggered.
ACTION POTENTIALS. Action potentials are the language of neurons; they’re what they use to communicate. These potentials are abrupt waves of electric discharge triggered by a change in charge inside the axon. When this change occurs, we can describe the neuron as “firing,”
similar to the firing of a gun. Much like a gun, neurons obey the “all or none” law: They either fire or they don’t. Action potentials originate in the trigger zone near the cell body and continue all the way down the axon to the axon terminal. During an action potential, positively charged particles flow rapidly into the axon and then flow out just as rapidly, causing a spike in positive charge followed by a sudden decrease in charge, with the inside charge ending up at a slightly more negative level than its original resting value (see FIGURES 3.3 and 3.4). These sudden shifts in charge produce a release of electricity. When the electrical charge reaches the axon terminal, it triggers the release of neurotransmitters—chemical messengers—into the synapse.
THE ABSOLUTE REFRACTORY PERIOD. Neurons can fire extremely rapidly, up to 100 to 1,000 times per second. At this very moment, energy is traveling down tens of millions of your axons at breakneck speeds of about 220 miles per hour. Pause to think about that fact for a moment; it’s remarkable. Each action potential is followed by an absolute refractory period, a brief interval during which another action potential can’t occur. This period limits the fastest rate at which a neuron can fire, much as it takes us a while to reload some guns after firing them. The rate at which action potentials travel becomes a limiting factor in very long axons, such as the sciatic nerve, which runs from the spinal cord down the leg.
In humans, this axon extends a whopping 3 feet on average.
Chemical Communication: Neurotransmission
Whereas electrical events transmit information within neurons, chemical events triggered by neurotransmitters orchestrate communication among neurons. After neurotransmitters are released into the synapse, they bind with receptor sites along the dendrites of
At rest. During an action potential,
positive particles rapidly flow into the axon.
When the inside of the axon accumulates maximal levels of positive charge, positive particles begin to flow back out of the axon.
When the action potential reaches the axon terminal, it triggers release of neurotransmitters.
Direction of action potential
Neurotransmitter release
+ +
+
+ + +
++
+ + +
+ +
++ + +
+ +
+ +
+
+ +
++ ++
+ ++
+ + +
–
– –
– –
– –
– – –
–
– – –
– + ++ +
++ ++ + +
+ + +
+
+ +
+ + +
–
– – –
–
threshold
membrane potential necessary to trigger an action potential
action potential
electrical impulse that travels down the axon triggering the release of neurotransmitters
Time (ms)
Membrane potential (mV)
Action potential
Threshold of excitation
–90 –80 –70 –60 –50 –40 –30 –20 –10 0 +10 +20 +30 +40 +50
1 2 3
FIGURE 3.4 Voltage across the Membrane during the Action Potential. The membrane potential needed to trigger an action potential is called the threshold. Many neurons have a threshold of –55 mV. That means only 5 mV of current above resting (at –60 mV) is needed to trigger an action potential.
Factoid
The neurons of the largest animal on earth, the blue whale, contain axons that reach up to 60 feet.
absolute refractory period
time during which another action potential is impossible; limits maximal firing rate
receptor site
location that uniquely recognizes a neurotransmitter
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