You'll recall from Chapter 1 that a monist approach assumes that the mind and body are one. In other words, if we want to understand the mind, we can do so by studying the physiological structure and processes of the body. The biological approach to psychology follows this assumption, whether we are trying to understand a relatively simple process like moving your arm, or a complex process like treating depression. While this approach to psychology can be criticized as reductionist (i.e. thinking of a complex problem like depression only in terms of neurotransmitterneurotransmitterA chemical messenger released by a neuron that crosses the synapse and binds to receptors on the receiving neuron. function) the preference towards parsimony (looking for the simplest explanation of a complex problem) allows psychologists to study underlying processes and identify reliable and predictable physiological interactions. With this approach in mind, we'll begin by looking at the fundamental building blocks of most organisms: neurons. Neurons are the individual nerve cells which help make up the entire nervous system and understanding how neurons communicate is a key to understanding thought and behavior.

In order to understand how approximately 85 billion neurons in the human brain communicate with one another, we first need to know the parts of a neuronneuronThe basic building block of the nervous system — a specialized cell that transmits electrical and chemical signals. and the function each part serves.

The DendritesDendritesBranching extensions of a neuron that receive incoming signals from other neurons.– Derived from the Greek word for “tree”, dendrites are the parts of a neuron that reach out like branches to receive messages from other neurons. Dendrites are able to receive messages via chemical signals which interact with receptor sites on the dendrites. These receptor sites can be stimulated by messages from other neurons or by other chemical messengers which are traveling in the body.

The Cell Body – all of the dendrites lead to the cell body, or soma, which collects and aggregates the messages that are being received by the dendrites and it is also where you will find the nucleus of the cell.

The AxonAxonThe long fiber of a neuron that carries electrical impulses away from the cell body toward other neurons. – When a certain thresholdthresholdThe level of stimulation required to trigger an action potential in a neuron. of stimulation is reached by the dendrites, an electrical signal is sent down the axon, which is the long section of the neuron that leads away from the cell body and out to other neurons (or in some cases to a muscle or organ).

The axon of most (but not all) neurons is covered with a layer of fatty material called myelin, which helps to insulate the axon and allows it to send messages faster and more efficiently. You can think of the myelin coating just like the rubber insulation on an electrical wire. A difference, however, is that the myelin is broken up into sections with small gaps between them. These gaps are known as nodes of Ranvier (pronounced Ran-vee-ay, named after Louis-Antoine Ranvier, the French anatomist who discovered them). These nodes allow the message to travel more quickly by “jumping” along the axon. Each node essentially re-sends the message, preventing its strength from being dissipated along the way. This “jumping” is known as saltatory conduction, derived from the Latin word saltare - “to jump”.

Imagine you and a friend are each standing at either end of a very long hallway. If you wanted to say something, the sound would dissipate and wouldn't reach your friend, so you would need to yell extremely loudly. Now imagine, instead, that many other people were spaced throughout the hallway, and each could repeat your message to pass it along. Now you wouldn't need to shout so loudly, and the message could still reach your friend. This is comparable to how myelin improves the efficiency of neural communication.

The Terminal Button – At the end of the axon, the neuron has swelling terminal buttons, which are simply the endpoints of the neuron. These terminal buttons allow the neuron to connect to other nearby neurons. Rather than connecting electrically, most neurons communicate with one another chemically. Inside each terminal button are vesicles; special bags which contain chemical messengers known as neurotransmitters. These neurotransmitters are released into the space between neurons, known as the synapsesynapseThe tiny gap between neurons across which neurotransmitters are released to pass signals from one cell to another., where they can float across and interact with the next neuron.

Camillo Golgi (1843-1926) developed a silver staining technique (which he called “black reaction” but became known as Golgi staining) which showed the dendrites and axons of individual neurons. Golgi incorrectly believed that neurons were all connected to one another, creating a mesh network of neurons (known as reticular theory). Ironically, Santiago Ramón y Cajal (1852-1934) adapted Golgi's staining method in order to demonstrate that Golgi was wrong, and that neurons, in fact, did not touch. Ramón y Cajal argued that neurons were actually separated by tiny gaps, which he romantically referred to as “protoplasmic kisses”. These tiny gaps between neurons are more formally known as synapses (from the Greek for “conjunction”), and they allow neurons to communicate chemically. Ramón y Cajal and Golgi shared the Nobel Prize for Physiology in 1906 (despite their conflicting views – in fact in their Nobel addresses they gave contradictory explanations for the structure of neural networks) and it wasn't until the 1950s that electron microscopes were able to confirm that Ramon y Cajal's neuron doctrine was indeed correct, and that neurons were separated by tiny gaps.

Now that we know the general structure of the neuron, let's examine in more detail at how it sends messages to communicate with other neurons around it. The communication process for neurons consists of two main types of messages; an electrical message, which carries information within a neuron, and a chemical message, which carries information between neurons.

When the dendrites of a neuron are stimulated enough to reach a certain threshold, an electric signal travels down the axon of the neuron. This signal is known as an action potentialaction potentialAn electrical impulse that travels down the axon when a neuron fires — follows the all-or-nothing principleall-or-nothing principleA neuron either fires at full strength or not at all — there is no partial action potential... An important point here is that neuron firing is “all-or-none”. A neuron either fires an action potential (if a threshold is reached) or it doesn’t. There is no in-between. In this way, a neuron is like a gun. It can’t be fired a little bit by pulling the trigger more softly and it doesn’t fire any harder by pulling the trigger firmly. It simply fires, or it doesn’t. Neuron firing is the same, and once the threshold for firing is reached, the action potential generated is always the same. To continue the analogy, after firing an action potential, there is a brief period before the neuron is ready to fire again, which is similar to a machine gun. Holding down the trigger (i.e. continuous stimulation) doesn’t generate a solid beam out of the gun barrel, but rather a series of individual firings with brief spaces of time between them. This is also true of neurons. Continuous stimulation doesn't cause a neuron to stay “turned on”, but instead causes the neuron to fire repeatedly, with a brief pause between each firing.

To better understand this firing process, let's take a closer look at what actually happens when a neuron is stimulated. The cell membrane is covered with channels (which can be open or closed) that allow for the movement of charged particles (ions) in or out of the cell. Stimulation of dendrites causes the movement of charged ions (particularly sodium and potassium) in or out of this semipermeable cell membrane.

This ion movement changes the electrical charge inside the neuron. When a neuron is not firing, the balance of ions inside and outside the cell gives it an electrical charge of about -70millivolts. This is known as the resting potential. Stimulation opens channels for positively-charged sodium ions (Na+) to move into the neuron. When enough sodium moves in and the threshold is reached, many more sodium channels open, allowing even more sodium in. This sudden rush of sodium creates a brief positive electrical charge of about +40millivolts. This positive charge moves along the axon like a wave, traveling from the cell body (soma) to the end of the neuron (terminal button), as sodium channels open sequentially, like a falling line of dominoes. Each sodium channel is open only briefly before closing again while sodium-removing pumps and other ion channels help to restore the neuron to the resting state. The neuron must return to the resting state before it can fire again, and this time delay between firings is known as the refractory period. This process of firing an action potential then returning to resting potential happens quickly, allowing some neurons to fire hundreds of times per second.

It's important to remember that when an action potential travels down the axon, the individual ions themselves aren't actually moving down the axon. This would be far too slow. They are each simply moving in, then back out of the cell membrane in roughly the same place. It's like a baseball stadium doing “the wave”. Each person simply stands, then sits, and this triggers the next person to do the same. In this way, the message travels across the entire stadium without the individual people needing to travel the entire distance. You can imagine an action potential the same way; a wave of ion movement that carries a message all the way to the end of the axon.

I mentioned earlier that myelin helps to insulate axons and improve the efficiency of messages. While we can think of the previous hallway example as demonstrating greater efficiency (you don't need to use as much energy yelling so hard), we can use the baseball stadium analogy to understand the improvement in speed provided by myelin. Imagine that instead of every person in the crowd needing to stand, then sit, we decided that only the first person in each section would stand, then sit. This would trigger the next “section leader” to stand, then sit. In this way, the message could travel the distance of the stadium even more quickly. This is essentially what happens at the nodes of Ranvier. The message traveling down the axon jumps along each section, allowing it to reach the terminal button more quickly. As mentioned before, this is known as saltatory conduction – from the Latin saltare - “to jump”.

This improved speed and efficiency makes myelin essential, and unfortunately, we can see this importance in diseases which damage myelin (known as demyelinating diseases) such as multiple sclerosis. In the case of multiple sclerosis, patients' immune systems erroneously attack and destroy their myelin cells. This breakdown of myelin affects the ability to send and receive messages, resulting in problems in movement, coordination, and balance, as well as problems in sensation and cognition.

It's also worth noting that while we are primarily going to focus on neurons in this chapter, we shouldn't completely ignore all the other cells (including myelin) that provide support, insulation, nutrition, and waste removal for neurons. The understanding of these different types of glial cells (from the Greek for “glue”) has improved greatly in the last few years and researchers are beginning to find that glial cells are involved in more processes than previously thought. They are more than just the glue of the nervous system, and there's evidence that besides the maintenance functions listed above, glial cells may play a role in helping neurons to form new connections.

When the action potential reaches the terminal buttons at the end of the neuron, chemical messengers called neurotransmitters are released from containers called vesicles. These neurotransmitters then float across the gap between neurons – the synapse - and interact with receptor sites on the next neurons. When a neurotransmitter binds with a receptor site, it influences the flow of ions into the postsynaptic neuron. The neurotransmitter released by the initial (or presynaptic) neuron can either make it more likely that the next (or postsynaptic) neuron will fire (excitatory) or make it less likely that the next neuron will fire (inhibitory).

You may be wondering what happens to the neurotransmitter after it has been released. There are essentially 3 main ways of clearing out the neurotransmitter after a message has been sent.

ReuptakeReuptakeThe process by which the sending neuron reabsorbs excess neurotransmitters from the synapse. (the vacuum cleaner)

In reuptake, neurotransmitter is sucked back into the presynaptic neuron, where it can be recycled into vesicles and used again.

Enzyme Deactivation (the Pac-man)

Enzymes break the remaining neurotransmitter down into parts which are either recycled or become waste products.

Autoreception (the Thermostat)

The presynaptic neuron also detects levels of neurotransmitter in the synapse, and if the level is high, may prevent more release of neurotransmitter from flooding the synapse.

There are many different neurotransmitters used throughout the body and brain, but let’s take a look at a few key examples of neurotransmitters and their related functions. It’s important to note that the same neurotransmitter can influence many different behaviors by being used in different areas of the brain. Given the complexity of behavior and the multiple functions of each neurotransmitter, the examples below will, of course, be simplifications of these interactions.

AcetylcholineAcetylcholineA neurotransmitter involved in muscle movement and memory; depleted in Alzheimer's disease. (ACh) (ah-see-tyl-koh-leen) is one of the main excitatory neurotransmitters used in the body and brain. ACh is used throughout the body to control muscle contractions and is also used in brain areas associated with learning, memory, and attention. Alzheimer’s Disease involves deterioration of ACh-producing neurons which causes deficits in memory, learning, and attention. When these neurons cannot produce adequate amounts of ACh, the postsynaptic neurons no longer receive enough stimulation to fire properly. To remember the association between Acetylcholine and Alzheimer's, notice both start with the letter A.

DopamineDopamineA neurotransmitter associated with reward, movement, and motivation; linked to Parkinson's disease and addiction. is a key neurotransmitter in areas of the brain relating to control of movement and also in areas relating to the experience of pleasure and motivation (the “Reward Area” of the brain). Parkinson’s Disease involves a deterioration of dopamine-producing neurons in an area of the midbrain known as the substantia nigra, resulting in problems with coordinating movements. This causes shakes and tremors, one of the main symptoms of this disease. Noticing that a “P” is an upside-down “d” may help you remember the relationship between Parkinson's and dopamine. In the section on drugs, we'll look at how addictive recreational drugs influence the dopamine-rich “reward area” of the brain.

Gamma-aminobutyric acid, or GABAGABAThe main inhibitory neurotransmitter in the brain — it reduces neural activity and is affected by alcohol and anti-anxiety drugs., is one of the main inhibitory neurotransmitters used in the brain. GABA binds to receptor sites and prevents the flow of positive ions into the neuron, reducing the likelihood that the neuron will reach its threshold and fire an action potential.

SerotoninSerotoninA neurotransmitter involved in mood, sleep, and appetite; targeted by antidepressant medications (SSRIs). is a neurotransmitter that is used in pathways related to mood and well-being and is also involved in the regulation of sleep and dreaming. Major depressive disorder is believed to be associated with reduced activity of serotonin in some brain areas. Lower levels of serotonin affect the functioning of certain neurons, which leads to decreases in mood. The most commonly prescribed type of medication for depression is an SSRI (Selective Serotonin Reuptake Inhibitor), which increases the level of serotonin available in the synapse by blocking reuptake. This is like clogging up the vacuum cleaner so that it can no longer pull away any of that precious serotonin. This results in serotonin staying in the synapse longer and being better able to influence subsequent neurons, which may help elevate mood.

NorepinephrineNorepinephrineA neurotransmitter and hormone involved in alertness and the fight-or-flight stress response. (also known as noradrenaline) - Norepinephrine is an excitatory neurotransmitter which is involved in physiological arousal and the regulation of heart rate. In a stressful situation, more norepinephrine is released, which then stimulates the heart to beat more quickly.

Because neurons rely on chemicals to communicate, their communication can be altered by the introduction of certain chemicals in the form of psychoactive drugs. One of the main ways that drugs affect the body and brain is by influencing the communication between neurons. By increasing or decreasing the activity of different neurotransmitters in different areas of the brain, drugs are able to have a variety of effects on behavior. Most drugs have multiple effects on the body and brain, but we’ll be simplifying the following examples to focus on relationships with particular neurotransmitters.

When it comes to influence over a particular neurotransmitter’s activity, drugs are often classified as being either agonists or antagonists. Substances which are agonists for a neurotransmitter increase the activity of the neurotransmitter. Drugs which are antagonists, however, reduce the activity or effectiveness of a particular neurotransmitter. Let’s take a look at a few specific drug/neurotransmitter interactions in order to see how some well-known drugs influence neural communication.

Nicotine is an example of an agonistagonistA drug or chemical that mimics or enhances the effect of a neurotransmitter by binding to its receptor. for the neurotransmitter Acetylcholine (ACh). Nicotine’s structure resembles that of ACh, allowing it to bind to the same receptor sites on neurons, opening ion channels and increasing the likelihood that certain neurons will fire, particularly those in brain areas associated with attention and learning. While this may sound like a good thing, over time this repeated stimulation of neurons from nicotine reduces the sensitivity of those neurons. As a result, greater amounts of nicotine are required for the same effect. In addition, ACh production is reduced because there appears to be a surplus of ACh with all the increased neuron activity. When nicotine is not available to assist the reduced level of ACh, smokers experience difficulty concentrating, as well as other symptoms of withdrawal.

Alcohol (more specifically ethanol) is technically not an agonist, but it does enhance the effects of the neurotransmitter GABA (gamma-aminobutyric acid). You may recall that GABA is an inhibitory neurotransmitter, meaning that its presence reduces the likelihood that postsynaptic neurons will fire. Ethanol increasing the effects of GABA means that it is less likely certain neurons will fire when alcohol is consumed (which is why it is known as a depressant). As consumption increases, this inhibition affects different areas of the brain. This can be seen in the progressive deficits that alcohol consumption causes; initially there is a reduction of activity in neurons which regulate and monitor behavior for appropriateness (Should I make a sexually suggestive remark to this person I just met? Should I take my shirt off and dance on the bar?), followed by reduced firing of neurons coordinating movements (stumbling) and speech production (slurring) and eventually inhibiting enough function to cause unconsciousness or even death.

In understanding any kind of substance addiction, remember that the body is always working to compensate for the changes that drugs bring about, in order to restore balance and maintain normal functioning. In the case of alcohol, the nervous system attempts to counteract the inhibition that alcohol causes by increasing the strength of excitatory messages.

It does this by increasing levels of the excitatory neurotransmitter glutamate. This is how a tolerance for alcohol's effects builds up with regular consumption, but with chronic excessive consumption this tolerance can become a dangerous dependency. In this case, the body relies on the inhibitory effect of alcohol to maintain functioning, and without it experiences excessive stimulation. This excitotoxicity causes withdrawal symptoms which can include anxiety, shakes, tremors, heart palpitations, and in extreme cases, even death. Similar types of withdrawal can occur with sudden cessation of other depressant drugs like benzodiazepines or barbiturates.

Methamphetamine and Cocaine each have a number of different effects on the brain, but one they share is that they are both agonists for the neurotransmitter dopamine. In the nucleus accumbens, the “reward area” of the brain, dopamine stimulates neurons which trigger feelings of pleasure, well-being, and euphoria. While these neurons are normally triggered by behaviors like eating or sex, drugs like meth and cocaine (and to a lesser extent, nicotine) also activate these neurons by influencing the release of dopamine. It is this activation of the reward area that makes these drugs particularly addictive. With repeated drug consumption, these dopamine areas can become damaged, which can lead to reduced ability to experience pleasure (known as anhedonia). Meth and coke both stimulate norepinephrine release, causing an increase in heart rate. In the case of overdose, the heart contracts so rapidly that blood cannot properly flow in and out of it, which can lead to unconsciousness or even death.

Caffeine is an example of an antagonistantagonistA drug or chemical that blocks or reduces the effect of a neurotransmitter. drug for the neurotransmitter adenosine (in addition to other effects on the brain and body). Adenosine is an inhibitory neurotransmitter which is mostly produced as a result of ATP metabolism. The adenosine produced inhibits activity of some neurons, and is partially responsible for feelings of tiredness. Caffeine binds to the receptor sites for adenosine, blocking it from being detected but not actually inhibiting the neurons. As a result, we don’t experience the same level of tiredness. Once the caffeine has been broken down, however, the receptors are flooded with the adenosine that has been accumulating, leading to sudden inhibition of the neurons and the feeling of a “crash” we’re probably all familiar with.

Now that we've got a general understanding of neural communication, let's take a broader view and look at the nervous system as a whole. The nervous system can be broadly divided into two major sections, the central nervous systemcentral nervous systemThe brain and spinal cord — the main processing center of the nervous system. and the peripheral nervous systemperipheral nervous systemAll nerves outside the brain and spinal cord, connecting the CNS to the body..

The Central Nervous System (CNS) includes the brain and the spinal cord, and these vital structures are “armored” by being encased in bone (the skull and the vertebrae).

The Peripheral Nervous System (PNS) includes all the other nerves, blood vessels, organs, and glands outside of the brain and spinal cord. Since this includes a wide variety of systems, it is further divided into sections.

One section is the somatic division of the peripheral nervous system. This includes skeletal muscles and their nerves, which are generally under voluntary control. You can decide when and how to move your arms, legs, facial muscles, etc.

The second division of the peripheral nervous system is the autonomic division. The autonomic division contains nerves, muscles, organs, and glands which are not under voluntary control. This would include systems regulating your breathing, heart rate, perspiration, sweating, and digestion, all of which are generally outside of conscious control. Our bodies have automated these essential processes in order to free up resources for other tasks (you can remember the word autonomic sounds similar to automatic). You can imagine how difficult life would be if we didn't relinquish control and instead had to consciously remember to take each breath, pace our heart's rhythm, or command the processes of digesting our dinner. If these processes weren't on auto-pilot we simply wouldn't have the cognitive resources left for more complex behaviors like moving gracefully, reading great literature, or contemplating the meaning of our existence.

Control of these autonomic processes can be further subdivided into two main systems. The sympathetic nervous systemsympathetic nervous systemThe autonomic division that activates the body for fight-or-flight responses. works to excite the autonomic division and can be most clearly seen in the face of acute stress which triggers the “fight or flight” response. In the face of a sudden threat, our survival may depend on escaping or fighting off this threat. Despite this name, “fight” and “flight” aren't the only possible reactions to a threat, and there is also a “freeze” response.

The sympathetic nervous system is activated through a combination of processes, including the release of hormones, which are chemical messengers carried throughout the body via the bloodstream. Hormones like adrenaline prime our bodies for action. Activation of the sympathetic nervous system increases our level of arousal, our heart rate, blood pressure, respiration, muscle tension, and sweating, while simultaneously decreasing less essential processes like digestion, salivation, and immune response. Escaping from a predator may require all the energy you have available, so for the moment, using energy to digest your lunch or fight germs may not be the best use of your resources.

While we may not be fleeing from tigers very often in the modern age, we still experience the same sympathetic activation in response to threats and stress, which may help explain those knots in your stomach, dry mouth, rapid heart rate, and profuse sweating as you prepare to make a presentation in class. You may wish you had greater conscious control over your autonomic nervous systemautonomic nervous systemThe division controlling involuntary functions like heart rate and digestion. to command your body to “stop sweating” or “slow heart rate” as easily as you move your arms, but as mentioned above, it's generally a good trade-off that we don't have this kind of conscious control (and thus responsibility) for these systems.

In contrast to the sympathetic nervous response, the parasympathetic nervous systemparasympathetic nervous systemThe autonomic division that calms the body and supports rest-and-digest functions. relaxes the autonomic division, helping us to recover from stress. We cannot always be on high alert, so after escaping from that fierce tiger, we need to put the brakes on the stress response and restore our body to a resting state. Activation of the parasympathetic system causes a decrease in arousal, lowered heart rate, respiration, and muscle tension, reduced levels of stress hormones, and increases in digestion and immune function. Sitting quietly, breathing deeply, or practicing meditation are ways to help activate the parasympathetic nervous system and these behaviors can induce what Herbert Benson calls the “relaxation response”. Engaging in these behaviors can be seen as a way of taking greater control over your autonomic nervous system, particularly if you are plagued by chronic stress. So while you can't readily command your heart rate to slow or your immune system to step things up, you can engage in behaviors that will help to accomplish these feats.

Now that we've covered the general organization of the nervous system, let's look in greater detail at its crowning structure; the brain.

In the past, the ability to study structures in the brain was mostly limited to studying the brains of the deceased. Technologies for looking at brain function in living humans didn't exist, and the closest approximation was to study cases of brain damage to particular areas and attempt to relate these to impaired functions. Noticing that a blow to the back of the head was associated with subsequent visual problems would indicate that the back of the brain may be related to vision. One could also study the effects of stroke damage on patients' subsequent behavior. A stroke is a blockage of blood flow in the brain which can cause brain tissue in that particular area to die. By analyzing changes in behavior before and after a stroke, and analyzing the location of brain damage in autopsy, one could make inferences about the role of those areas.

One of the most famous examples of brain damage and clues to function is the unfortunate case of Phineas Gage. Gage was a 25 year-old foreman working on a railroad in Vermont in 1848. While he was working, a charge accidentally detonated and sent a 3-foot iron tamping rod into his left cheek and clear through the top of his head. Along the way, it damaged his left eye, but more importantly, took out a piece of the left frontal lobefrontal lobeThe brain lobe behind the forehead involved in planning, decision-making, motor control, and language production. of his brain. Miraculously, Gage remained conscious immediately following the accident, even explaining the event to a local doctor (though Gage was later comatose and his recovery was slow). He survived this experience, though there were claims his personality changed following the ordeal. While he was described as previously being a dependable worker and polite young man, following his accident he was described as fitful and profane and his ability to regulate his behavior was questioned.

We can't be too sure of the exact changes in Gage as details are scant. Just how long-lasting any changes were has been called into question, as later Gage was able to work successfully as a stagecoach driver in Chile, a job which would require social skills, planning, and behavioral control. Despite distortions and unsubstantiated claims about the extent of personality change in Gage, his case still demonstrates a way to study brain function and consider what role certain brain structures may play in behavior and personality.

Another famous analysis of brain damage was carried out by physician Paul Broca in the 1860s. Broca saw one patient who was referred to as “Tan” (real name Louis Victor Leborgne). Leborgne's comprehension of language was intact, but he was only able to produce the syllable “tan” when he spoke. Following Leborgne's death, Broca performed an autopsy and found damage to a region in the left frontal lobe. He correctly surmised that this area of the brain must be involved in speech production, and he then collected confirming evidence from autopsies of other patients with the same speech production problem (known as aphasia) and similar damage to the left frontal lobe. This is considered to be one of the first cases of direct evidence for localization of brain function and we now know that this area (called Broca's area) helps send messages to the motor cortex to coordinate the muscle movements necessary for speech production.

While these attempts at understanding the brain were crucial milestones of discovery, they pale in comparison to the modern brain imaging techniques that have been developed in the last few decades. One of the oldest methods for analyzing living brain function is the EEGEEGElectroencephalogram — a technique that records electrical brain activity through electrodes on the scalp. or electroencephalogram, first used on humans in 1924. The activity of neurons firing produces tiny surges of electrical activity, which can be detected through the skull. By placing electrodes on the scalp, an EEG picks up on these electrical impulses and graphs them as waves of activity, which are referred to as brain waves. As we'll see in chapter 8, different states of consciousness have differing brain wave patterns.

A CAT scan (also called a CT scan) uses X-rays to reveal the structure of the brain. Short for Computerized Axial Tomography (tomography refers to making a 2D image “slice” of a 3D object), a CT scan sends a series of X-rays through the skull at a variety of angles. A computer then combines how the X-rays pass through varying densities of different brain structures and creates a 2D image of a “slice” of the brain, allowing us to see structural abnormalities or physical damage.

An even more detailed way of looking at brain structure is Magnetic Resonance Imaging (MRI). An MRI machine sends a magnetic pulse through the brain, causing molecules to temporarily twist, then relax in response to the magnetic field. This slight movement releases energy, and by recording the pattern of energy, an MRI is able to create a detailed image of the brain's structure.

A PET scanPET scanPositron emission tomography — a brain imaging technique that tracks a radioactive tracer to show areas of metabolic activity. (Positron Emission Tomography) is a functional imaging technique, meaning that it is able to show regions of activation in a living brain. In a PET scan, the patient first ingests a small amount of a harmless radioactive substance. This substance travels in the bloodstream to the brain. Brain areas which are working harder will require more oxygen (and thus greater blood flow) so by looking at concentrations of the radioactive substance we can see which brain areas have greater blood flow, and thus more activation. While a PET scan can show us general levels of activation, it isn't able to provide clear images of specific regions of activation over short periods of time. For this, we turn to fMRIfMRIFunctional magnetic resonance imaging — measures blood flow to active brain regions, revealing which areas are engaged during tasks..

fMRI (functional magnetic resonance imaging) is similar to MRI in that it uses a magnetic pulse to briefly twist molecules, but in this case, an fMRI machine acts on molecules of hemoglobin. This allows it to reveal levels of blood flow in specific areas of the brain over much shorter periods of time, without the patient needing to ingest a radioactive substance. For now, this is the closest we can get to seeing real-time brain function. Participants in an fMRI machine can carry out cognitive tasks while researchers watch areas of the brain change their levels of activation, allowing us to see localization of brain function in action.

The brain has a lot of responsibilities spread across a number of different areas and structures, so it’s often divided up into categories to simplify things a bit. Generally it’s broken up into three main areas, the hindbrain, the midbrain, and the forebrain.

You may also sometimes hear of the “old brain” and the “new brain”, which has nothing to do with a person’s age or development. This is a way of categorizing brain areas in terms of evolutionary time, with the structures that have been around the longest being referred to as the “old brain” (generally areas that are crucial for survival – the hindbrain and midbrain), while structures that appeared later in human evolutionary history are referred to as the “new brain” (areas that are useful but less essential – the forebrain).

The structures of the hindbrain control the most basic elements of survival, giving us a pulse and allowing us to be alert and mobile. The medulla regulates several activities which are absolutely essential for survival; heart rate and respiration. The reticular formation is involved in the regulation of wakefulness and states of vigilance. The cerebellumcerebellumThe 'little brain' at the back of the skull that coordinates movement, balance, and motor learning. (from the Latin for “little brain” – based on its appearance) helps to coordinate and fine-tune motor activity, allowing for smooth and graceful movements. The cerebellum is connected to the rest of the brain via the pons (Latin for “bridge”) which helps relay messages back and forth between the brain, cerebellum, and spinal cord.

The Midbrain

The two areas of the mid-brain, the tectum and the tegmentum, are primarily involved in orientation and coordination of movement. The substantia nigra, an area of the tegmentum which uses dopamine as a neurotransmitter, can be affected by Parkinson’s disease, resulting in problems with motor control and tremors.

Life is about more than just having a pulse and moving around, and this is where the structures of the forebrain really come into play. The forebrain is divided into two categories; the cerebral cortexcerebral cortexThe wrinkled outer layer of the brain responsible for higher mental functions — thought, language, perception., which is the thin outer layer of the brain, and the subcortical structures underneath (literally “under-cortex”).

We'll start with the subcortical structures and work our way up.

The thalamus is a relay station for information. Information from our senses comes to the thalamus first and is then sent to appropriate areas of the cortex. You can think of the thalamus like an old-timey telephone switchboard operator, receiving calls and then redirecting them out to the appropriate connections.

The hypothalamushypothalamusA small but powerful structure that regulates hunger, thirst, body temperature, and links the nervous system to the endocrine system. (literally the “under-thalamus”) is the area underneath the thalamus which is involved in regulating hunger, thirst, and body temperature, and it plays a key role in hormone release for the fight-or-flight response. This area is where you’ll find the nucleus accumbens, the “reward area” of the brain, which is associated with motivation for behaviors like eating or having sex, and as mentioned previously, is involved in drug addiction. A useful bad joke for remembering the four main functions of the hypothalamus is to refer to the four Fs: feeding, fighting, fleeing, and mating.

The limbic systemlimbic systemA set of brain structures involved in emotion, memory, and motivation — includes the amygdalaamygdalaAn almond-shaped limbic structure critical for processing fear and emotional memories. and hippocampushippocampusA seahorse-shaped limbic structure essential for forming new long-term explicit memories.. is a group of structures (including the hypothalamus) related to emotion and memory. The amygdala (Latin for “almond”) attaches emotional significance to events and triggers the neighboring hippocampus to form memories, allowing us to keep track of emotionally-charged events and stimuli (hippocampus is Greek for “sea-horse”; obviously there were some imaginative early anatomists).

The pituitary gland is the “master gland” because it releases hormones which can stimulate other glands to release their hormones.

The basal ganglia is involved in voluntary motor control and the initiation of movements.

Finally we reach the cerebral cortex, the wrinkled outer layer of the brain (about 2-4 millimeters thick) where the most complex processing occurs. The reason for all the wrinkling and folding of the cortex is that this allows a greater surface area to fit inside our already over-sized heads. If it were smoothed out, the cortex would cover an area about the size of an open sheet of newspaper. Fortunately we don’t need to have giant, flat newspaper heads, and crumpling the cortex allows us to fit more brain into a smaller skull.

The cortex is divided into different areas that handle different tasks. The first general division is that of the left side of the brain and the right side. These two hemispheres are connected by a band of nerve fibers called the corpus callosumcorpus callosumThe thick band of nerve fibers connecting the left and right cerebral hemispheres., which allows each half-brain to know what the other half is up to. Each of these hemispheres specializes in different types of tasks and is able to function independently.

When it comes to sensations and movement of the body, the hemispheres have contralateral control, which means that the left hemisphere controls the right side of the body and the right hemisphere controls the left side of the body. Other tasks are specialized as well, such as language and speech production occurring mostly in the left hemisphere, while the recognition of faces and musical patterns generally occurs in the right hemisphere. These differences in task management may vary slightly from person to person, particularly when someone is left-handed (like myself). In the next section of this chapter, we'll see some examples of patients with split brains who initially helped give us these insights into the specialized functions of each hemisphere.

Each hemisphere of the brain can be divided up into 4 distinct lobes, each of which is specialized for particular tasks.

The occipital lobes are located at the very back of each hemisphere. The main task of the occipital lobeoccipital lobeThe brain lobe at the back of the head dedicated to visual processing. is to process visual information. Information originating from the optic nerves goes to the thalamus and from there is passed on to the primary visual cortex (known as V1) in the occipital lobe. To help you remember that the occipital lobe processes visual information, just imagine the O of Occipital is an eyeball located on the back of your head.

The parietal lobes are located just under the top of your head in each hemisphere. One of the functions of the parietal lobeparietal lobeThe brain lobe at the top of the head that processes touch and spatial information. is to process touch information coming from the body. Each hemisphere’s parietal lobe contains an area known as the somatosensory cortex. The somatosensory cortex is like a map of your skin surface, where body parts are represented according to their sensitivity. Greater sensitivity requires a greater amount of space in the cortex. If we were to make a representation of a person based on the amount of brain area in the cortex, this person (known as a homunculus – “little man” in Latin) would have giant-sized hands, lips, and other ummm… how should I put it…particularly sensitive areas. Less sensitive areas of the skin surface, such as your legs or torso, require less area in the somatosensory cortex.

The temporal lobes are located on either side of your head. One of the main functions of the temporal lobes is to process auditory information. Just like with vision, information coming from the auditory nerves goes to the thalamus and is then passed to the primary auditory cortex in the temporal lobetemporal lobeThe brain lobe on the sides of the head involved in hearing, language comprehension, and memory. (an area known as A1 – not to be confused with the delicious steak sauce). Auditory input is not strictly contralateral, and both hemispheres receive information from each ear. How each hemisphere processes the information is somewhat specialized, and in general, the left temporal lobe specializes in processing speech, while the right temporal lobe is specialized for processing music. You can remember the temporal lobes relate to hearing by considering that they are located near your ears (just behind your temples).

Lastly we come to the frontal lobes, which are the brain areas just behind your forehead. Near the border with the parietal lobes, adjacent to the somatosensory cortex, the frontal lobes contain the motor cortices (cortices is the plural of cortex) which control voluntary movement of different areas of the body. These are arranged contralaterally (left hemisphere controls the right side of the body, and vice versa). These are laid out in a similar manner to the somatosensory cortices, in that movements involving greater dexterity require larger amounts of cortex. So again, the hands and mouth (consider the intricacy of producing speech) take up large amounts of space, while areas corresponding to simpler movements (knee, elbow, etc.) require less space.

More importantly, the frontal lobes can be seen as being the “executives” of the brain which can control and regulate our behaviors. In many ways the frontal lobes set us apart from other primates (notice their sloping foreheads in comparison to ours – they have considerably smaller frontal lobes) and these lobes give us those traits that make us most human. The frontal lobes carry out tasks relating to planning and reasoning, thinking about the future, regulating emotions and making decisions. When a harsh comment and low score on a paper has you ready to physically assault your teacher, the frontal lobes (hopefully) step in and allow you to consider the consequences of your actions, imagine your future life in a prison cell, and come up with an alternative (and more reasonable) course of action.

One way of seeing differences between the two hemispheres comes from cases of patients with “split-brains”. These patients have had their corpus callosum severed in order to prevent the spread of epileptic seizures. While this process effectively stops the seizures, it also creates a few interesting side effects of having two hemispheres which are no longer able to communicate with one another.

This doesn't have a major effect on the patients' lives, as most visual and auditory information is received by both hemispheres, but Roger Sperry and colleague Michael Gazzaniga devised a number of clever experiments to demonstrate some of the specializations of each hemisphere, for which Sperry was awarded the Nobel Prize in 1981. As mentioned when discussing Broca's work on aphasia, speech production is predominantly located in the left hemisphere. This means that split-brain patients are able to talk about information that is in their left hemisphere, but they are unable to verbalize information that is solely in the right hemisphere.

If a split-brain patient were blindfolded and a key were placed in her right hand, she would be able to recognize it and verbally identify it because that sensory information would be in her left hemisphere (remember contralateral control). If, on the other hand (literally), the key were placed in her left hand, she would not be able to say what it was. She would, however, be able to point to the object or even draw it using the left hand. This shows that the right hemisphere is able to have knowledge that cannot be verbally expressed without the help of the left hemisphere.

If a split-brain patient focuses his vision on the center of a screen, anything to the left of the focal point (left visual field) goes to the right hemisphere, while anything in the right visual field goes to the left hemisphere. Note that this division is by visual field not by eye; each eye sends information to both hemispheres, with the left half of what that eye sees going to the right hemisphere and the right half going to the left hemisphere. By selectively presenting images to a particular hemisphere and then assessing the patient's response, we can clearly see how some tasks are localized to that hemisphere.

saw +hammer

For instance, if the words above were flashed on a screen (with the cross as the center focal point), the split-brain patient would say that he saw the word “hammer”, yet if he were asked to draw what he saw with the left hand (right hemisphere) he would draw a picture of a saw. In a similar study, Michael Gazzaniga presented images of faces made out of objects and showed that split-brain patients are only able to recognize the faces when they are presented to the right hemisphere, indicating that this hemisphere is specialized for face recognition.

Unfortunately, the popular press frequently exaggerates the importance of these hemispheric differences as though we had to choose which hemisphere to use for each task. It's certainly not the case that artists are “right-brained” or that mathematicians are more “left-brained”. These differences in skills and preferences cannot be so easily explained by which hemisphere they use. The truth is that we all use both hemispheres all the time, as most of our behaviors are complex enough to require many areas of brain activation in both hemispheres simultaneously. So while it is true that some processes (like speech production or face recognition) are generally confined to particular hemispheres, this doesn't mean that your left hemisphere is twiddling its thumbs while you look at a face or that your right hemisphere shuts down while you're speaking. Both hemispheres are constantly working and processing information, and assuming that you have an intact corpus callosum, they're also constantly letting each other know what's happening on the other side.

Another one of the main assumptions of the biological approach to psychology is that traits and behaviors are heritable, meaning that they can be passed from one generation to the next via biological means. Here’s a basic look at how this happens.

We’ve all heard of genes, but what are they exactly? A gene is the name used for a single unit of hereditary information passed from parent to offspring. This information contains instructions used to code for proteins and build the cells of the offspring. All of our genetic information is known as our genome. You may be surprised to learn that we share a great number of genes with other species, in fact, humans share about 96% of our genes with chimpanzees. This may seem like a lot, but when we consider the role of genes in building all of our cells, we realize the many commonalities with chimps. Our genes need to tell our bodies how to make hair cells, skin, eyes, ears, a heart, blood vessels, neurons, and so on, and chimps also need to make many very similar structures. With this in mind, we shouldn't be quite so shocked that so many of the instructions are similar.

Our genes are located on our DNA (deoxyribonucleic acid) which is organized into strands called chromosomes. These chromosomes are arranged in pairs, and abnormalities aside, we each have 23 pairs of chromosomes. For each chromosome pair, one half came from your dad’s DNA, and the other half came from your mom’s DNA. This means that overall, you will share half of your genes with your father and half of your genes with your mother. Exactly which genes you get from mom and which you get from dad, however, is randomly determined.

If you have siblings, they will also randomly receive half of their genes from mom and half from dad, so, on average, you’ll share about half of your genes with each of your siblings. Identical twins, or more formally, monozygotic twins will share 100% of their genes because they result when a single fertilized egg or zygote splits to become two individuals. Since both twins come from the same sperm cell and same egg, their genes are identical (For the nit-pickers, technically it isn't 100% shared genes because development can result in mutations and copy number variation but for our purposes we will ignore these).

Fraternal, or dizygotic, twins, however, result from 2 separately fertilized zygotes, (two different eggs and two different sperm cells) and so they are just like any other siblings, and will share about 50% of their genes. It's worth noting that when we talk about shared genes among family members, the 50% refers to the percent of genes that may possibly vary among all humans, not the overall difference (as in the chimp example above). In other words, you share somewhere around 99.9% of your genes with all humans, but of the remaining 0.1% that can vary, 50% will be identical with your mom, dad, or siblings, (or 100% of it if you have an identical twin).

Since these different types of twins have different amounts of shared genes, we can use them to estimate the amount of genetic influence on a particular trait. For example, we might look at a trait like IQ and see if monozygotic twins tend to have more similar IQs than dizygotic twins have. If monozygotic twins are more similar, this would indicate that genes play a role in determining IQ because these twins share more genes. Twin studies like these, along with studies of family histories and adoption studies, attempt to estimate the heritabilityheritabilityThe proportion of variation in a trait within a population that is attributable to genetic differences. of certain traits or behaviors. A heritability score (usually denoted with the coefficient h2) is a number ranging from 0 to 1 which represents how much of the variance of a trait is due to genetic influence. A heritability score of 0 means that genes have no influence on the differences between people, while a score of 1 would indicate the sole influence of genes in explaining why people differ.

For example, in the case of IQ, the heritability score is generally estimated to be around 0.5, meaning that about half of the reason for people’s differences in IQ is genetic, and the other half is explained by their different environments and experiences (like nutrition, parenting, school, access to books, etc).

It’s important to remember that heritability scores are always about groups of people, not individuals, and that estimated heritability scores will vary in different places, time periods, and populations. A heritability score of 0.5 for IQ doesn’t mean that half of your individual IQ score comes from your genes. It means that in comparing IQ scores to each other, the reason for differences is partly explained by the fact that people have different genes and partly explained by the fact that people have different environments. It’s also important to note that while heritability indicates the relative strength of these forces, it doesn’t tell us which genes or which aspects of the environment are influencing a particular trait.

While the behavioral geneticsbehavioral geneticsThe study of how genes and environment jointly influence behavior and psychological traits. techniques above can identify relationships between genes and traits, they aren't able to isolate the individual genes responsible. In some cases, however, we are able to specify individual genes that are connected to particular behaviors, traits, problems, or illnesses, and this type of genetic research is known as molecular genetics.

Molecular genetics includes the study of chromosomal abnormalities that have certain characteristic features. In copying the genetic material from parent to offspring, occasionally an entire half of a chromosome pair is duplicated or missing. Having a particular chromosomal abnormality then predicts a number of symptoms that you may experience. Here are a few examples of possible chromosomal abnormalities and their effects.

Down Syndrome occurs when an extra chromosome is copied on the 21st chromosome pair. This results in the characteristic symptoms of Down Syndrome, including a rounded face, thin lips, and moderate mental retardation.

With the following chromosomal abnormalities, occurring on the 23rd chromosome pair, we can see how sex isn't always an either/or distinction of male/female. Generally, the 23rd pair for females contains 2 X chromosomes (XX), while males have an X chromosome and a Y chromosome (XY).

Turner Syndrome – Turner Syndrome occurs when a female child only has a single X chromosome and is missing the other half of the chromosome pair. The physical characteristics of Turner Syndrome include a webbed neck, swollen feet, widely spread nipples, and abnormal genital development. Girls with Turner Syndrome will not menstruate and will not be able to bear children.

Klinefelter Syndrome occurs when there is an extra X chromosome present in a male child. In this case, the child is XXY, with physical characteristics including above average height, breast development, and smaller testicles. Some males with Klinefelter Syndrome are able to produce sperm (and thus have offspring) but not all.

In addition to understanding chromosomal abnormalities, molecular genetics can reveal the structures and functions of individual genes. Genes code for proteins and amino acids and particular versions of some genes will create anomalies in the amino acids they code for. By looking at a person's genetic profile and also identifying the presence or absence of a particular version of a protein, enzyme, or amino acid, we can establish a link between particular genes and certain physiological outcomes.

One such case is the disease PKU or phenylketonuria. PKU results from the mutation of just one of the 3 billion base pairs that make up the human genome. In this case, the body's ability to create phenylalanine hydroxylase (PAH), an enzyme that breaks down phenylalanine, is impaired. Phenylalanine is a toxic amino acid found in certain foods like meat, cheese, and fish that is broken down by PAH into tyrosine, rendering it harmless. Without the correct form of the PAH enzyme, however, people with PKU are unable to break down phenylalanine. As consumption continues, phenylalanine builds up in the body, hindering brain development and resulting in seizures and cognitive deficits.

Fortunately, PKU can be detected early, and a diet which strictly avoids phenylalanine can be adopted. By following a strict diet and also supplementing with some amino acids, people born with PKU can avoid the damaging effects of phenylalanine and live normal, healthy lives.

While these are just a few examples of possible mutations and abnormalities, they can get us started in exploring exactly how our genes make us who we are. We will return to these genetic approaches in future chapters to look for clues in understanding complex subjects like intelligence or personality traits or disorders like depression and schizophrenia.