Kalat Chapters 12-15 Notes

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Kalat Chapters 12 – 15 Notes
CHAPTER 12
EMOTIONAL BEHAVIORS
Chapter Outline
I.
What Is Emotion?
A. Strong emotions tend to increase readiness for action. Most general theories of
emotion deal with the relationship between emotion and action.
B. Emotions, Autonomic Arousal, and the James-Lange Theory
1. Emotional situations arouse the sympathetic and the parasympathetic
branches of the autonomic nervous system. The sympathetic nervous
system prepares the body for brief, vigorous action while the
parasympathetic nervous system alters the body’s activities to save energy
and prepare for later events.
2. One theory on emotion is that when you feel an emotion, your heart rate
responds and then prompts other responses.
3. James-Lange theory: Autonomic arousal and skeletal actions occur before
an emotion. An emotion is the label we give to our physiological responses.
4. In this theory, emotions have three components—cognitions, actions, and
feelings. Cognitive appraisal of a situation comes first, which leads to some
action, and then the emotional feelings follow last.
5. Is Physiological Arousal Necessary for Emotions?
a. People with severe spinal cord injuries, who cannot move or feel from
the damaged area downwards still report that they feel emotions at the
same rate/level as before the injury. This suggests emotions do not
require feedback from muscle movements.
b. Pure autonomic failure: Uncommon condition in which output from
the autonomic nervous system to the body fails, either completely or
almost completely. People with this disorder have no changes in
autonomic response to psychological or physical stress. These people
report having the same emotions as anyone else, although the emotions
are much less intense. The decreased emotional feeling is consistent
with predictions of the James-Lange theory.
c. A study of people who have received BOTOX suggest that they
experience weaker than usual emotional responses to videos, which
implies that body changes (i.e., facial expressions and movements) are
important for feeling an emotion.
6. Is Physiological Arousal Sufficient for Emotions?
a.
b.
Panic attack: A condition marked by extreme sympathetic nervous
system arousal, which is sometimes brought on by the occurrence of
rapid breathing and a racing heartbeat. Such symptoms, when
spontaneously occurring, lead people to believe that a panic attack is
about to happy, and thus trigger the panic attack.
People forced to smile rated a comic strip as funnier than people not
manipulated into expressing a smile.
c. However, a smile is now necessary for happiness. People with a rare
disorder that does not allow them to smile, Möbius syndrome, still
experience happiness and amusement.
C. Brain Areas Associated with Emotion
1. Attempts to Localize Specific Emotions
a. Limbic System: A forebrain area that forms a border around the
brainstem, traditionally regarded as critical for emotion.
b. Brain areas responsible for different types of emotion have been
investigated and found to be highly variable. One of the best-localized
emotions is disgust, which has been shown to be in the insular cortex.
The same part of the brain reacts to something that tastes badly.
2. Contributions of the Left and Right Hemispheres
a. Activity in the left hemisphere is termed as Behavioral Activation
System (BAS), marked by low to moderate autonomic arousal, which
could be characterized as either happiness or anger.
b. Activity in the frontal and temporal lobes of the right hemisphere is
associated with the Behavioral inhibition System (BIS), which
increases attention and arousal, inhibits action, and stimulates emotions
such as fear and disgust.
c. People with great activity in the frontal cortex of the left hemisphere
tend to be happier, more outgoing, and more fun-loving. People with
greater right-hemisphere activity tend to be socially withdrawn, less
satisfied with life, and prone to unpleasant emotions.
d. The right hemisphere appears to be more responsive to emotional
stimuli than the left. The right hemisphere is especially activated by
unpleasant emotions.
D. Functions of Emotion
1. The adaptive advantages of some emotions are clear: Fear alerts us to
danger and disgust helps us avoid illness-inducing substances. They may
also help us make quick “gut” decisions.
2. Emotions and Moral Decisions
a. When making moral decisions, we consider how the outcomes will
make us feel.
b. The trolley dilemma, the footbridge dilemma, the lifeboat dilemma, and
the hospital dilemma are all examples where you can save five people
(sometimes including yourself) by killing one person.
c. Most people say it is right to pull the switch in the trolley dilemma,
while fewer say yes in the footbridge and lifeboat dilemmas.
d.
3.
When we are making a decision about right and wrong, we seldom
work it out rationally. Most people go with what feels right and then
think of a logical justification afterwards.
Decision Making After Brain Damage that Impairs Emotions
a. If confronted with the trolley car dilemma, people with prefrontal
damage are more likely than average to choose the utilitarian option of
killing one to save five, even in situations where most people find the
choice emotionally unacceptable.
b. The most famous example is of Phineas Gage, who suffered massive
damage to his prefrontal cortex and survived. Reports about his
behavior and temperament after the accident suggested that he became
impulsive and made poor decisions.
c. Antonio Damasio, who also suffered prefrontal cortex damage,
expressed almost no emotions. It resulted in bad decision-making that
cost him his job, his marriage, and his savings.
d. Damage to the ventromedial prefrontal cortex results in the loss of a
sense of guilt. People with damage to the prefrontal cortex or the
amygdala are slow in processing emotional information.
II. Attack and Escape Behaviors
A. Attack Behaviors
1. What you are doing or about to do affects how you feel. Research shows
that a bout of anger will often prime a more intense and rapid bout of anger,
if provoked, at a later point.
4. Heredity and Environment in Violence
a. Research shows that people who were abused as children, people who
witnesses abuse of parents, and people who live in violent
neighborhoods are at greater risk of violence themselves.
b. Environmental factors, including exposure to lead and fetal exposure to
nicotine, may lead to violence in individuals.
c. One study found that monozygotic twins were more likely to resemble
each other in adult crimes and aggressive behaviors than were dizygotic
twins, and adopted children resemble their biological parents.
d. No single gene accounts for aggression. Instead, there is an interaction
between heredity and environmental factors.
e. Violence is particularly enhanced in people with both a genetic
predisposition and a troubled early environment. Low MAOA activity
and serious maltreatment in childhood results in significantly higher
antisocial behavior.
4. Hormones
a. Male aggressive behavior and increased striving for social dominance
depends heavily on testosterone. In humans, men with higher levels of
testosterone have, on average, slightly higher rates of violent activities
and criminal behaviors than do other men.
b.
Aggression tends to be highest when testosterone levels are high and
cortisol levels are low (as cortisol increases fear).
c. A recent study found young women injected with testosterone were less
accurate at identifying angry facial expressions. Other studies show that
testosterone increases the response of the amygdala to angry facial
expressions.
5. Serotonin Synapses and Aggressive Behavior.
a. Nonhuman Animals
 Increased aggressive behavior was seen in decreased serotonin
turnover in mice. Serotonin turnover can be inferred by measuring
the concentration of 5-hydroxyindoleacetic acid (5-HIAA), a
serotonin metabolite.
 Luigi Valzelli found that social isolation induced a drop in
serotonin turnover in the brains of male mice, an effect that further
increased the possibility of aggressive behavior toward other
males. These effects are not found in female mice.
 In a study of 2-year-old male monkeys, researchers found that
monkeys with the lowest serotonin turnover had the highest
amount of aggressive behaviors. Moreover, these monkeys died
before the age of 6, while monkeys with higher serotonin turnover
were alive at 6.
b. Humans
 Studies have found that lower-than-normal serotonin turnover is
present in those convicted of violent crimes as well as those who
committed or attempted suicide by violent means. Follow-up
studies on people released from prison have found that those with
lower serotonin turnover had a greater probability of further
convictions for violent crimes.
 Neurons synthesize serotonin from tryptophan (an amino acid
found in proteins). A diet high in other amino acids, but low in
tryptophan, impairs the brain’s ability to synthesize serotonin. One
study found an increase in aggressive behavior in young men a few
hours after eating a diet low in tryptophan.
 Less active forms of the genes for the enzyme tryptophan
hydroxylase (which convert tryptophan into serotonin) may be
responsible for the low serotonin levels and increased aggression.
c. How Do We Explain Serotonin Effects?
 High levels of serotonin inhibit a variety of impulses, and low
levels remove inhibitions.
 Serotonin’s role in aggression is complicated: Some people with
low serotonin levels become depressed, not aggressive. However,
the brain has been found to release serotonin during aggressive
actions. In addition, low serotonin activity prior to aggravation
magnifies the response when serotonin is suddenly released at the
start of an aggressive encounter.
B. Fear, and Anxiety
1.
2.
3.
4.
5.
Fear, Anxiety, and the Amygdala
a. Startle reflex: Response one makes to a sudden, unexpected loud
noise. People with post-traumatic stress disorder show a much
enhanced startle reflex.
Studies of Rodents
a. The amygdala enhances the startle reflex by sending axons to the
hypothalamus (for controlling autonomic fear responses) and by
relaying information to the midbrain, which in turn sends axons to the
pons, triggering the startle reflex.
b. Toxoplasma gondii is a protozoan that exploits the consequences of
amygdala damage. The parasite enter a rat and migrates to the brain,
where it damages the amygdala. The rat fearlessly approaches a cat,
guaranteeing that the parasite will find its way back into a cat (where it
reproduces and excreted in the feces).
c. If a rat receives shocks after fear conditioning, it learns to fear the
stimulus, as well as the cage, new cages, and new situations. The same
is true of humans.
d. The amygdala is important for knowing what to fear. When people are
attacked or have traumatic experiences, they become more fearful in a
wide variety of situations. This long-term, generalized emotional
arousal depends on a brain area called the bed nucleus of the stria
terminalis.
Studies of Monkeys
a. Klüver-Bucy syndrome: Tameness and placidity in monkeys following
damage or removal of the amygdala. Monkeys with amygdala lesions
have decreased fear and are more likely to approach an object they
normally avoid, while other monkeys are withdrawn and fearful.
b. Those with a more vigorously reactive amygdala tend to show the
greatest fear in response to a noise or an intruder.
Response of the Human Amygdala to Visual Stimuli
a. Studies using fMRI have demonstrated that the amygdala is activated in
response to emotional expressions, especially fear and anger. It also
responds, to a lesser extent, to faces showing happiness or sadness.
b. The amygdala responds most strongly when a facial expression is a bit
ambiguous or difficult to interpret. Presumably, arousal indicates that
it is working harder to make sense of the stimulus.
Individual Differences in Amygdala Response and Anxiety
a. In a study of college students, researchers found that amygdala activity
correlated highly with the number of unpleasant emotions they had
recorded. Presumably, unpleasant emotions are biologically
predisposed.
b. Soldiers with the greatest amygdala response to unpleasant faces later
reported the greatest amount of combat stress.
c. The amygdala is strongly associated with fear responses. The
interpretation is that people with a highly reactive amygdala are likely
to perceive dangers and therefore to support strong protection against
those dangers.
6. Damage to the Human Amygdala
a. Some people with damage to the amygdala continue to experience the
cognitive aspect of emotions (they can classify emotional photos as
pleasant or unpleasant) but not the feeling aspect.
b. Urbach-Wiethe disease is a genetic disorder that causes gradual atrophy
of the amygdala. In one example, an individual known as SM views
scary movies and experiences only excitement, is curious when
touching exotic and venomous snakes, and is happy when going
through a haunted house. In addition, she was held up at gun point and
knife point and only remembers being angry, not scared. Her preferred
talking distance was ½ that of normal people, and she did not show
discomfort when an unknown man approached her so close that their
noses touched.
c. Such people fail to recognize the emotional expressions in faces,
especially expressions of fear and disgust. Instead of making eye
contact, she always looks at people’s noses. When asked to look at the
eyes, those like SM quickly recognize fear.
d. This research suggests that the amygdala may not be responsible for
feeling fear, as much as it is responsible for detecting emotional
information and directing other brain areas to pay attention to it in the
proper way.
C. Anxiety Disorders
1. Anxiety disorders are characterized as such when the major symptoms is
increased anxiety. They include panic disorder, generalized anxiety
disorder, and phobias.
2. Panic disorder: A type of anxiety disorder characterized by frequent
periods of anxiety and occasional attacks of rapid breathing, increased heart
rate, sweating, and trembling. More common in women than men, and more
common in adolescent and young adults than in older adults.
3. Pharmacological Relief from Anxiety.
a. CCK (cholecystokinin) is one of the main excitatory neuromodulators
in the amygdala. Injections of CCK-stimulating drugs into the
amygdala enhance the startle reflex. Injections of CCK type B receptor
blockers will block this anxiety.
b. GABA (gamma amino butyric acid) is the main inhibitory
neurotransmitter found in the amygdala. Injections of GABA blockers
can induce outright panic.
c. Benzodiazepines: Commonly used class of anti-anxiety drugs. The
benzodiazepines include diazepam, chlordiazepoxide, and alprazolam.
These drugs bind to a receptor site on the GABAA receptor, which
causes the receptor to change shape, allowing GABA to attach more
easily and bind more tightly to it.
d.
4.
Benzodiazepines exert their antianxiety effects in the amygdala and
hypothalamus, midbrain, and several other areas. They produce a
variety of effects, including the possibility of addiction.
Relearning as Relief from Anxiety
a. Anti-anxiety drugs provide temporary relief and are not intended for
use with chronic anxiety, like that which results from trauma.
b. To help relieve chronic anxiety, clinical psychologists generally use
exposure therapy to gradually expose the individual to the feared
object. However, although extinction training suppresses the original
learning with new learning, it does not eliminate it altogether. Adults
seldom fully extinguish a learned reaction.
c. In general, it is easier to extinguish a learned response immediately
after original learning than it is later. After time has passed, the
learning becomes consolidated (has a stronger effect).
d. Propranolol: A drug that interferes with protein synthesis at certain
synapses in the amygdala. This drug weakens the emotional response
that occurs after a feared stimulus is presented, and the result is a
persisting decrease in fear intensity.
III. Stress and Health
A. Behavioral medicine: Emphasizes effects of diet, smoking, exercise, and other
behaviors on health.
B. Concepts of Stress
1. Stress: The nonspecific response of the body to any demand made upon it.
Events that are interpreted as threatening to an individual and which elicit
physiological and behavioral responses.
2. General Adaptation Syndrome: A generalized response to stress that
includes the following three stages: alarm (characterized by increased
activity of the sympathetic nervous system), resistance (adrenal cortex
secretes cortisol and other hormones that enable the body to maintain
prolonged alertness, fight infections, and heal wounds), and exhaustion (the
individual is tired, inactive, and vulnerable because the nervous system and
immune systems no longer have the energy to sustain their heightened
responses).
3. Changes in one’s life can also induce stress, such as getting fired or
promoted.
C. Stress and the Hypothalamus-Pituitary-Adrenal Cortex Axis
1. Stress activates both the autonomic nervous system and the HPA axis
(hypothalamus, pituitary gland, and adrenal cortex). In fact, prolonged
stress increasingly activates the HPA axis.
2. Stress activates the hypothalamus, which sends messages to the anterior
pituitary gland to secrete adrenocorticotropic hormone (ACTH); this
hormone stimulates the adrenal cortex to secrete cortisol, which increases
blood sugar levels and enhances metabolism.
3.
4.
5.
Brief and moderate stress improves attention and memory formation,
improves performance on relatively simple tasks, impairs performance that
requires complex, flexible thinking, and enhances the activity of the
immune system.
The Immune System
a. Immune system: Comprised of cells that protect the body against
intruders such as bacteria and viruses. An autoimmune disease is the
result of the immune system attacking normal cells.
1. Leukocytes: White blood cells that are produced in the
bone marrow before migrating to the thymus gland, spleen,
and peripheral lymph nodes. Leukocytes patrol the blood
and other body fluids, looking for intruders.
2. There are several types of leukocytes, including B cells:
Leukocytes that mature in the bone marrow and produce
specific antibodies to attack an antigen.
3. Antibodies: Y-shaped proteins that circulate in the blood
and attach specifically to one kind of antigen. The body
develops antibodies against antigens that it has encountered
in the past.
4. Antigens (antibody-generator molecules): Proteins located
on a cell surface. When leukocytes discover cells with
antigens different from the rest of the body, they attack
those cells.
5. T cells: Leukocytes that mature in the thymus. T cells are
of two types: cytotoxic T cells, which directly attack
intruder cells, and helper T cells, which stimulate other T
cells or B cells to multiply more rapidly.
6. Natural killer cells: Blood cells that attach to cells infected
with viruses and certain kinds of tumor cells.
7. Cytokines: Chemicals released by the immune system that
cross the blood-brain barrier and influence neuronal
function.
Effects of Stress on the Immune System
a. Psychoneuroimmunology: Deals with the ways in which experiences,
especially stressful ones, alter the immune system, and how the
immune system in turn influences the central nervous system.
b. In response to a stressful experience, the nervous system activates the
immune system to increase its production of natural killer cells and the
secretion of cytokines. The elevated cytokine levels help combat
infections, but also trigger the brain to produce the same symptoms as
if one were ill.
c. In prosperous countries, the immune system responds more often to
events such as taking exams in college, seeing photos of sick or injured
people, or giving a public lecture.
d. Results of one study show that people who reported a brief stressful
experience were at no more risk for catching a cold that were people
who reported no stress. However, for those who reported stress lasting
longer than a month, the longer it lasted, the greater the risk of illness.
e. High cortisol levels impair memory and increase the vulnerability of
neurons in the hippocampus, so that toxins or overstimulation will kill
the neurons.
D. Stress Control
1. In humans, resilience in the face of stress correlates with stronger
connections between the amygdala and the prefrontal cortex.
2. In order to control stress, people have developed techniques like breathing
routines, exercise, meditation, and distraction. Social support is a powerful
method for coping with stress. Brain scans correspond to people’s selfreports that social support from a loved one helps reduce stress.
E. Post-traumatic Stress Disorder
1. PTSD: Psychiatric disorder that occurs in some people who have had a
traumatic experience of being severely injured or threatened or seeing other
people harmed or killed.
2. Symptoms of PTSD, which last at least a month after the experience,
include frequent distressing recollections (flashbacks) and nightmares about
the traumatic event, avoidance of reminders of it, and exaggerated arousal
in response to noises and other stimuli.
3. There are differences in vulnerability to PTSD. Victims have a smaller than
average hippocampus and have lower than normal cortisol levels.
F.
CHAPTER 13
THE BIOLOGY OF LEARNING AND MEMORY
Chapter Outline
I.
Learning, Memory, Amnesia, and Brain Functioning
A. Localized Representations of Memory
1. Classical Conditioning: After repeated presentations (although a strong
stimulus will work with only one pairing) of a conditioned stimulus (CS),
which initially elicits no response, with an unconditioned stimulus (UCS),
which automatically elicits an unconditioned response (UCR), the subject
begins responding to the CS because they have come to associate it with the
UCS. For example, Pavlov classically conditioned a dog to respond to have
a salivating response to a bell after continuously pairing the bell with the
dog’s food.
2. Instrumental Conditioning: Behavior is followed by a reinforcer (which
increases the future probability of a response) or punishment (which
suppresses the frequency of a response).
Lashley’s Search for the Engram
a. Engram: Physical representation of learning.
b. Karl Lashley’s work on learning (using cortical lesions in varying
locations within the brains of rats) led him to propose two principles
about the nervous system.
c. Equipotentiality: All parts of the cortex contribute equally to complex
behaviors like learning; any part of the cortex can substitute for any
other.
d. Mass action: The cortex works as a whole, and the more cortex the
better.
e. Lashley’s work was based on the assumption that the cerebral cortex
was the best place to search for an engram and that all memories are
physiologically the same. Researchers that followed found neither
assumption was necessary true.
f. Years later, Richard F. Thompson located an engram of memory in the
cerebellum.
g. Lateral interpositus nucleus (LIP): An area essential for learning.
Damage to this area of the cerebellum leads to permanent loss of a
classically conditioned eyeblink response in rabbits. Temporary
suppression of the area led to zero effectiveness of classical
conditioning training.
B. Types of Memory
1. Short-Term and Long-Term Memory
a. Short-term memory: Memory of events that have just occurred.
b. Long-term memory: Memory of events from previous times.
c. Short-term and long-term memory differ in capacity. Short-term
memory holds no more than seven items, while long-term memory is
vast and more difficult to estimate.
3.
d.
2.
Short-term memory depends on rehearsal and long-term memory does
not.
e. With short-term memory, once you forget something, it is lost. Longterm memories may be recalled with hints and reconstructed.
f. Information initially entered into short-term storage can be
consolidated into long-term memory.
Our Changing Views of Consolidation
a. Many short-term memories are not simply temporary stores on their
way to being long-term memories. Once something changes (like the
score to a hockey game), it doesn’t turn into a long-term memory.
b. The time needed for consolidation varies enormously. Memorizing
interesting facts will take less time than memorizing boring ones.
Emotionally significant memories form quickly. Small to moderate
amount of cortisol activate the amygdala and hippocampus, where they
enhance the storage and consolidation of recent experiences.
c.
It was previously thought that once formed, long-term memories were
permanent. However, it is now clear that consolidated memories are not
always permanent. They can change, fade, and vary in detail.
d. If a reminder is followed by a similar experience, the memory is
reconsolidated. New experiences during the reconsolidation process
can modify the memory.
3. Working Memory
a. Working memory: Temporary storage of memories about a task that
one is attending to at the moment.
b. Delayed-response task: Memory task in which a subject is given a
signal to which it must give a learned response after a delay. A
common test for working memory.
c. Damage to the prefrontal cortex impairs performance on working
memory tasks, and the deficit can be amazingly precise.
d. Older people have impairments of working memory, probably because
of changes in the prefrontal cortex.
C. The Hippocampus
1. Amnesia: Memory loss. Damage to the hippocampus produces a powerful
kind of amnesia.
2. People with Hippocampal Damage
a. Patient H. M. had his hippocampus and surrounding brain tissue
removed from both hemispheres in 1953 to treat his severe epilepsy.
b. Anterograde and Retrograde Amnesia
i. H.M. suffered moderate retrograde amnesia (loss of memory for
events that occurred shortly before brain damage) and severe
anterograde amnesia (loss of long-term memories for events that
happened after brain damage) as a result of the bilateral
hippocampal removal.
c. Intact Working Memory
i. H.M.’s short-term memory or working memory remained intact.
d.
e.
f.
Impaired Storage of Long-Term Memory
i. The surgery severely impaired H. M.’s ability to form long-term
memories. Even newer words to the English language, like Jacuzzi
and granola, were regarded as nonsense.
ii. When distracted, he would underestimate his own age by 10 years
or more.
Severe Impairment of Episodic Memory
i. He showed no ability to form episodic memories (memories of a
single event). He could describe facts that he learned before the
operation but could not recount personal events.
ii. He did retain the ability to weakly retain semantic (factual)
memories. Memory loss also affected his ability to describe the
future.
Better Implicit than Explicit Memory
3.
i. Nearly all patients with amnesia show better implicit memory
(influence of a recent experience on behavior, even if one does not
realize that he or she is using memory at all) than explicit memory
or declarative memory (deliberate recall of information that one
recognizes as a memory).
g. Intact Procedural Memory
i. Procedural memory: the development of motor skills and habits;
a special kind of implicit memory. H.M. acquired new skills
without apparent difficulty.
ii. People with amnesia usually have normal working memory, severe
anterograde amnesia for declarative memory, some retrograde
amnesia, better implicit than explicit memory, and nearly intact
procedural memory.
Theories of the Function of the Hippocampus
a. The Hippocampus and Declarative Memory
i. People with hippocampal damage acquire new skills but have
enormous trouble learning new facts. This leads researchers to
believe that the hippocampus is critical for declarative memory,
especially episodic memory.
ii. Delayed matching-to-sample task: Task used to measure
declarative memory in animals. In this procedure, animals see an
object (the sample) and after a delay get to choose between two
objects, one of which matches the sample.
iii. Delayed nonmatching-to-sample task: The procedure is the same
except that the animal must choose the object that is different from
the sample.
iv. Hippocampal damage impairs performance on both delayed
matching-to-sample and delayed nonmatching-to-sample tasks.
b. The Hippocampus and Spatial Memory
i. In rats, many hippocampal neurons are tuned to particular spatial
locations. In human cab drivers, imaging data has shown that the
hippocampus is activated when answering spatial questions and
they have a larger than normal posterior hippocampus.
ii. Radial Maze: Maze with eight or more arms used to test spatial
memory in animals. Damage to the hippocampus impairs
performance on this task.
iii. Morris Water Maze: Procedure where an animal has to find a
hidden platform, usually under murky water. This procedure is
used to test spatial memory in animals and, like the radial maze,
performance is negatively impacted by hippocampal damage.
iv. In certain closely related species of birds, the larger the
hippocampus, the better their performance on spatial memory
tasks.
c. Hippocampus and Contextual Memory
i. The hippocampus is important for remembering details and
context. Recent memories have significant detail and depend on
the hippocampus.
ii. Older memories have fewer details and are less reliant on the
hippocampus.
iii. Recalling recent memories activates the hippocampus; recalling
older memories may not require the involvement of the
hippocampus.
D. The Basal Ganglia
1. The basal ganglia is responsible for implicit learning or habit learning,
which is gradual.
2. People with amnesia from hippocampal damage perform randomly on the
weather task (when asked what the weather will be like based on images).
However, if they continue for long enough, they show gradual improvement
based on habits supported by the basal ganglia.
3. This suggests that the hippocampus is more important for declarative
memory and the basal ganglia is more important for procedural memory.
Psychologists no longer believe in a strict separation between the tasks of
the two structures as nearly all tasks activate both areas.
E. Other Types of Amnesia
1. Korsakoff's Syndrome
a. Korsakoff’s Syndrome or Wernicke-Korsakoff’s syndrome: Brain
damage caused by prolonged thiamine deficiency (this disorder is most
commonly seen in chronic alcoholics).
b. Thiamine deficiency leads to brain cell loss in the mammillary bodies
of the hypothalamus and the dorsomedial nucleus of the thalamus,
which projects to the prefrontal cortex.
c. Korsakoff's patients show apathy, confusion, and have trouble
reasoning about their memories. Patients with Korsakoff’s syndrome
also have both anterograde and retrograde amnesia.
d. Confabulation: Making up an answer to a question and accepting the
invented answer as if it were true (a common symptom of Korsakoff's
syndrome).
2. Alzheimer’s Disease
a. Alzheimer's disease: A dementia that becomes more prevalent with
advancing age. Symptoms include short-term and long-term memory
loss, confusion, restlessness, hallucinations, and disturbances of eating
and sleeping.
b. People with Alzheimer’s disease have better procedural than
declarative memory and better implicit than explicit memory.
c.
People with Down syndrome (a type of mental retardation caused by
having three copies of chromosome 21) usually get Alzheimer's disease
if they survive into middle age. This led researchers to discover a gene
on chromosome 21 linked with early-onset Alzheimer’s disease, but
this form of the disease only accounts for 1% of total cases.
d. Abnormal genes located on several different chromosomes can lead to
an accumulation of amyloid- deposits in the brain. Deposits of
amyloid cause neuronal degeneration in the brain, and the dying axons
and dendrites form plaques in many areas of the cerebral cortex and
hippocampus, as well as other brain areas.
e. The tau protein also accumulates and produces tangles, structures
formed from degeneration within neurons
f. Curcumin, a component of the turmeric spice, has been shown to
inhibit amyloid- in animals. Research on human applications has just
begun.
g. What Patients with Amnesia Teach Us
i. People do not lose all aspects of memory equally.
ii. People have several somewhat independent kinds of memory that
depend on different brain areas.
D. Other Brain Areas in Memory
1. Almost all cortical and subcortical structures are involved in some aspect of
memory.
2. The amygdala is important for fear learning.
3. Parietal lobe damage affects the ability to associate one type of information
with another.
4. Damage to the anterior and inferior temporal lobes results in semantic
dementia, in which semantic memories are impaired.
5. Damage to the prefrontal cortex impairs the ability to learn about rewards
and punishments.
II. Storing Information in the Nervous System
A. Learning and the Hebbian Synapse
1. Hebbian synapse: A synapse that increases in effectiveness because of
simultaneous activity in the presynaptic and postsynaptic neurons.
B. Single-Cell Mechanisms of Invertebrate Behavior Change
1. Aplysia as an Experimental Animal
a. Aplysia is a marine invertebrate related to the common slug, often used
for physiological studies of learning. Aplysia have fewer neurons than
any vertebrate, and many are large and easy to study. A commonly
studied behavior in the Aplysia is the gill withdrawal response.
2. Habituation in Aplysia
a. Habituation: A decrease in response to a stimulus that is presented
repeatedly and is accompanied by no change in other stimuli.
Habituation in Aplysia reflects a change in the synapse between the
sensory neuron and a motor neuron.
3.
Sensitization in Aplysia
a.
Sensitization: An increase in response to a mild stimulus after an
intense stimulus has been presented. Sensitization in Aplysia depends
on the release of serotonin by a facilitating interneuron onto the
synapses of many presynaptic sensory neurons; this process ultimately
blocks potassium channels and thereby prolongs the release of
transmitter from that neuron.
C. Long-Term Potentiation in Vertebrates
1. Long-term potentiation (LTP): Increased responsiveness to axonal input
as a result of a previous period of rapidly repeated stimulation. LTP has
three properties that make it an attractive candidate for the cellular basis of
learning and memory:
a. Specificity: Only activated synapses become strengthened.
b. Cooperativity: Nearly simultaneous stimulation by two or more axons
produces LTP; stimulation by just one axon produces it weakly.
c. Associativity: Pairing a weak input with a strong input enhances later
responses to the weak input.
2. Long-term depression (LTD): A prolonged decrease in responsiveness to
synaptic input after repeated pairing with some previous input that is
generally of low frequency. LTD occurs in the cerebellum and
hippocampus.
3. Biochemical Mechanisms
a. AMPA and NMDA Synapses
i. In a few cases, LTP depends on changes at GABA synapses.
ii. Most cases of LTP depend on changes at glutamate receptors.
iii. The AMPA receptor and the NMDA receptor are both usually
excited by the neurotransmitter glutamate, but can respond to drugs
abbreviated AMPA and NMDA respectively.
iv. Usually glutamate produces neither excitatory nor inhibitory
effects at NMDA receptors because magnesium blocks ion
channels located on this receptor.
v. About the only way to activate NMDA receptors is first to
repeatedly stimulate nearby AMPA glutamate receptors, thereby
depolarizing the dendrite. Depolarization repels the magnesium
ions and allows glutamate to open NMDA channels so that sodium
and calcium ions can enter the cell.
vi. Calcium ions induce the expression of otherwise inactive genes,
which produce proteins that alter the activities of more than a
hundred other known chemicals within the dendrites. This
increases the future responsiveness of these glutamate receptors.
vii. Calcium enhances the responsiveness to glutamate by activating a
protein called CaMKII, leading to the following effects:
 The dendrite may build more AMPA receptors or move them
into a better position.
 Neurons make more NMDA receptors.
 The dendrite may make more branches, thus forming additional
synapses with the same axon.
 The AMPA receptors become more responsive than before.
viii. The effects of CaMKII and CREB are magnified by BDNF, a
neurotrophin similar to nerve growth factor.
ix. Once LTP has been established, it no longer depends on NMDA
synapses. Drugs that block NMDA prevent the establishment of
LTP, but they do not interfere with the maintenance of LTP.
b. Presynpatic Changes
i. LTP causes presynaptic changes through the release of a
retrograde neurotransmitter from the postsynaptic cell. These
changes include reduced threshold for producing action potentials,
increased neurotransmitter release, expanded size of the
presynaptic axonal membrane, and release of neurotransmitter
from more sites on the axon.
4. Consolidation, Revisited
a. fMRI studies found that progressively older events produced more
activity in the cerebral cortex and less in the hippocampus and
amygdala. This demonstrates a shift to the cerebral cortex both over a
period of one day and over a period of many years.
D. Improving Memory
1. The relationship between LTP and learning is unknown at this time, but
studying the biochemistry of LTP has improved our understanding of what
could impair or improve memory.
2. LTP depends on production of several proteins, and enhancing production
of these proteins enhances memory in rodents.
3. Moderate doses of stimulant drugs enhance learning by increasing arousal.
Caffeine and methylphenidate are both examples.
CHAPTER 14
Cognitive Functions
Chapter Outline
I.
Lateralization of Function
A. The Left and Right Hemispheres
1. The brain has two hemispheres; each hemisphere controls the contralateral
(opposite) side of the body. For example, the right hemisphere is connected
to sensory receptors and muscles mainly on the left half of the body (the
opposite holds true for the left hemisphere). Both hemispheres control the
trunk muscles and facial muscles. Taste and smell are uncrossed (each
hemisphere gets taste information from its own side of the tongue.
2. Corpus Callosum: A set of axons that allows the two hemispheres to
exchange information with one another. The anterior commissure, the
hippocampal commissure, and a couple of other small commissures also
help in the exchange of interformation.
3. Lateralization: Refers to the behaviors and cognitive abilities that each
hemisphere specializes in. For example, language ability is primarily
localized in the left hemisphere.
B. Visual and Auditory Connections to the Hemispheres
1. Light from the right visual field (what is visible at a particular moment)
shines onto the left half of both retinas; this information is then relayed to
the left hemisphere. The right half of each retina connects to the right
hemisphere, which sees the left visual field.
2. Optic chiasm: Point where half of the axons from each eye cross to the
opposite side of the brain.
3. Each ear receives sound waves from one side of the head, but each sends
the information to both sides of the brain. If the two ears receive different
information, each hemisphere pays more attention to the ear on the opposite
side.
C. Cutting the Corpus Callosum
1. Severing the corpus callosum prevents the sharing of information between
the two brain hemispheres.
2. Epilepsy: Condition characterized by repeated episodes of excessive
synchronized neural activity (i.e., seizure). Most people with epilepsy
(90%) use drugs to suppress their seizure activity.
3. If seizure activity is not controlled by drug therapy, some people have
surgery to remove the focus (point of origin of the seizure). Alternatively,
epileptics sometimes have their corpus callosum severed to prevent seizure
activity from crossing from one hemisphere to the other.
4.
5.
6.
7.
8.
Evidently, epileptic activity rebounds back and forth between the
hemispheres and prolongs seizures. Without the bounce back effect, a
seizure may not develop at all. These individuals are often referred to as
split-brain people.
Split-brain people can point to objects with their left hand (but not with
their right hand) if visual information is presented from the left visual field
to their right hemisphere. Information presented in the right visual field
(thus going to the left hemisphere) allows patients to name or describe what
they see.
The left hemisphere is dominant for speech production in 95% of righthanded individuals and for approximately 80% of left-handed individuals.
Speech comprehension is less lateralized.
The two hemispheres of a split-brain person can process information
independently of each other. This allows split-brain people to do tasks that
some find difficult, like drawing circles with both hands simultaneously
with one hand going slightly faster than the other.
Split Hemispheres: Competition and Cooperation
a. In the first weeks after surgery, split-brain people find that the
hemispheres act like separate people sharing one body. For example,
7.
8.
D.
1.
2.
3.
one person repeatedly took items from the grocery shelf with one hand
and returned them with the other.
b. Later, the brain eventually learns to use smaller connections between
the left and right hemispheres to avoid conflicts between them.
c. Sometimes, the hemispheres learn to cooperate. This is tested using
words that are flashed simultaneously on both sides of the visual field.
Some split-brain people will combine the two words into one concept.
The Right Hemisphere
a. The right hemisphere is better than the left at perceiving the emotions
in people’s gestures and tone of voice.
b. People with right-hemisphere damage speak with less inflection and
expression, plus they often have trouble interpreting the emotions that
other people express through their tone of voice.
c. Research findings suggest that the right hemisphere is more adept than
the left at comprehending spatial relationships.
d. The left hemisphere is more focused on details and the right
hemisphere is better at perceiving overall patterns.
Hemispheric Specializations in Intact Brains
a. Differences in hemisphere specialization can be demonstrated in people
without brain damage, but most of these differences are small.
b. For example, research shows that you will be more accurate if you
smelled the two substances with the same nostril, and therefore the
same hemisphere.
Development of Lateralization and Handedness
Anatomical Differences Between the Hemispheres
a. Planum temporale: A section of the temporal cortex that is larger in
the left hemisphere in approximately 65% of the population. This
difference in size is apparent at age 3 months in humans. Children with
the biggest ratio of left to right planum temporale performed best on
language tests.
b. Smaller but still significant differences are found between left and right
hemispheres of chimpanzees, bonobos, and gorillas. This is evidence
that specialization in the human brain is built upon specializations
already present in apelike species.
Maturation of the Corpus Callosum
a. The corpus callosum gradually grows and thickens during childhood
and adolescence.
b. The corpus callosum matures slowly over the first 5 to 10 years of
human life. Because the neurons connected by the corpus callosum take
years to develop their mature adult pattern, the behavior of young
children sometimes resembles that of split-brain people.
c. In one study using fabrics, five-year olds did equally well with one
hand or with two, while three-year olds made 90% more errors with
two hands that with one.
Development Without a Corpus Callosum
a.
People born without a corpus callosum can perform some tasks that
split-brain people fail, possibly due to larger-than-normal hemispheric
connections developing elsewhere in the brain. For example, they can
describe what they feel with either hand and what they see in either
visual field. The following two commissures are often larger than
normal in people born without a corpus callosum:
a. Anterior commissure: Connects the two hemispheres around the
anterior parts of the cerebral cortex.
b. Hippocampal commissure: Connects the left hippocampus to the right
hippocampus.
4. Most people (90%) are right-handed, and in 95% of this group, the left
hemisphere is dominant for speech. Left-handed people are more variable.
Most left-handers have a left hemisphere dominance for speech, but some
have right hemisphere dominance or a mixture of left and right.
E. Avoiding Overstatements
1. One should not conclude from this research that they are not good at certain
things because they are either “left-brained” or “right-brained”. It is
doubtful that any individual habitually relies mostly on one hemisphere.
II. Evolution and Physiology of Language
A. Human language stands out from others because of its productivity, its ability
to produce new signals to represent new ideas.
B. Nonhuman precursors to language
1. Common Chimpanzees
a. Common chimpanzees cannot learn to talk, but can learn some
language skills using American Sign Language or other visual systems.
Their use of language- related symbols differs from human language in
many ways.
b. The chimpanzees seldom used the symbols in new original
combinations. They lack productivity.
c. The chimpanzees used their symbols almost always to make a request,
only rarely to describe.
d. Chimpanzees show moderate understanding and can answer “What”
and “Who” questions accurately.
2. Bonobos
a. Bonobos (Pan paniscus) given language training used symbols in
several ways that more resemble humans than common chimpanzees.
 They understand more information than they produce.
 They use symbols to name and describe objects even when they are
not requesting them.
 They request items that they do not see.
 They occasionally use the symbols to describe past events.
 They frequently make original, creative requests.
b. The reason for the better language skills in the bonobos is unknown,
but three reasons have been suggested:


Bonobos have more language potential than common chimpanzees.
The bonobos trained so far have been very young, unlike the
chimpanzees in other studies.
 The bonobos trained so far have learned by observation and
imitation rather than formal language training.
4. Nonprimates
a. Alex, an African gray parrot, could say a variety of words in
conjunction with specific objects. Alex's language abilities caused
many to rethink some assumptions about what sort of brain
development is necessary for language.
b. These studies indicate that human language evolved from precursors
present in other species.
C. How Did Humans Evolve Language?
1. Most theories fall into two categories:
a. The first is that we evolved it as a byproduct of overall brain
development.
b. The second is that we evolved it as a specialization.
2. Language: Byproduct of Intelligence, or Specialized Adaptation?
a. People with Normal Intelligence but Impaired Language
i. Presumably because of a dominant gene, 16 (out of 30) people
of normal intelligence within one family have severe language
deficiencies.
ii. Cases such as this suggest that genetic conditions that affect
brain development can impair language without impacting other
aspects of intelligence.
b. People with Mental Retardation but Relatively Spared Language
i. Williams syndrome: A rare disorder in which retarded
individuals have skillful use of language, but limited abilities in
other regards. This disorder is caused by a deletion of several
genes from chromosome 7.
c.
Language as a Specialization
i. An alternate view of the evolution of language is that language
evolved as an extra brain module, called a language acquisition
device. This is a built-in mechanism for acquiring language.
This idea is supported by the fact that children learn language
with amazing ease and that children learn language despite the
fact that they do not hear enough examples to learn the
grammatical structure of language (this is called the poverty of
the stimulus argument).
ii. Researchers have begun to explore this genetic explanation.
Looking at the family with severe language deficiencies,
researchers found a nutation on the genre designated FOXP2,
which has an impact on the development of the jaw and throat
and is essential for speech.
3. A Sensitive Period for Language Learning
a. While testing the hypothesis that there is a sensitive period for language
acquisition early in life, researchers found that adults are better than
children at memorizing the vocabulary of a second language.
However, children have a great advantage on learning the
pronunciation and grammar.
b. Research shows that the younger language acquisition starts, the better.
People who start learning a second language beyond age 12 or so
almost never reach the level of a true native speaker.
c. Those who grow up in a bilingual home show substantial bilateral brain
activity during speech, for both languages. In addition, their temporal
and frontal cortex grow thicker than average.
d. Language has a critical period; if you don’t learn language when you
are young, you will forever be language-disadvantaged.
D. Brain Damage and Language
1. Broca’s Aphasia
a. Aphasia: Severe language impairment.
b. Broca’s area: Small part of the frontal lobe of the left cerebral cortex
that when damaged, leads to language impairments.
c. Broca's aphasia or nonfluent aphasia: A language impairment whose
most prominent symptom is a deficit in language production. Caused
by damage to Broca’s area and surrounding areas.
d. Patients suffering from Broca’s aphasia speak meaningfully, but omit
pronouns, prepositions, conjunctions, and qualifiers from their own
speech; they also have trouble understanding these same kinds of
words.
e. Difficulty in Language Production
i. Broca’s aphasia relates to language, not just vocal muscles.
English speakers with Broca’s aphasia speak most pronouns,
prepositions, conjunctions, auxiliary verbs, quantifiers, and tense
and number endings.
ii. The problem seems to be with word meanings, not just
pronunciation.
f. Problems in Comprehending Grammatical Words and Devices
i. People with Broca’s aphasia have trouble understanding the same
kinds of words that they omit when speaking. They also
misunderstand complex sentences.
ii. However, they generally recognize when something is wrong in a
sentence and have some knowledge of grammar.
g. Broca’s Area One Step at a Time
i. In some studies, physicians expose someone’s brain to explore
options for treating severe epilepsy. In a few cases, researchers
implanted electrodes to record activity in Broca’s area while the
person listened to sentences or processed them in other ways.
ii. The cells that responded first made the same response regardless of
what, if anything, the person was supposed to do with the word.
iii. A second group of cells responded a bit later, and responded more
strongly if the instruction was to change the tense.
iv. A third group, with the latest response, was active in preparation
for saying the word.
v. This research suggests Broca’s area goes through at least three
stages in controlling speech.
2. Wernicke’s Aphasia (Fluent Aphasia)
a. Wernicke's aphasia or fluent aphasia: Damage to Wernicke’s Area,
near the auditory part of the temporal cortex, leads to difficulty in
comprehending the verbal and written communications of others.
Although patients can still speak smoothly, their speech content is often
nonsensical. They also have anomia (difficulty recalling the names of
objects).
b. Typical characteristics of Wernicke’s aphasia are: articular speech,
difficulty finding the right word, and poor language comprehension.
c. People with Wernicke’s aphasia have anomia, difficulty recalling
names of objects.
d. Language requires the activation of many different areas other than the
frontal cortex (Broca’s area and surrounding regions) and the temporal
cortex (Wernicke’s area).
E. Music and Language
1. Music and language have many parallels, suggesting that they may have
arisen together
a. Trained musicians and music students tend to be better than average at
learning a second language.
b. In both language and music, we alter the timing and volume to add
emphasis or to express emotion.
c. English speakers average about .5 to .7 seconds between one stressed
syllable and another in speech, and prefer music with about .5 to .7
seconds between beats.
d. Greek and Balkan languages have less regular rhythms than English,
and much of the music written by speakers of those languages has
irregularly spaced beats.
F. Dyslexia
1. Dyslexia: Inability to read despite adequate vision and intelligence.
Dyslexia is more common in boys than girls and has been linked to at least
four genes that produce deficits in hearing or cognition.
2. As a rule, a dyslexic person is more likely to have a bilaterally symmetrical
cerebral cortex (i.e., the planum temporale and other structures are the same
size on the left and right hemisphere).
3. Different researchers have hypothesized different explanations for dyslexia
including:
a. Dyslexia reflects a subtle hearing impairment.
b.
c.
d.
Dyslexia is caused by a problem detecting the temporal order of
sounds.
Dyslexia is caused by a problem converting vision to sound or vice
versa, as if one part of the brain were poorly connected to another.
Dyslexia is a function of attentional differences.
III. Consciousness and Unconscious Processes and Attention
1. If a cooperative person reports the presence of one stimulus, but not of a
second, they were conscious of the first but not the second.
2. Consciousness is roughly equivalent to attention.
3. Can be driven by features of the stimulus, such as brightness, motion, or size,
or due to “top-down” processes.
4. Inattention blindness: You are conscious of only a few things in your visual
field at a time. If things change slowly or during a blink, you are unlikely to
notice the change.
A. The Mind-Brain Relationship
1. The mind-brain problem: What is the relationship between the mind and the
brain?
2. The most widespread view among nonscientists is dualism, the belief that
mind and body are different kinds of substance that exist independently.
3. The alternative is monism, the belief that the universe consists of only one
kind of substance.
4. Various types of monism are:
a. Materialism: the view that everything that exists is material, or
physical
b. Mentalism: the view that only the mind really exists and that the
physical world could not exist unless some mind were aware of it
c. Identity position: the view that mental processes and certain kinds of
brain processes are the same thing
B. Brain Activity Associated with Consciousness
1. Researchers used fMRI images to record brain activity in a young woman
who was in a persistent vegetative state. When she was told to imagine
playing tennis, the fMRI showed increased activity in motor areas of her
cortex, similar to that of healthy volunteers.
2. One problem in solving the mind-body problem is we cannot observe
consciousness.
3. Researchers use the operational definition: If a cooperative person reports
awareness of one stimulus and not another, then he or she was conscious of
the first and not the second.
4. The next step is to present a given stimulus under two conditions. For
example, in “flash suppression,” you may be unable to see a stationary dot
while other dots are flashing around it.
5. Experiments using Masking
a. Masking: a brief visual stimulus is preceded and followed by longer
interfering stimuli.
b.
Backward Masking: the same method as above but only the later
stimulus is presented.
c. Data on masking studies shows that consciousness of a stimuli depends
on the amount and spread of brain activity.
6. Experiments Using Binocular Rivalry
a. Binocular rivalry: Gradual changes in perception when two different
stimuli are presented to the two eyes
b. Consciousness seems to be all or none; you cannot be partially
conscious of a stimulus.
7. The Fate of an Unattended Stimulus
a. Much of brain activity is unconscious and can influence behavior.
b. Brain attends to some things even if you are not conscious of the
stimulus.
8. Consciousness as a Threshold Phenomenon
a. One study suggests that consciousness is a yes/no phenomenon. When
shown blurry words on a screen, participants almost never said they
were partly conscious of something. They always rated words as 0 or
100 in terms of how conscious they were of it.
9. The Timing of Consciousness
a. Phi phenomenon: If you see a dot in one position alternating with a
similar dot nearby, it will seem that the dot is moving back and forth.
b. Later perceptions alter earlier perceptions.
C. Attention
1. Attention is closely aligned with consciousness.
2. Inattentional blindness or change blindness: If something in a complex
scene changes slowly, you probably will not notice it unless you are paying
attention to the particular item that changes.
3. Brain Areas Controlling Attention
a. Bottom-up process: a reaction to a stimulus
b. Top-down process: intentional. For example, when you look for
someone in a crowd.
c. Stroop effect: the difficulty of ignoring words and saying the color of
ink
4. Unilateral Neglect
d. Spatial neglect: a tendency to ignore the left side of the body and its
surroundings, including visual, auditory, and touch stimuli after
damage to the right hemisphere.
a. If the damage to the right hemisphere is to the inferior part of the
parietal cortex, the person tends to neglect everything to the left of their
own body. People with damage to the superior temporal cortex neglect
the left side of objects, regardless of their location.
b. Spatial neglect can be reduced by doing manipulations to increase
attention to the left side, such as giving instructions to attend to the left
side or having the person look left while at the same time feeling
something with the left hand.
CHAPTER 15
MOOD DISORDERS AND SCHIZOPHRENIA
Chapter Outline
I.
Mood Disorders
A. Major Depressive Disorder
1. Major Depression: According to the DSM-IV, people with major
depression feel sad, helpless, and lacking in energy and pleasure for weeks
at a time. Individuals with major depression also feel worthless, have
trouble sleeping, cannot concentrate, get little pleasure from sex or food,
may contemplate suicide, and in many cases, can hardly imagine being
happy.
2. Studies show that people with major depression reacted normally to sad or
frightening depictions, but seldom smiled at comedies or pleasant pictures.
In similar studies, people with depression show a decreased response to a
likely reward.
3. Approximately 5% of adults in the U.S. have a “clinically significant”
depression.
4. Childhood depression is equally common for boys and girls, but beyond age
14, depression is more common in females.
5. Although some people suffer from long-term depression, it is more common
to have episodes of depression separated by periods of normal mood.
Generally, the first episode is longer than subsequent episodes. The more
one experiences an episode, the easier it is to start another one.
6. Genetics
a. Evidence of genetic or other biological predispositions to depression
exist.
b. People with early-onset depression (before age 30) have a high
probability of other relatives with depression, anxiety disorders,
ADHD, alcohol or marijuana abuse, obsessive compulsive disorder,
bulimia, migraine headaches, and irritable bowel syndrome.
c. People with late onset depression (especially after 45 to 50) have a high
probability of relatives with circulatory problems.
7. Other Biological Influences
a. A few cases of depression are linked to viral infections, like Borna
disease, which affects farm animals. One third of those with severe
depression or bipolar disorder have Borna, which suggests it
predisposes people to those illnesses.
b. About 20 percent of women experience postpartum depression
(depression after giving birth) and most recover quickly.
8. Abnormalities in Hemisphere Dominance
a.
Most people suffering from depression have decreased activity in the
left hemisphere and increased activity in the right prefrontal cortex.
B. Antidepressant Drugs
1. Drugs used for the treatment of depression and other mood disorders.
2. Types of Antidepressants
a. Tricyclics: Prevent the presynaptic neuron from reabsorbing
catecholamines or serotonin after releasing them (this allows the
neurotransmitter to remain longer in the synaptic cleft thus stimulating
postsynaptic receptors).
b. Selective serotonin reuptake inhibitors (SSRIs): These drugs are
similar to tricyclics, but are specific to the neurotransmitter serotonin.
The most popular drug in this class is fluoxetine (Prozac).
c. Serotonin norepinephrine reuptake inhibitors (SNRIs): Block the
reuptake of serotonin and norepinephrine.
d. Monoamine oxidase inhibitors (MAOIs): Block the enzyme
monoamine oxidase (MAO) from metabolizing catecholamines and
serotonin into inactive forms.
e. Atypical antidepressants: A miscellaneous group of drugs with
antidepressant actions and mild side effects, including bupropion
(Wellbutrin), which inhibits reuptake of dopamine and to some extent
norepinephrine.
3. How Do Antidepressants Work?
a. People with depression have approximately normal levels of release of
neurotransmitters. Some studies show that people with depression have
an increase in serotonin release.
b. Although some patients respond to one drug and not another, we have
no clear evidence that any antidepressant drug produces any different
effects from any other.
c. Antidepressant drugs produce their effects on neurotransmitters in the
synapses within minutes to hours but it takes weeks before patients
experience mood elevation.
4. How Effective Are Antidepressants?
a. Depression occurs in episodes so even those with untreated depression
recover within a few months.
b. The best comparisons of the benefits of drugs are comparisons between
those who are treated with medication and those who are administered
a placebo. Placebo results often overlap with drug group results. One
study suggests that for people with mild to moderate depression, there
is no clear benefit of a drug over a placebo. Furthermore, even for those
with severe depression, antidepressants don’t always work.
c. Another type of treatment is psychotherapy. While drugs work better
for dysthymia, therapy works better for those who suffered abuse or
neglect during early childhood. For such cases, antidepressants are
usually ineffectual. Psychotherapy is also more likely to have long
term benefits, reducing the likelihood of relapse.
d.
e.
On average, people receiving both treatments improve more than those
receiving one treatment alone.
Electroconvulsive Therapy (ECT)
i. Electroconvulsive therapy (ECT): Inducing seizures with an
electric shock to the head. ECT is usually applied every other day
for about two weeks.
ii. Invented by Ladislas Meduna in the 1930’s for schizophrenia, the
treatment was mostly ineffectual on schizophrenia and became
overused in the 1950’s on patients without their consent.
iii. One common side effect was memory loss for the few months
following the shock.
iv. About half of those who respond well to ECT relapse into
depression within six months unless they are given antidepressant
drugs or other therapies to prevent it. TMS has similar effects on
depression symptoms.
f. Altered Sleep Patterns
i. Most depressed people have sleep problems, which precede mood
changes.
ii. Most depressed people enter REM sleep within 45 minutes after
going to bed compared to about 80 minutes for non-depressed
people and they have more than the usual number of eye
movements during REM sleep. This pattern resembles someone
who has traveled west for a few time zones.
iii. One way to treat depression is to have the depressed person stay
awake all night. Another method is to alternate the sleep schedule.
5. Other Therapies
a. Regular, non-strenuous exercise increases blood flow to the brain and
provides other benefits that are especially helpful to people with
depression.
C. Bipolar Disorder
1. Depression can be unipolar or bipolar. People with unipolar disorder vary
between depression and normality. People with bipolar disorder (formerly
known as manic-depression disorder) alternate between episodes of
depression and mania (characterized by restless activity, excitement,
laughter, self-confidence, rambling speech, and loss of inhibitions).
2. Bipolar I disorder: A type of bipolar disorder where the person has fullblown episodes of mania.
3. Bipolar II disorder: A type of bipolar disorder where the person has much
milder manic phases, called hypomania.
4. Genetics
a. There is a strong hereditary basis for bipolar disorder, as shown by twin
studies. Two genes appear to increase the probability of bipolar II
5.
disorder. They have also demonstrated that some of the same genes
that predispose major depression also predispose bipolar disorder.
Treatments
a. Lithium salts are the most effective therapy for bipolar disorder, but
how it works remains unknown. Other drug treatments include
anticonvulsant drugs such as valproate and carbamazepine.
Encouraging bipolar patients to keep a consistent sleep schedule may
reduce the intensity of the mood swings.
D. Seasonal Affective Disorder
1. Seasonal affective disorder (SAD): Depression that reoccurs seasonally,
usually in the winter.
2. SAD is most common in regions closest to the poles, where the nights are
very long in winter and very short in summer.
3. It is possible to treat SAD by exposing the person to very bright lights for
about an hour either early in the morning or in the evening.
II. Schizophrenia
A. Diagnosis
B. Schizophrenia was originally called dementia praecox. Eugen Bleuler came up
with the term schizophrenia in 1911, which has been preferred ever since.
C. Schizophrenia: A disorder characterized both by deteriorating ability to
function in everyday life and by some combination of the following:
1. Delusions: Unjustifiable beliefs, such as “beings from outer space are
controlling my actions”
2. Hallucinations: False sensory experiences, such as hearing voices when
alone
3. Disorganized speech: rambling or incoherent
4. Grossly disorganized behavior
5. Weak or absent signs of emotion, speech, and socialization
D. Positive symptoms: Behaviors that are present that should be absent. Positive
symptoms fall into two clusters that do not correlate strongly with each other:
E. Negative symptoms: Behaviors that are absent that should be present, such as
deficits of social interaction and emotional expression.
F. Cognitive symptoms: Limitations of thought and reasoning that are common in
schizophrenia.
G. The main problem is disordered thinking, which results from abnormal
interactions between the cortex and the thalamus and cerebellum. This may lead
to the hallucinations, delusions, and other symptoms.
1. Demographic Data
a. Schizophrenia occurs in all ethnic groups and is slightly more common
in men than in women; however, it usually develops at an earlier age in
men and is more severe. About 1% of people suffer from schizophrenia
at any given time.
b.
c.
Schizophrenia is 10 to 100 times more common in the United States
and Europe, as compared to many third world countries. The cause of
this discrepancy is unknown.
The older the age of the father at time of the baby’s birth, the greater
the risk of schizophrenia.
H. Genetics
1. Twin Studies
a. For monozygotic schizophrenic twins, there is about a 50%
concordance (agreement), and a 15% concordance for dizygotic twins.
b.
The greater concordance in monozygotic twins does not necessarily
mean a genetic cause, as a pure genetic effect would have a 100%
concordance. The greater environmental similarity in monozygotic
twins, as compared to dizyogotic twins, may also influence
concordance rates.
c. Dizygotic twins have the same genetic resemblance as siblings but
greater environmental similarity, including prenatal environment.
2. Adopted Children Who Develop Schizophrenia
a. One study found that 12.5% of the immediate biological relatives and
none of the adopting relatives had schizophrenia.
b. These results suggest a genetic basis for schizophrenia. There is also
the possibility of a prenatal influence. For example, many women with
schizophrenia drink and smoke during pregnancy.
3. Efforts to Locate a Gene
a. One gene has consistently been linked with schizophrenia. A dozen
genes appear to be more common in people with schizophrenia.
b. DISC1 (disrupted in schizophrenia 1) gene controls the production of
dendritic spines and the generation of new neurons in the hippocampus.
c. Other genes linked to schizophrenia are important for brain
development, transmission of glutamate synapses, and connections
between the hippocampus and the prefrontal cortex.
d. Schizophrenia may result from a combination of genetic and
environmental factors.
C. The neurodevelopmental hypothesis: Schizophrenia is caused in large part by
abnormalities to the nervous system during the prenatal or neonatal periods.
1. Prenatal and Neonatal Environment
a. Several factors could have affected the infant’s brain development,
including poor nutrition of the mother during pregnancy, premature
birth, low birth weight, and complications during delivery.
b. If a mother is Rh-negative and her baby is Rh-positive, the baby’s Rhpositive blood may trigger an immunological rejection by the mother.
The result is hearing deficits, mental retardation, and twice the usual
probability of schizophrenia.
c. Season-of-birth effect: the tendency for people born in winter to have
a slightly greater possibility of developing schizophrenia. Some reason
this may occurs is nutrition during winter, viral infections, fever, and
influenza.
d. Childhood infections, like toxoplasma gondii, also infect humans and
leads to memory disorders, hallucinations, and delusions. Because this
bacteria only reproduces in cats, people with schizophrenia are more
likely than other people to have a pet cat in childhood.
2. Mild Brain Abnormalities
a. On average, people with schizophrenia have less than average gray
matter and white matter, and larger than average ventricles—the fluidfilled spaces within the brain.
b. The strongest deficits are in the left temporal and frontal areas of the
cortex. The thalamus is also smaller than normal for people with
schizophrenia.
c. The areas with consistent signs of abnormality include some that
mature slowly such as the dorsolateral prefrontal cortex. Most people
with schizophrenia show deficits in memory and attention because of
these deficiencies.
d. Lateralization also differs, with the left hemisphere slightly larger than
the right.
e. The areas of the brain that most consistently show signs of abnormality
in schizophrenics are the ones that mature the most slowly, such as the
prefrontal cortex.
f. At a microscopic level, people with schizophrenia have smaller than
normal cell bodies, especially in the frontal cortex and hippocampus.
g. Research has not yet determined whether these brain damages will
worsen with time.
3. Early Development and Later Psychopathology
a. It is currently thought that the early brain damage is done in areas that
are slow to mature, such as the prefrontal cortex. For this reason, the
damage produces only minor symptoms in childhood, but increasing
impairments when the brain area fully matures.
b. Those later developed with schizophrenia often have other problems in
childhood, like deficits in attention, memory, and impulse control.
D. Treatments
1. Antipsychotic Drugs and Dopamine
a. Chlorpromazine (Thorazine): First drug used successfully for the
treatment of schizophrenia.
b. Antipsychotic drugs (neuroleptic drugs): Drugs used for the
treatment of schizophrenia. These drugs work primarily by blocking
dopamine receptors.
 Phenothiazines: A class of neuroleptic drugs that includes
chlorpromazine.
 Butyrophenones: A class of neuroleptic drugs that includes
haloperidol (Haldol).
c. Dopamine hypothesis of schizophrenia: According to this hypothesis,
schizophrenia results from excess activity at certain dopamine
d.
e.
f.
2.
3.
synapses. The primary evidence for this hypothesis is the type of drugs
that relieve and aggravate the symptoms of schizophrenia.
Substance-induced psychotic disorder: Disorder characterized by
hallucinations and delusions caused by drugs such as cocaine,
amphetamine, and LSD, which increase the activity of dopamine
synapses.
Schizophrenic people have about twice as many D2 receptors occupied
by dopamine as normal people.
Excess activity of dopamine cannot be the sole cause of schizophrenia.
Drugs that block dopamine receptors do so almost immediately, but
their effects on behavior build up gradually over 2 or 3 weeks.
Role of Glutamate
a. Glutamate hypothesis of schizophrenia: Idea that schizophrenia
results from deficient activity at certain glutamate synapses. Because
dopamine inhibits glutamate activity in many parts of the brain, much
of the evidence supporting the dopamine hypothesis of schizophrenia
also supports the glutamate hypothesis of schizophrenia.
b. Researchers have found that the brains of schizophrenic people release
lower than normal amounts of glutamate in the prefrontal cortex and
hippocampus. Schizophrenics also have fewer glutamate receptors.
c. Phencyclidine (PCP): A drug that blocks NMDA glutamate receptors.
PCP administration produces a type of psychosis more similar to
schizophrenia than drugs like cocaine, as PCP induces both negative
and positive symptoms. Moreover, PCP does not produce psychosis in
preadolescents and PCP produces a much more severe psychosis in
people with a history of schizophrenia.
d. Because increasing glutamate activity in the brain would be extremely
risky, there are no drugs used to treat schizophrenia that directly
stimulate glutamate activity. However, there are some experimental
compounds that may someday be used to treat schizophrenia, such as
the amino acid glycine, which enhances the effects of glutamate at
NMDA synapses. Glycine is not an effective antipsychotic by itself but
it increases the effects of other antipsychotic drugs.
New Drugs
a. Mesolimbocortical system: A set of neurons which project from the
midbrain tegmentum to the limbic system. The mesolimbocortical
system is believed to be the area in which antipsychotics have their
beneficial effects.
b. Tardive dyskinesia: A serious side effect of antipsychotics; this
disorder is characterized by tremors and other involuntary movements.
Tardive dyskinesia is caused by the prolonged blockade of dopamine
receptors in the basal ganglia.
c.
d.
Second generation (atypical) antipsychotics: New drugs (e.g.,
clozapine) that alleviate the symptoms of schizophrenia while seldom,
if ever, producing movement problems. These drugs have less intense
effects on dopamine type D2 receptors, but stronger effects at D4 and
serotonin 5-HT2 receptors.
Atypical antipsychotics are more effective than typical antipsychotics
at relieving the positive symptoms and, to some extent, the negative
symptoms of schizophrenia, but they do not improve overall quality of
life more than the typical antipsychotic drugs.
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