Shackman Psyc210 Module20 SemesterRecapAndFinalExamReview

When a scientist doesnt know the answer to a
problem, he is ignorant. When he has a hunch as

to what the result is, he is uncertain. And when
he is pretty damn sure of what the result is
going to be, he is still in some doubtScientific
knowledge is a body of statements of varying
degrees of certaintysome most unsure, some
nearly sure, but none absolutely certain.
Richard Feynman (1955), Nobel Laureate
PSYC 210: Temperament and

Personality
Developmental Origins,
Biological Bases,
and Implications for Psychopathology
Dr. Alex Shackman
University of Maryland
Spring 2015
Semester Recap
AJ Shackman
08 December 2014
Where Did We Begin Our

Adventure?

Adventure?
For most of us, we started from a place of
ignorance, informed by some combination of
Prior training and course work in psychology and
biology (e.g., hazy recollections from Intro to Psyc)
Attitudes and ideasabout traits, personality,
temperament, heritability, mental illness, and the
brain that we passively absorb from our culture,
from friends and family, and from the media. Folk
psychology, in other words

Adventure?

Adventure?
Use Science to Dispel Ignorance

Leverage recent scientific research in humans and other species in order to
Understand the core dimensions of T&P
Become experts on how T&P influence our daily lives and some of the mechanisms
that link T&P to important outcomes (e.g., temptation and self-control, academic
attainment, divorce, dieting, depression, drug and alcohol abuse, and death)
Develop a working knowledge of the psychological and neurobiological
mechanisms that underlie T&P
Understand the strengths and limitations of a broad spectrum of biological,
behavioral, and statistical tools
Broaden the way you think about connections between the mind, brain, genes, and
behavior
Become a more critical consumer of psychological and neurobiological research
Become a more thoughtful and informed patient, tax payer, voter, and citizen

Leverage recent scientific research in humans and other species in order
to
Know how T&P influence our daily lives and some of the mechanisms that link T&P
to important outcomes (e.g., temptation and self-control, academic attainment,
divorce, dieting, depression, drug and alcohol abuse, and death)
Broaden the way you think about connections between the mind, brain, genes,
and behavior

to
and behavior

to
and behavior

to
and behavior

to
and behavior

to
and behavior
What did we actually learn?

A ton!
What did we actually learn?

A ton!
Models
Models
BIS/BAS (Gray)
Behavioral Inhibition (Kagan/Fox)
Big 3 (Caspi)
Big 5 (OCEAN; Costa & McCrae)
Scientific Concepts
Scientific Concepts
Affective chronometry (e.g., time-to-peak, recovery, etc.)
Appetitive motivation
Approach/Withdrawal
Biomarkers, Endophenotypes & Intermediate Phenotypes
Epigenetics and Non-genomic transmission of acquired traits
Fear vs. Anxiety
Garbage In/Garbage Out
G * E interactions
Hedonic hotspots
Heritability (common misconceptions)
Incentive sensitization model
Liking vs. Wanting
Natural language hypothesis
Pavlovian fear conditioning (and the conditioned emotional response/CER)
Scientific skepticism
Self-stimulation
Sensitivity, Specificity, and Reliability
Serotonin transporter (5-HTT) polymorphism
Statistical Tools and Concepts
Statistical Tools and Concepts

Correlation (vs. causation)
Construct validity
Factor analysis
Meta-analysis
Reliability (Internal-consistency, TestRetest)
Brain Regions and Systems
Brain Regions and Systems

Basal forebrain cholinergic system
Extended amygdala (including the BNST)
Lateral prefrontal cortex (PFC)
Midcingulate cortex (MCC)
Orbitofrontal cortex (OFC)
HPA axis
Medial forebrain bundle
Mesocorticolimbic dopamine system
Ventral striatum/Nucleus accumbens
Methods and Measures
Methods and Measures

ASL MRI
BART
Cortisol
Daily diary
Deep brain stimulation (DBS)
EDA/SCR/GSR
ERP (including N2, ERN, FRN, and P3b)
Eriksen flanker task
Excitotoxic lesions
Experience sampling
FDG-PET
Fear-potentiated startle
fMRI (task-related and resting-state)
Frontal EEG asymmetry
GWAS
Limitations of introspective measures and self-report (e.g., peak-end rule)
NeuroSynth
Pharmacological methods (e.g., benzodiazepines)
Stop-signal task
Disorders
Disorders
Anxiety
Depression
Impulse control disorders
Substance abuse
Parkinsons
People
Famous and Not-So-Famous Patients
Famous and Not-So-Famous Scientists

Ralph Adolphs; Yair Bar-Haim; David Barlow; Kent Berridge; Jenni
Blackford; Jack Block; Ryan Bogdan; Turhan Canli; Avshalom
Caspi; Michelle Craske; Tony and Hannah Damasio; Richie
Davidson; Mike Davis; Hans and Mike Eysenck; Nathan Fox;
Jeffrey Gray; Christian Grillon; Dan Grupe; Amad Hariri; Jerry
Kagan; Ken Kendler; Carl Lejuez; Joe Ledoux; Schmuel Lissek;
Jerry Kagan; Ned Kalin; Ken Kendler; Roman Kotov; Seymour
Gig Levine; Colin Macleod; Michael Meaney; Walt Mischel; Temi
Moffitt; Jack Nitschke; Danny Pine; Diego Pizzagalli; Tony Rangel
and Todd Hare; Terry Robinson; Kerry Ressler; Alex Shackman;
Andy Tomarken; Mike Treadway; Peter Visscher; David Walker;
David Watson; Paul Whalen; Tal Yarkoni; David Zald and many
others
People
Famous and Not-So-Famous Patients
B-19, EVR/Eliot, SM, and Phineas Gage
Famous and Not-So-Famous Scientists
Ralph Adolphs; Yair Bar-Haim; David Barlow; Kent Berridge; Jenni
Blackford; Jack Block; Ryan Bogdan; Turhan Canli; Avshalom
Caspi; Michelle Craske; Tony and Hannah Damasio; Richie
Davidson; Mike Davis; Hans and Mike Eysenck; Nathan Fox;
Jeffrey Gray; Christian Grillon; Dan Grupe; Amad Hariri; Jerry
Kagan; Ken Kendler; Carl Lejuez; Joe Ledoux; Schmuel Lissek;
Jerry Kagan; Ned Kalin; Ken Kendler; Roman Kotov; Seymour
Gig Levine; Colin Macleod; Michael Meaney; Walt Mischel; Temi
Moffitt; Jack Nitschke; Danny Pine; Diego Pizzagalli; Tony Rangel
and Todd Hare; Terry Robinson; Kerry Ressler; Alex Shackman;
Andy Tomarken; Mike Treadway; Peter Visscher; David Walker;
David Watson; Paul Whalen; Tal Yarkoni; David Zald and many
others
New Answers to
Fundamental Qs
New Answers to
Fundamental Qs
New Answers to
Fundamental Qs
What is temperament?
What is personality?
Are temperament and personality

fundamentally different?
Is T&P emotional, cognitive, or a blend of both?
Are dimensions of T&P comprised of more
basic psychological or neural ingredients?
New Answers to
Fundamental Qs
How many dimensions or types of

personality are there?
Where did these dimensions come from;

how were they discovered?
New Answers to
Fundamental Qs
What exactly does it mean to be neurotic?

What makes Woody Allen tick?
What is self-control? Where does it come
from? What are the implications of my niece
grabbing that marshmallow?
Is reward one thing? What motivates us to
seek out pleasure and reward?
New Answers to
Fundamental Qs
Is The Situation the primary determinant of

thoughts, feelings, and actions?
Is T&P predictive of meaningful outcomes? Is
it impactful or can we safely ignore
individual differencestreat them as noise
or error in our equations?
New Answers to
Fundamental Qs
How stable are trait-like individual

differences in T&P across the life span?
How well can I predict your personality at
age 70, knowing what you're like when you
are 2 or 3 years old?
My son or daughter is extremely shy and
reticent Should I hit the panic button? Is
s/he destined to develop a debilitating
emotional disorder?
New Answers to
Fundamental Qs
How are traits related to emotional states?
How does T&P interact with cues, challenges, and

perturbations in the environment?
Do people tend to exert control over those challenges
and the feelings they evoke or are they passive
recipients?
Does T&P go away in the absence of challenges or is it
discernible all the time? (Is our brain ever really at rest?)
Does T&P lead individuals to construct different
environments for themselves?
New Answers to
Fundamental Qs
Does T&P reflect nature, nurture, or both?

Does T&P breed true? Does it reflect a few
genes or many?
Are heritable traits fixed and immutable or
plastic? How informative is heritability is
one group ALWAYS going to come out on top?
If T&P is somewhat malleable, should we
intervene in the case of high-risk T&P?
New Answers to
Fundamental Qs
Is depression just being really sad?
Is addiction just an excess of approaching highs and

avoiding lows?
Why do we so often succumb to temptation and
immediate gratification? What mechanisms are
involved?
Do drugs of abuse exert lasting consequences on
reward circuitry?
Is dopamine a natural joy juice?
Some Broad Take Home

Points
T&P Are Important,

But Incompletely Understood
Individual differences in temperament, which first
emerge early in life, can exert a profound impact on
disease and wellbeing, socioeconomic status, and
academic and occupational attainment
One important way in which temperament influences

these diverse outcomes is by conferring risk for the
development of psychopathology.
The challenge is to understand the psychological and
biological mechanisms that link dispositional risk to
positive and negative outcomes.
T&P Are Important,


development of psychopathology
biological mechanisms that link stable differences in risk
and resilience to important positive and negative
outcomes in the real world
T&P Are Important,


development of psychopathology
biological mechanisms that link trait-like differences in
risk and resilience to important positive and negative
outcomes in the real world
I am really proud of you guys and all that you

have accomplished and learned this semester
Be Proud of Your New Knowledge and New Ways

of Thinking,
But Not Too Proud
https://www.youtube.com/watch?v=zM
xatjSLngc
(546 to 7:37)
Take Home Question

(Just 1)
Take Home Question

(Just 1)
Complete the course evaluation
https://www.courseevalum.umd.edu/
The numeric/quantitative portion ofthe evaluation directly
impacts me, in terms of promotion and retention (tenure)
The narrative/free-response portion directly impacts students
enrolled in future classes. I take your feedback and suggestions
very seriously and use it to revise the class.
In CANVAS, submit a brief statement to the effect that
I, <Your Name> , pledge on my honor that I have truthfully
completed the Course Evaluation for Psychology 612
Take Home Question

(Just 1)
Take Home Question

(Just 1)
Take Home Question

(Just 1)
The End.
Good luck with your
end of term responsibilities
and the final examination
and
Have a great summer!
Exam Review
Based on fear conditioning studies in the

psychophysiology lab, we can say that
children and adults with extreme anxiety
tend to show
A. Amplified signs of anxiety

(startle) in response to
certain threat (CS+)
B. Exaggerated anxiety to
uncertain, ambiguous,
unpredictable dangers
(CS- , ITI; evidence of
over-generalization or
deficient safety learning)
C. Anxiety-related responses
which are strictly limited
to immediate danger
Real-time fMRI neurofeedback

studies demonstrate that
A. Subjects report that in order to
increase activation, they were
imagining engaging in different
kinds of high arousal, negative
activities
B. Subjects can learn to regulate
activation in the VS/NAcc,
providing important mechanistic
insights into the neural circuitry
underlying reward
C. Subjects who experienced the
most intense positive affect
showed the smallest increases in
VS/NAcc activation
D. A and B
E. B and C
Family, twin, and adoption studies (aka

behavioral genetics) teach us that:
A. Psychiatric disorders and
T&P are not heritable
B. Psychiatric disorders and
T&P aggregate in families
C. Things that blood
relatives share (e.g., SES,
toxin exposure, stress,
habits) are irrelevant to
understanding
psychopathology or T&P
D. A and C
E. B and C
Many or most individuals with diagnosable

major depression or an anxiety disorder
A. Fail to receive
high-quality,
evidence-based
treatment
(under-treated)
B. Receive highquality
pharmacological
or cognitivebehavioral
T&P reflect trait-like individual differences in

emotional and cognitive (and neural) biases that:
A. First emerge in mid-life

B. Are fixed at a relatively
young age
C. Account for consistency
and biases in behavior,
inner experience, and
risk across time and
contexts
D. A and B
E. B and C
Mechanistic studies in animal models

tell us absolutely nothing about
A. Mechanism/Causat
ion, as this can
only be achieved
in studies of
human patients
with circumscribed
brain damage
B. Subjective
experience and
feelings
Are there pleasure centers in the

brain?
A. Yes! Hedonic
hotspots; opioid
and
endocannabinoi
d signaling
B. No!
C. Yes! Medial
forebrain bundle
D. Yes! Dopamine
Orbitofrontal cortex
A. Signals value, such as
tastiness
B. Signals value, such as
healthiness
C. Appears to be
regulated by lateral
prefrontal cortex (i.e.,
attend to health,
downweight taste)
D. All of the above
Individuals who show increased

activation in the ventral
striatum/nucleus accumbens
(VS/NAcc) when looking at yummy
foods in the scanner, tend to
A. Experience more
intense food desires in
daily life and are more
likely to give in to their
temptations to eat
B. b. Experience less
intense food desires in
daily life and are less
likely to give in to their
temptations to eat
fMRI signals in the ventral striatum are

A. Highly specific to
particular kinds of
rewards
B. Nonspecific
C. Predictive of rewardmotivated behavior in
real life (sex, food
consumption)
D. A and C
E. B and C
Substance abuse disorders are associated

with
A. High N/NE
B. Low C/SC
C. Both
Which is the more correct

statement?
A. Nearly every aspect of
human behavior is
somewhat heritable and
reflects the activity of the
brain, suggesting that all
behaviors are biological
B. Very few aspects of
human behavior are
heritable; heritable
behaviors are especially
biological; biologically
mediated behaviors are
special
Which is FALSE: Height is

A. Among the most heritable
mammalian traits, although
offspring show considerable
variation (probabilistic, not
deterministic)
B. A trait-like phenotype that is
associated with variation in a
small number of genetic
polymorphisms
C. Cannot be markedly affected by
interventions (diet, nutrition, and
healthcare access), underscoring
that public policy and other kinds
of interventions can have a huge
impact on highly heritable traits
D. A and B
E. B and C
Substance abuse disorders reflect

A. Incentive sensitization
(permanent changes) in the
mesolimbic dopamine system
that creates Motivational
Magnets
B. Problems bringing regulatory
circuits centered on the lateral
prefrontal cortex on-line
(inhibitory failure); activity in
this braking system predicts
real life impulse control
problems (e.g., giving in to food
temptations)
C. Both
Which statement is MORE scientifically TRUE, based

on the latest evidence (through 2015) discussed in
class?
A. Today few neuroscientistsassertthat
dopamine causes pleasureFor example
Wisewas recently quoted [as saying],
I no longer believe that the amount of
pleasure felt is proportional to the
amount of dopamine floating around in
the brain, and pleasure is not a
necessary correlate of dopamine
elevations
B. Today most neuroscientistsassertthat
dopamine causes pleasureFor example
Wisewas recently quoted [as saying],
the dopamine junctions represent a
synaptic way station . . . where sensory
inputs are translated into the hedonic
messages we experience as pleasure,
euphoria or yumminess
Amygdala damage/lesions is
associated with
A. a. Attenuated (but not
abolished) signs of fear/anxiety
in the presence of learned
threats (CS+) and unlearned
threats (snakes, spiders),
suggesting a causal role in N/NE
B. b. A profound increase in
fear/anxiety elicited by
naturalistic threat (haunted
houses, armed muggers, scary
film clips), suggesting a causal
role in N/NE
C. c. Elevated levels of selfreported N/NE and trait anxiety
D. d. All of the above
E. e. None of the above
Some Parkinsons patients on the

dopamine augmenting agent Pramipexol
A. Display impulse control
disorders (e.g.,
hypersexuality, compulsive
shopping)
B. This appears to reflect
problems turning dopamine
off in the ventral striatum
C. Both, suggesting that the
mesolimbic dopamine
system can play a causal
role in impulse disorders
such as substance abuse
Recent meta-analyses demonstrate that
A. A variety of anxiety disorders,

much like N/NE, are
associated with heightened
amygdala activation to
potential threat
B. Depression, much like N/NE, is
associated with increased
amygdala reactivity to
aversive cues
C. Both A and B, providing
evidence for a common or
overlapping biological
substrate
D. Neither A nor B, suggesting
dissociable substrates
Which is more TRUE: Addiction

involves
A. The
development of
long-lasting
changes in the
brain
B. Fleeting
processes that
rapidly subside
after a transient
period of acute
Deep brain stimulation (DBS) provides

important mechanistic (causal) clues about
the neurobiology of E/PE. In particular, DBS
of the human ventral striatum (VS) / nucleus
accumbens
A. a. Attenuates the VS
response during reward
anticipation
B. b. Ameliorates depression
and increases behavioral
engagement, suggesting a
causal role in behavioral
approach and reward
responsiveness
C. c. Increases resting
metabolic activity in the VS
D. d. A & B
E. e. B & C
Are there pleasure centers in the brain
A. Yes
B. No
Which is more TRUE: Reward, addiction,

fear, anxiety and other key emotional
features of T&P emerge from
A. The activity of
isolated brain
regions
B. The coordinated
activity of
widely
distributed brain
circuits
Is the neurotransmitter dopamine the

source of pleasure and reward?
A. Yes
B. No
Which is FALSE: The

amygdala:
A. Helps to orchestrate states of
fear and anxiety via
connections to brainstem and
subcortical regions
B. Is a fear hotspot in the brain
and is uniquely and
specifically associated with
fear
C. Shows enhanced activation in
response to drug-related cues
in addicts, consistent with the
idea that it helps to prioritize
the processing of emotionally
and motivationally salient
cues in the environment
In rodents, increasing dopamine transmission or

signaling in a circuit centered on the nucleus
accumbens
A. Increases liking
(oro-facial
expressions of
pleasure)
B. Increases
wanting (e.g.,
bar pressing)
C. Both A and B
Is Reward
A. One thing
B. A set of processes
that normally
work together to
support adaptive
behavior (e.g.,
foraging for food)
Self-control in the face of temptation

reflects interactions between
A. A wanting/approach/go circuit
centered on the amygdala
B. Inhibitory/stop circuitry
encompassing the right
posterior parietal cortex
C. Regions of the orbitofrontal
cortex (OFC) that are sensitive
to overall value and preferences
and that integrate information
about long-term health and
short-term reward
D. Regions of the lateral prefrontal
cortex that help to represent
impulsive preferences (yummy!)
E. All of the above
Is the neurotransmitter dopamine the

source of pleasure and reward?
A. Yes
B. No
Is Reward
A. One thing
B. A set of processes
that normally
work together to
support adaptive
behavior (e.g.,
foraging for food)
Deep brain stimulation of the ventral

striatum / nucleus accumbens
A. Ameliorates depression
B. Increases metabolic
activity in the VS
C. Potentiates the VS
response during reward
anticipation
D. All of the above, suggesting
a causal role for this
system in the wanting
component of E/PE/BAS as
well as depression
Which is more true of liking and

wanting?
A. They represent
the same
underlying
construct
B. They are
difficult to tease
apart with selfreport and
behavioral
(reaction time)
In humans, pharmacological
manipulations that increase dopamine
transmission in the ventral striatum
A. Increase
willingness to
work for reward
B. Decrease
willingness to
work for reward
Depression is associated with blunted activation in the

ventral striatum/nucleus accumbens. Manipulations
(ketamine, deep brain stimulation) that increase
VS/Nacc activation ameliorate depression. Collectively,
these observations are consistent with the idea that
A. Major depression
reflects sensitization
of the psychological
function of this
circuit (e.g. wanting)
B. Blunted VS/NAcc
activation in the
face of reward is a
proximal cause of
depression
In humans, nucleus accumbens / ventral

striatum activation is
A. Is trait-like
B. Associated with
N/NE
C. Both
D. Neither
Sensory pleasure appears to reflect the

action of
A. So called hedonic hotspots in
the medial shell of the nucleus
accumbens and other brain
regions; stimulation increases
liking facial expressions
B. Hedonic hotspots that rely on
dopamine
C. Hedonic hotspots that rely on
opioids (opium) and
endocannabinoids (marijuana)
D. A and B
E. A and C
Which is FALSE? Reduced reward

responsiveness
A. Shows good test-retest
stability; is trait-like
B. Is a candidate
endophenotype for
depression
C. Is not heritable
D. Prospectively predicts
symptoms & treatment
response
E. Avoids the limitations of
self-report (mnemonic
distortions, biases, lying)
Increasing dopamine levels in the circuit

centered on the nucleus accumbens
A. Increases liking
(facial
expressions)
B. Increases
wanting (e.g.,
bar pressing)
C. Both
Michael Meaneys group has provided

evidence that the impact of experimenter
handling on rodent temperament (N/NE
or stress reactivity) is
A. Reflects decreased expression

of benzodiazepine receptors in
the amygdala
B. Proximally mediated by a
maternal behavior,
underscoring the importance
of early nurture for adult T&P
and highlighting the fact that
parents can regulate the
development of their
offsprings brains
C. Mediated by genes that
increase maternal LG-ABN and
decrease offspring reactivity
(i.e., a common genetic cause)
Dopamine is
A. Necessary for
experiencing
sensory pleasure
B. Sufficient for
experiencing
sensory pleasure
C. Neither
Which is TRUE: Behavioral Activation

therapy for depression:
A. Focus on cognitive and
emotional change; attempt to
directly regulate thoughts and
feelings
B. Is an evidence-based treatment
for depression with a large
effect size
C. Provides mechanistic evidence
that high levels of behavioral
activation and increased
engagement with reward serve
to maintain pathological
depression
D. A and B
E. B and C
Blockade or disruption of the mesolimbic

dopamine system
A. Disrupts liking
(facial
expressions)
B. Disrupts wanting
(e.g., bar
pressing)
C. Both
Increasing dopamine levels in the circuit

centered on the nucleus accumbens
A. Increases liking
(facial
expressions)
B. Increases
wanting (e.g.,
bar pressing)
C. Both
Dopamine is
A. Necessary for
experiencing
sensory pleasure
B. Sufficient for
experiencing
sensory pleasure
C. Neither
Rats, chimps, and humans

A. Show similar emotional
facial expressions in
response to liked and
disliked food and drink
B. These oro-facial
expressions provide a
direct behavioral readout of liking
C. Both
The mesolimbic dopamine system

A. Is activated by natural
rewards and all major
drugs of abuse
B. When blocked
(pharmacologically,
lesions, genetic
engineering), radically
amplifies rewardmotivated behavior
(e.g., bar pressing for
cocaine)
Attentional biases to
threat:
A. Attentional bias modification
is not clinically effective,
according to the metaanalyses reviewed in class
B. Retraining the attentional
bias produces a lasting
diminution in anxiety in the
lab (e.g. in a public speaking
task), suggesting that it is
an "active ingredient" in the
development of extreme
anxiety.
C. Both A and B
D. Neither A nor B
Which is true of depressed

individuals?
A. They express blunted
liking of rewards and
positive stimuli in the
lab
B. They under-invest in
meh (low-reward)
activities in daily life
C. They are more willing
to work for reward
D. A and B
E. B and C
The mesolimbic dopamine system

A. Underlies hedonic
pleasure and
consummatory
reward
B. Supports wanting
and appetitive
behaviors aimed
at getting rewards
Activation of the medial forebrain bundle
A. Supports robust,
frequent selfstimulation in
rodents and
humans
B. Activates
pleasure centers
in the brain
T&P predicts:
A. Motivated behavior:
Approach or avoidance
in the absence of traitrelevant challenges
B. Emotion regulation &
recovery following
challenges
C. Anticipatory thoughts
and feelings (e.g.,
worry) before challenges
D. All of the above (A-C)
E. None of the above
Which is FALSE: Over time, the repeated

experience of social failure among
individuals with high levels of BI may
A. Train them to interpret
ambiguous social
situations as threatening
B. Cause them to believe
that poor social outcomes
are their fault
C. Promote excessive
anxiety about social
situations and public
performance
D. Reduce the risk of
developing depression
and substance abuse
FILL IN THE BLANKS: ______s (or their absence) do not hardwire people for certain behaviors. There is no _____ for
understanding calculus [or extraversion or neuroticism or selfcontrol] Specific behaviors are [not biologically] hard-wired.
M.I.T. math majors arent born doing calculus Its not just
______s make brain make behavior. You have ___________ too.
A. Experience;
Experience;
Experience;
Gene
B. Gene; Gene;
Gene;
Experience
Individuals with elevated

N/NE are:
A. Less likely to be exposed to
daily conflicts in their
relationships
B. More likely to de-escalate
negative affect during conflict
C. More likely to express toxic
social behaviors (criticism,
contempt, defensiveness, &
stonewalling), perhaps
contributing to increased
marital dissatisfaction and
higher rates of divorce among
highly neurotic individuals
D. All of the above
Rewards are liked (hedonic pleasure

during consumption) and wanted. Liking
and wanting
A. Are challenging to
tease apart
B. Reflect dissociable
neural substrates
C. Are differentially
related to substance
abuse, according to
rodent models
(Berridge & Robinson)
D. All of the above
Reduced reward responsiveness. Which is

false?
A. Is a candidate
endophenotype for
depression
B. Prospectively
predicts symptoms
& treatment
response
C. Not heritable
Depressed individuals
A. Show blunted liking of
positive stimuli and rewards
B. Are less willing to invest
effort in obtaining rewards
and overinvest in lowreward activities
C. Are more responsive to
rewards in the lab and in
daily life
D. A & B
E. B & C
(Tomarken:) Measures of T&P need

to:
A. Exhibit adequate
construct validity
(sensitivity and
specificity)
B. Show adequate internalconsistency reliability
C. Display sufficient testretest stability (traitlike)
D. All of the above (A-C)
E. None of the above (A-C)
In humans, nucleus accumbens /

ventral striatum (VS)
A. Activation during
reward anticipation
is trait-like
B. Activation is
associated with
trait-like individual
differences in E/PE
and BAS
C. Both A and B
D. Neither A nor B
Electrical signals generated in the

midcingulate cortex and measured on the
scalp are trait-like and predict
A. Greater caution and
inhibition following negative
feedback or errors
B. Enhanced avoidance of cues
associated with punishment,
loss, and negative feedback
C. Both, suggesting that this
circuit accounts for anxious
individuals excessively riskand threat-avoidant profile of
choices and behaviors
When cumulated over many individuals

or experiences (e.g. job interviews of a
minority candidate), tiny or weak
statistical effects (e.g. small correlations)
A. Are never of any

practical importance
B. Can be of substantial
practical importance
when cumulated over
many individuals or
experiences; they may
also provide key clues
about important
therapeutic targets for
drug development (as in
the cholesterol example)
The Adaptive Control Hypothesis claims

that
A. Anxiety and cognition
engage a common
territory in the MCC
B. MCC uses punishment
related information to
bias behavior in the face
of uncertainty
C. These signals are
enhanced in anxious,
inhibition individuals
D. All of the above
The mesolimbic dopamine

system
A. Underlies hedonic
pleasure and
consummatory reward
("neural joy juice")
B. Supports wanting and
appetitive behaviors
aimed at getting rewards
C. Is activated by natural
rewards (food, sex) and
all major drugs of abuse
D. A & B
E. B & C
Pete & Paul: With regard to anxiety,

cognitive and behavioral avoidance is
A. An adaptive coping
mechanism that reduces
short-term distress and
arousal
B. Maladaptive because it
prevents exposure that
might contradict inflated
negative expectations
(i.e., lost opportunity for
extinction)
Which is FALSE?
A. Individual common
genetic polymorphisms
(the SNPs measured by
SNP chips) generally have
strong effects on brain
function, behavior, and
T&P (e.g., 50+%)
B. Such big effects are easy
to reliably detect in small,
inexpensive samples
C. Both A and B
D. Neither A nor B
Clinically effective anti-anxiety drugs

A. Selectively
decrease fear
elicited by clear
and imminent
danger
B. Selectively
attenuate anxiety
elicited by
uncertain threat
Substance use disorder has been linked to

which of the following core dimensions of T&P
A. Elevated E/PE
B. Attenuated C/SC;
indeed, low levels of
self-reported
Conscientiousness/Sel
f-Control is among the
strongest prospective
risk factors
C. Amplified N/NE
D. A and B
E. B and C
Uncertainty, unpredictability, and

ambiguity
A. Increase anxiety,
indexed by fearpotentiated
startle or ratings
B. Decrease anxiety,
indexed by fearpotentiated
startle or ratings
Unpredictable, neutral tones are sufficient

to
A. Increase amygdala
activation in the rat
B. Decrease behavioral
manifestations of
anxiety in the rat
C. Amplify amygdala
reactivity in humans
D. A & C
E. B & C
Which is true?
A. Anxiety and
cognition (attention,
inhibition, memory)
are completely
separable and
different in kind
B. Anxiety and
cognition are deeply
and intimately
connected
Orbitofrontal cortex (OFC)

A. Is sensitive to
preferences and value,
such as tastiness and
healthiness
B. Appears to be
regulated by lateral
prefrontal cortex
C. Damage often leads to
anhedonia
D. A & B
E. B & C
Which is correct? My friend, Dr. X,

comes from a family of alcoholics
A. Alcoholism is not
heritable
B. Dr. X is more likely to
develop a substance
use disorder (e.g.
alcoholism)
C. Dr. X can choose to
abstain from alcohol
and eliminate the risk
D. Both A and B
E. Both B and C
In particularly tempting moments, subjects

with low activation in the inferior frontal
gyrus (IFG; as indexed using fMRI during the
performance of simple go/no-go task) are
A. less likely to give in to a food

desire and actually eat than
subjects with High IFG
activation, suggesting that this
region of the lateral PFC serves
as an "accelerator" in
situations demanding selfcontrol
B. more likely to give in to a food
desire and actually eat than
subjects with High IFG
activation, suggesting that this
region of the lateral PFC serves
as a "brake" in situations
demanding self-control
Which is true?
A. The error related negativity
(ERN) is an event-related
potential (ERP) generated in the
mid-cingulate cortex (MCC);
bigger in individuals with an
anxious T&P
B. The ERN is increased by
clinically effective anti-anxiety
drugs (anxiolytics) eg
benzodiazepines
C. Errors (endogenous negative
feedback ) are aversive and are
associated with potentiation of
the startle reflex
D. A & C
E. B & C
Negative life events & psychological

pathogens such as stress tend to:
A. Cause individuals to
cross the diagnostic
boundary and
experience a depressive
episode
B. Increase the risk of
developing a
diagnosable anxiety
disorder
C. Decrease N/NE
D. A and B
E. B and C
Individuals with elevated N/NE and

frank anxiety disorders tend to show
A. Heightened
avoidance of
potential threat (I
cross the street to
avoid someone I
know)
B. Abnormally
infrequent attempts
to control or avoid
distress by worrying
Heightened anxiety in response to uncertain,

ambiguous, unpredictable dangers (CS- ,
ITI/context paired with shocks)
A. Is observed in teens with a childhood
history of stable, extreme behavioral
inhibition (Fox lab) , suggesting that
it confers increased risk and may
contribute to disease etiology
B. Retrospectively predicts the first
onset of a depressive disorder (i.e.,
who will get sick) [Craske lab] and is
observed in many patients with
bipolar disorder [Lissek lab]
C. Appears to reflect alterations in the
posterior parietal cortex
D. Is selectively amplified by clinicallyeffective medications for anxiety,
such as the benzodiazepines, as well
as low doses of ethyl alcohol
E. All of the above
Amygdala damage/lesions is
associated with
A. pathologically reduced
trust and paranoia
B. increased social
approach (i.e. reduced
social distancing),
underscoring that the
amygdala does much
more than just
orchestrate states of
fear and anxiety
C. Both A and B
D. Neither A nor B
Individuals with high levels of N/NE

are characterized by
A. Inflated
estimates of
threat likelihood
B. Abnormally low
estimates of
threat intensity
Anxious individuals tend to

show
A. Heightened
anxiety (startle) in
response to clear
and imminent
threat (CS+)
B. Excess anxiety to
uncertain and
ambiguous
danger (CS- , ITI)
disorder with Pramipexol exhibit severe impulse

control problems (e.g., pathological gambling,
hypersexuality, compulsive shopping, and binge
eating). Recent research using PET indicates that
these patients show (i) reduced expression of the
dopamine transporter in the ventral striatum/VS (i.e.,
they are hypersensitive to Pramipexol-induced
increases in VS dopamine signalling) as well as (ii)
increased VS activation and enhanced dopamine
release in the VS in response to reward cues.
Behaviorally, their impulse control problems rapidly
decline as soon as they stop taking the drug.
Collectively, these pharmacological, clinical, and
brain imaging findings provide unique and compelling
evidence that
A. Low C/SC and impulse control

disorders likely reflect, at least in part,
decreased magnitude and duration of
DA transmission in the VS
B. Low C/SC and impulse control
disorders likely reflect, at least in part,
increased magnitude and duration of
DA transmission in the VS
C. Low C/SC and impulse control
disorders is unrelated to striatal
dopamine transmission
Anxious individuals attentional bias to threat can be

re-trained using computerized tasks. Which is the best
answer?
A. This is clinically effective,
albeit weakly
B. Retraining the bias
produces a lasting
diminution in anxiety (e.g.
in a public speaking task)
C. Furthermore, CBT
targeting excess anxiety
reduces the attentional
bias (reverse effect)
D. Collectively, these
mechanistic findings
indicate a causal role

A. Allocate excess
attention to threat
B. Are faster to
respond to the
dot-probe when it
occurs at the
same location as a
negative word
C. Both
Amygdala reactivity to threatrelated cues

A. predicts N/NE and anxious
temperament in humans and
monkeys
B. is increased in a dosedependent manner by drugs,
such as benzodiazepines,
suggesting that it does not play
a mechanistic (causal) role in
N/NE
C. retrospectively predicts the
development of PTSD symptoms
in individuals who lived through
the Boston Marathon bombingAll
of the above
D. None of the above
Hypervigilance may reflect

A. The direct influence of the
amygdala on sensory
cortex
B. Robust projections from
the amygdala to the
visual cortex
C. An indirect influence of
the amygdala, mediated
by acetylcholine neurons
sitting in the basal
forebrain (nucleus basalis
of Meynert); wake up!
D. All of the above

A. Overgeneralize
anxiety to cues
that resemble
genuine dangers
(e.g., Lisseks
parametric rings)
B. Show anxiety
that is strictly
limited to threat
Individuals with anxiety

disorders
A. Have difficulties tuning
their anxiety and learning
what is safe (safety
learning deficit)
B. This promotes to chronic,
pervasive anxiety,
arousal, and stress; they
dont know when its safe
to relax
C. And predicts who will
develop an anxiety
disorder
D. All of the above
Individuals with a childhood history

of extreme BI, a facet of N/NE, show
A. Hypervigilance
on the dot-probe
task
B. Elevated startle
during periods
of objective
safety
C. Both
Exam Review:
Material Covered During the
Middle Third of Course
The (fear-potentiated or emotionmodulated) startle reflex is

A. Is potentiated (increased)
during periods of stress,
fear, and anxiety
B. Can be measured using
similar techniques in
rodents, monkeys, and
humans
C. Is a widely used,
valence-sensitive
measure of conditioned
and unconditioned fear
D. All of the above
Conventional functional MRI (fMRI)

pulse sequences measure
A. Blood oxygenation (the
hemodynamic BOLD signal);
fMRI is an indirect measure
of neuronal firing
B. Neuronal firing
C. The release of
neurotransmitter-filled
vesicles into the synapse
(synpaptic cleft)
D. FDG metabolism
E. Electrical activity generated
by ensembles of neurons,
providing exquisite temporal
resolution
Which is true?
A. There is one
anxiety disorder
B. There is a whole
family of
anxiety
disorders
The most common family of

psychiatric disorders is
A. Anxiety
B. Depression
C. Schizophrenia
D. Somatoform
Anxiety disorders tend to onset

A. Late in life
B. Mid life
C. Early in life
Depression tends to onset

A. Early in life
B. Mid life
C. Late in life
The most burdensome disorder

(disability, illnes, death) in the US is
A. Depression
B. Heart Disease
C. COPD
D. Cancer
E. Alzheimers
Elevated N/NE is a risk

factor for
A. Anxiety
disorders
B. Depressive
disorders
C. Both
Anxiety and depression

symptoms
A. Form a coherent,
factor (internalizing)
B. Are categorically
distinct
C. Should be thought
of as natural kinds,
discrete entities that
exist in nature
waiting to be
discovered
Anxiety and depression

A. Are highly comorbid
B. Rarely co-occur
in the same
individual
Treatments targeting one emotional

disorder
A. Ameliorate
(decrease) the
symptoms of
other emotional
disorders
B. Decrease
ratings of N/NE
C. Both,
suggesting a
common cause
Negative life events & psychological

pathogens such as stress tend to
A. Cause individuals to
cross the diagnostic
boundary and
experience a frank
depressive disorder
B. Increase the risk of
developing a
diagnosable anxiety
disorder
C. Increase N/NE
D. All of the above
Anxiety disorders, depression, and

N/NE
A. Reflect
completely
separate genes
B. Are inherited
together
(shared
inheritance),
suggesting a
common genetic
underpinning
Recent meta-analyses demonstrate

that
A. A variety of anxiety
disorders, like N/NE, are
associated with
heightened amygdala
activation to potential
threat
B. Depression, like N/NE, is
associated with increased
amygdala reactivity to
aversive cues
C. Both, providing evidence
for a common biology
Barlow argues that the development of a

particular Dx (diagnostic specificity) reflects
A. N/NE and a
disorder-specific
learned
vulnerability (e.g.,
fear dogs)
B. N/NE and an innate
vulnerability
C. N/NE and other
non-specific risk
factors
N/NE is a
A. Cause of emotional
disorders
B. Symptom of
emotional disorders
C. Identical to or
synonymous with
the emotional
disorders
D. A symptom of too
much anxiety
When confronted by potential threat (robot, intruder),

children with high levels of behavioral inhibition (BI)
A. Exhibit heightened
avoidance and
freezing
B. Cease playing
C. Become quiet
D. Withdraw to the
proximity of their
caregiver
E. All of the above
Jenni Blackfords group uses a questionnaire to

retrospectively assess childhood BI. This is
A. Much more
practical than
starting a new
longitudinal study
(waiting 20 years)
B. Subject to the
usual concerns
about mnemonic
biases
C. Both
BI in toddlers
A. Parallels anxious temperament
(AT) in young monkeys
B. Echoes theoretical
descriptions of the BIS (Jeffrey
Gray)
C. Is associated with R > L frontal
EEG asymmetry, as in studies
of monkeys and human adults
D. Is considered a facet of N/NE
E. Is somewhat stable (testretest)
F. Is heritable (inherited)
G. All of the above
Most preschoolers with

high levels of BI __________
A. Stick with it
B. Grow out of it
C. Are likely to develop
an anxiety disorder
D. Just have an ageappropriate fear of
separation or
strangers
E. A and C
F. B and D
Kids with _____ & ______ are at risk

for developing ___________
A. Consistent, high
levels of BI,
substance and
emotional disorders
B. Stable, high levels
of BI, schizophrenia
and personality
disorders
Social anxiety disorder can be

characterized by
A. Heightened anxiety
about people and
performance
B. Pervasive worries about
being judged
C. Avoidance
D. Hyper-arousal
E. A disconnect between
what patients know to
be rational vs what they
feel
F. All of the above
BI is associated with
A. Less effective ways of
interacting with others
B. Worse social outcomes
C. Lower quality peer
relations
D. A loss of opportunity to
acquire critical social
skills
E. Challenges forging
strong relations with new
peers and schoolmates
F. All of the above
Over time, the repeated experience of social failure

among individuals with high levels of BI may
A. Train them to interpret

ambiguous social
situations as
threatening
B. Cause them to believe
that poor social
outcomes are their fault
C. Promote excessive
anxiety about social
situations and public
performance
D. All of the above
BI is a strong (candidate) _________ for

______________; but we still need to establish ______ .
A. Intermediate
phenotype,
dysthmia, causation
B. Endophenotype,
social anx disorder,
causation
C. Biomarker, emotional
disorders, heritability
D. Marker, overactive
insula, heritability
T&P reflect
A. Nature
B. Nurture
C. Both
Genes (nature) can influence

A. Environments
and experience
B. Neither. Nature
and nurture are
distinct and
independent
forces
Nature (heritability) is
A. Fixed and
immutable
B. Plastic and can
change in
response to
growing
autonomy or
due to
cumulative
impact
Heritability is
A. The proportion of
variation in a trait,
such as C/SC, that
is accounted for
by the pedigree
(family tree)
B. GV / Total PV = GV
/ GV + EV
C. A and B
Estimates of heritability
A. Are fixed
B. Can be influenced by
social and
environmental
influences (e.g., living
in a conservative
religious community)
that increase or
decrease the amount
of variation in the trait
(e.g., disinhibition,
partying, smoking)
Heritability
A. Is the % of
variation in a trait,
such as E/PE, that
is passed down
from your parents
B. Reflects the
inheritance of
genes, not
phenotypes or
traits
Heritability describes
A. The % of my trait that
is inherited (nature)
vs. environmental
(nurture)
B. The % of phenotypic
variation across a
group of individuals
that is influenced by
genetic factors
C. Individuals within a
population (e.g., Alex)
Highly heritable traits, such as

height
A. Are our destiny
B. Can potentially
be powerfully
influenced by
interventions
(environment)
Ryan Bogdan: The neurogenetic strategy

A. Involves correlating variation
in genetic polymorphisms
(SNPs) with variation in
intermediate phenotypes,
such as differences in
amygdala activation
B. Promises to address WHY
individuals differ in brain
activation (e.g., why do
individuals high in N/NE show
heightened amygdala
reactivity)
C. Opens the door to discovering
testable mechanisms for
genetic influence on behavior
D. All of the above
Which is false about the serotonin

transporter genetic polymorphism
A. Amygdala reactivity is correlated
with variation in the serotonintransporter linked polymorphic
region (5-HTTLPR) on the SLC6A4
gene
B. The L allele is bad: Individuals
with the more transcriptionallyefficient long allele (more
transporter proteins available to
clear serotonin from the synapse)
show heightened threat-related
amygdala reactivity relative to
individuals with the short allele
C. Meta-analyses suggest that this
allele accounts for 20-50% of the
variance in amygdala reactivity
D. B and C
Which is false?
A.
B.
C.
D.
Some have suggested that the

neurogenetics strategy can address
the molecular mechanisms linking
genes to brain to traits, such as N/NE
Some have suggested that if we
measure a genetic polymorphism with
a known function (e.g., serotonin
transporter) and we are willing to
make some assumptions, then we can
use SNPs as a proxy for individual
differences in brain chemistry
(serotonin in the amygdala). Which is
awesome because we usually cannot
measure neurochemistry in living
human brains.
In relation to the serotonin transporter
allele, a key assumption of this
strategy is that differences in the
allele are actually associated with
differences in the expression of the
serotonin transporter in the brain
Several groups (e.g., Kalin) have used
PET to show that there is in fact an
association between the allele
transporter expression in the
Which is true
A. The HPA axis is involved in
the release of cortisol,
epinephrine/adrenaline,
and
norepinephrine/noradrenali
ne in response to physical
and psychological stress,
which increases the
availability of energy for
the brain as well as
defensive behaviors
(fight/flight)
B. HPA = hippocampal,
pituitary, amygdala
Which is false
A. Remarkable life-long changes
happen to stress-reactivity when
neonatal rats are exposed to
experimenter handling, providing
a nonhuman animal model of
early experience & temperament
B. Handling leads to tighter, more
precise regulation of cortisol
C. Handling leads to increased
expression of the glucocortisoid
receptor in the hippocampus in
adulthood
D. As adults, rats who were handled
as pups are less exploratory,
more fearful, and more stress
reactive (N/NE)
Which is false: Michael Meaneys group

has provided evidence that the impact of
handling on temperament (N/NE or stress
reactivity) is
A. Related to increased
expression of benzodiazepine
receptors in the amygdala
B. Mediated by a social factor,
namely, maternal style (LGABN: licking, grooming, and
arched-back nursing)
C. Mediated by genes that
increase maternal LG-ABN and
decrease offspring reactivity
D. Not genetically transmitted
(i.e., moms can alter
adopted/cross-fostered pups)
Which is false about

epigenetics
A.
B.
C.
D.
E.
Refers to trait-like alterations in

the transcriptional (proteinmaking) potential of a cell (such
as a neuron) that are not due to
changes in the genome (DNA);
turning certain genes on/off,
without changing the genes
themselves
Often reflects methylation or
histone modification of the DNA
Explains cell differentiation (liver
vs brain cell) & developmentally
appropriate changes in the brain
and body
Can never be heritable
(transmitted to subsequent
generations)
Can be heritable, violating a key
tenet of modern biology
(inherited traits, such as T&P,
Which is false: How does maternal behavior produce

lasting changes in (rodent) temperament (N/NE)
A. Meaneys team showed that

maternal behavior (LG-ABN)
produces epigenetic
changes
B. Epigenetic changes lead to
increased expression of
glucocorticoid receptors in
the hippocampus,
supporting enduring
changes in stress reactivity
C. Epigenetic changes induced
by maternal behavior only
persist during the neonatal
period
Can paternal experience be transmitted to offspring without a

behavioral/social intermediary? Can we benefit (or suffer) from
our parents experience without them teaching (or grooming)
us? Can acquired characteristics be inherited, as Lamarck
posited in the 18th century?
A. Yes!
B. No!
C. Ressler and others have
provided tantalizing
evidence suggesting that
this is possible, but much
remains unclear (e.g., how
fear learning in the brain
influences epigenetics in the
sperm/gametes)
Which is false: Trait-like differences in T&P

reflect the brain. Differences in brain
structure and function reflect the influence
of
A. Genome/DNA
B. Epigenome
C. Experience/Enviro
nment
D. Experience
interacting with
the genome and
epigenome
Which is false: Trait-like differences in T&P reflect

the brain. Nature (genome/DNA, epigenome) and
nurture (experience) interact to change
A. Protein expression
B. DNA methylation
C. Neurochemical
receptor expression
and binding
D. Hippocampal
structure and
function
E. Histone status
F. None of the above
How does early experience (abuse, stress,

caregiver behavior) get into the brain
A. Changes in the
genetic code
B. Changes in the
epigenome that
alter the
expression of
genes, leading to
changes in protein
synthesis and,
ultimately, activity
* Taylors question in class
GWAS pretends that

A. Alleles (i.e.,
genetic variants)
do not interact
with or influence
one another (only
independent
effects are
considered)
B. Alleles do interact
with one another
GWAS genome-wide association

study
A. Brute force approach to
identifying correlations
between alleles and
phenotypes, such as N/NE
B. Often relies on SNP chips
C. Suffers from low statistical
sensitivity, because of the
very large number of tests
performed
D. Opens the door to
discovering new and
potentially important
molecular pathways
E. All of the above
Showing that a trait, such as E/PE, is

heritable indicates
A. A single,
coherent or
unified
biological cause
B. Nothing
whatsoever with
regard to the
number or kind
of substrates
Kagans model of BI
A. Shows a number of
parallels with N/NE and
Grays BIS, reinforcing the
idea that childhood
temperament and adult
personality are closely
related
B. Shows a number of
important differences from
N/NE and Grays BIS,
reinforcing the idea that
childhood temperament
and adult personality are
distinct kinds
An allele is
A. A genetic
polymorphism
B. A genetic variant
C. The thing; that gives
rise to geneticallydetermined
individual differences
in trait-like
phenotypes
D. All of the above
Family, twin, and adoption studies

(aka behavioral genetics) are
A. Correlational
B. Mechanistic
C. Provide a tool
for discovering
the molecular
substrates of
T&P
Family, twin, and adoption studies (aka

behavioral genetics) teach us that
A. Psychiatric disorders,
like T&P, aggregate
in families
B. Are heritable
C. Things that blood
relatives share (e.g.,
SES, toxin exposure,
stress, habits) are
important
determinants of
psychopathology
Which is true
A. In humans, DNA is organized
into 23 pairs of chromosomes,
one descended from Mom and
one from Dad
B. Chromosomes are organized
into genes, regions of DNA
corresponding to the
instructions for a protein
C. These proteins form neurons,
axons, the myelin sheath
covering axons, neurochemicals,
synapses and every other
component of our brains, the
wetware that gives rise to our
T&P
D. All of the above
Developing a mechanistic understanding of the

molecular neurobiology of T&P and associated
psychiatric disorders promises to
A.
B.
C.
D.
E.
F.
G.
Redefine diagnostic categories and

T&P traits in terms of quantifiable
etiology (root causes)
Accelerate the development of novel
treatments or prevention efforts
targeting links in the etiological chain
Identify at-risk individuals early (e.g.,
carriers of a particular polymorphism)
Predict treatment response or more
quickly pick the best treatment (e.g.,
carriers of a particular polymorphism)
Enhance prognosis: You have 3
months to live
Provide a novel discovery tool for
addressing some of the most
fundamental question about the
nature of T&P
All of the above
Children with elevated behavioral

inhibition (BI)
A. Are more likely to develop anxiety,
mood, and co-morbid substance
abuse disorders later in life
B. Are more likely to develop
psychopathology if they show
stable, high levels of BI across
development
C. Are shy and reticent in the face of
novelty and potential threat (e.g.,
scary robot, human intruder)
D. May show elevated levels of the
stress hormone cortisol
E. Show a R > L pattern of frontal EEG
F. Show heightened amygdala
reactivity to novel faces in
adulthood
G. All of the above
If a trait is highly heritable, this means that group

differences at one point in history will always be that
way
A. Yes
B. No
What are the long-term prospects for linking genes to

intermediate neural phenotypes to traits, such as
C/SC?
A. Awesome!
B. Terrible! What a waste
of taxpayer money!
C. It depends on the nature
of the linkages, which
we do not yet know
D. Current evidence
suggests somewhere in
between awesome and
terrible, but we do not
yet know
E. C and D
Which is true
A. Common genetic polymorphisms
(the SNPs measured by SNP
chips) have, at most, weak effects
on brain function and behavior
(e.g., 2-5%)
B. Such small effects are small and
hard to reliably detect without
using very large and expensive
samples
C. Such small effects have led to
many non-replications
D. Such small effects have led many
to wonder whether this research
strategy is worth the money
E. All of the above
Which is true
A. Hannah is a 6
y.o. boy
B. Micah is an 18
m.o. girl
C. Both of Dr. Ss
kids are cute as
all get out
D. All of the above
The Big 3 superfactors are

about
A. 10% heritable
B. 45% heritable
C. 90% heritable
In class, we discussed several arguments for why

even these small effects are potentially important
A. Small is mis-leading; a limited
number (on the order of a few
tens) of SNPs, each accounting for
a small % of the variance, can add
up to meaningful differences (as in
the height example)
B. The expense to date of this
research is modest compared to
military expenditures or even
large-scale physics projects
(colliders)
C. The discoveries are truly novel,
opening the door to models and
treatments that we probably never
would have predicted or
developed based on our existing
knowledge and intuitions
Which is inherited
(heritable)?
A. Genes
B. Trait-like
phenotypes,
such as E/PE
C. All of the above
Heritability reflects
A. The % of betweenindividual variation
predictable from
pedigree
B. The % of a trait
within an individual
(you!) that is
inherited from your
forebears
A wide variety of environmental

factors can
A. Trigger genetic
predispositions (e.g.,
to high levels of N/NE)
B. Compensate for or
regulate the
expression of genetic
predispositions
C. Enhance or
accentuate genetic
predispositions
D. All of the above
Heritability
A. Is probabilistic and
predictive of
average outcomes
B. Is deterministic if
you know the
parents, you know
exactly what to
expect of the
offspring regardless
of environment or
experience
Anxiety disorders, such as GAD, and

major depression are
A. Categorically different
B. Often co-morbid and
show a number of
other similarities, in
terms of therapeutic
response, heritability,
and do on, suggesting
that they are closely
related to one another
and form a spectrum
Treatments targeting anxiety

disorders
A. Tend to influence
N/NE as well as
depression
B. Selectively
influence the
targeted disorder
C. Only help some
patients
D. A and C
E. B and C
Anxiety disorders, depression, and

N/NE appear to share
A. Genes
B. Neural
substrates (e.g.,
amygdala
hyper-reactivity)
C. Both
Lesion studies in rodents, monkeys, and

humans demonstrate that the amygdala
A. Is required for the
normal acquisition
of new fear learning
(conditioned
emotional
response)
B. Not required
C. Is required for the
retention of already
learned fears
Elevated N/NE
A. Is common
among anxiety
patients
B. Is common
among
depression
patients
C. Both
Psychological pathogens, such as

stress and family conflict
A. Exert similar
effects on
depression, anxiety
disorders, and
N/NE, suggesting a
common substrate
B. Have distinct
effects on T&P vs.
depression vs.
anxiety disorders
In a widely cited paper published in Science in 2003, Caspi

and colleagues provided evidence that Individual differences
in the serotonin transporter SNP
A. predicted depression
B. interacted with life
stress to predict
depression, providing
evidence of a G x E
interaction and
suggesting a
neurochemical substrate
for psychiatric risk
C. Was completely and
utterly unrelated to
depression
Amygdala lesions in
monkeys block
A. The acquisition
of new
conditioned
fears
B. Innate anxiety
about snakes
C. Both
Height is
A. Trait-like
B. Among the most
heritable traits,
although offspring will
show considerable
variation
C. Can be markedly
affected by
interventions (diet,
nutrition, and
healthcare access)
Jerry Kagan argues that the root cause

of childhood behavioral inhibition (BI) is
A. An over-reactive
amygdala
B. Maladaptive
cognitive coping
mechanisms
C. Worry
D. Disress
E. Social reticence
F. Shyness
The administration of a benzodiazepine

(anti-anxiety medication)
A. Causes a dosedependent
reduction in
amygdala
activation
B. Causes a dosedependent
increase in
amygdala
activation
Why do some individuals develop particular

disorders, such as specific phobia of dogs?
A. Learning and experience
B. Core vulnerability
(heightened
neuroticism, hyperreactive amygdala,
inadequate regulation of
the amygdala)
C. Both, neither is
sufficient to explain the
development of specific
emotional disorders
The RoboGator Experiment: Amygdala

lesions in rodents attenuate
A. Reticence to get the food
pellet in the presence of
the remote-control
robogator, suggesting a
substrate for the reticence
demonstrated by BI kids,
consistent with lesioned
monkeys and the human
intruder
B. The amount of time hiding
in the nest area (outside
the arena containing the
Rgator)
C. All of the above
Heritability
A. Is informative
about the nature
and plasticity of
group differences
(men/women,
black/white) in
traits
B. Is not informative
about such mean
differences
Amygdala damage
A. Increases ratings
of trust and
approachability to
faces that are
normally deemed
untrustworthy
B. Has no
consequence of
social interactions
or social cognition
N/NE is
A. A specific risk
factor for
anxiety
disorders
B. A nonspecific
risk factor for a
broad range of
psychiatric
disease
Patient SM has circumscribed bilateral

destruction of her amygdalae. She
A. Picks up snakes and
spiders, despite
professing anxiety
B. Shows no fear in the
haunted house
C. Is unable to acquire
new conditioned fears
in the lab
D. Quickly returned to
the park where she
was assaulted
Is BI a viable intermediate phenotype

for social anxiety disorder
A. Yes
B. No
Emotional disorders and

N/NE
A. Are
fundamentally
different
B. Reflect a
common cause
C. Are
categorically
distinct
Exam Review:
Material Covered During the
First Third of Course
How can we identify the cause(s) of

T&P (e.g., low C/SC)?
A. Forge a link between
individual differences in a
trait and variation in a
relevant behavioral or
biological measure
B. Correlate traits and fMRI
activation
C. Compute a regression
(correlation) between task
performance (e.g., BART)
and traits of interest
D. Directly manipulate the
hypothesized cause.
E. All of the above
What's the problem with reducing a complex,

broad-band trait to a single number?
A. Mixes distinct
processes
B. Hinders our
ability to clearly
resolve the
underlying
substrates
C. Too simplistic
D. All of the above
One strategy for discovering the cause of

phenomenologically complex traits (and mental
disorders) is to
A. Decompose them
into simpler,
more manageable
intermediate
phenotypes
B. Give up
C. Search for
endophenotypes
D. A and C
Which of the following can we plausibly model in

nonhuman animal models (where we can perform
mechanistic experiments to determine causation)
A. Anti-social behavior
B. C/SC
C. Delay of
gratification
D. Turn-taking and
emotional irritability
E. Hyper-sensitivity to
reward-related cues
F. C and E
With respect to neurological soft signs

(trait), elevated lead levels in the hair are
A. Noncausal
symptom/marker of
the process that
causes the trait or
phenotype
B. Marker or scar of
the trait or the
organisms response
to the trait
C. Endophenotype
We discussed 2 kinds of intermediate

phenotypes. Both kinds are
A. Causal
B. Heritable
C. Aggregate in
families
D. Co-segregate in
families
Endophenotypes are
A. Simpler than the
trait one seeks to
understand
B. Causal
C. A bridge between
the genotype and
phenotype
D. Heritable
E. All of the above
Which is true
A. Intermediate
phenotypes cause
traits, markers do not
B. Markers cause traits,
intermediate
phenotypes do not
C. Endophenotypes
cause traits,
biomarkers do not
D. A and C
E. B and C
Remarkably
A. We know quite a bit
about the mechanisms
linking genes to
endophenotypes
B. We know quite a bit
about the mechanisms
linking endophenotypes
to traits (and disorders)
C. We know next to nothing
about either mechanism
for any established
endophenotype
EEG/ERP affords
A. Exquisite spatial
resolution
B. Exquisite
temporal
resolution
C. Neither
D. Both
Conventional fMRI signals

reflect
A. Blood
oxygenation
levels
B. Neuronal firing
Conceptually, activation in both ERPs

and event-related fMRI is estimated by
A. Computing the
average
response
evoked by a
particular
condition or
kind of event
B. Computing the
cross-correlation
among sensors
Which is true
A. EEG is relatively cheap,
tolerant of motion, and
reflects neuronal
electrical activity
(EPSPs)
B. fMRI is relatively
expensive, sensitive to
motion artifacts, and
does not directly
measure neuronal
activity
C. Both
EEG and fMRI are

A. Causal (like lesion
studies)
B. Mechanistic (like
manipulating brain
activity in rodents
with drug infusions)
C. Correlational (like
longitudinal studies
of behavior)
In his 1968 book Personality and Assessment, Walt

Mischel argued that the primary determinant of
moods, thoughts, and behavior is
A. The situation,
because T&P at
most predict
outcomes r = .
30 (9%
variance)
B. T&P
C. Both
But contemporary science suggests that moods,

thoughts, and behavior are determined by
A. The situation
B. T&P
C. Both
Trait-like individual differences in T&P are strongly

predictive of
A. Academic
performance (above
& beyond IQ)
B. Marital stability &
satisfaction
C. Mental & physical
health and wellbeing
(morbidity)
D. Death (mortality)
E. All of the above
Correlation and variance explained: If

two variables are correlated R = .50, the
amount of variance accounted for is:
A. 0.50 * 0.50 = .25 =

25%
B. 0.50 / 0.50 = 1 =
100%
C. Sqrt(.50) = .7071 =
70%
Longitudinal research studies
A. Provide strong evidence that

antecedants (childhood)
predict consequences
(adulthood), a precondition
for establishing causation
B. Complex, costly, and timeconsuming
C. Can not prove causation,
because they do not
manipulate the putative
cause of the outcome
D. All of the above
Moffitt et al PNAS: What is C/SC?
A. Do things by the book;

follow rules
B. Prefer order and neatness
C. Planful; not impulsive
D. Able to delay gratification;
self-disciplined
(marshmallow test)
E. Focused; not easily
distracted
F. All of the above
Which features of modern culture tend to magnify the

impact of individual differences in T&P, such as C/SC?
A. Longevity
B. Risk exposure (fast
food nation)
C. The relatively high
prevalance of
psychiatric disorders,
such as depression,
anxiety, and
substance abuse
D. All of the above
Moffitt et al PNAS: Key results:

Childhood C/SC predicted mid-life
A. Composite measure
of health
B. Composite measure
of personal wealth
C. Incarceration,
criminal conviction
and other indices of
public safety
D. All of the above
Moffitt et al PNAS: Key results:

Which is true?
A. Kids with low C/SC are prone to

smoke, become parents, and
drop out of school as teens
B. Teen snares explain the
negative adult outcomes
experienced by many kids with
low C/SC
C. Teen snares are only part of the
story. Might make more sense to
target the root cause (low
childhood C/SC) for intevention,
rather than teen symptoms
D. All of the above
Moffitt et al showed that childhood self-control predicts health, wealth &

public safety in midlife. What was one intervening mechanism during
adolescence that partially explained the link from kid temperament to
deleterious adult outcomes?
A. Smoking
B. Becoming a parent
C. Excessive video
game playing
D. Violence in the
media
E. High-caffeine energy
drinks
F. A & B
G. C & D
Correlation and variance explained: If

two variables are correlated R = .50, the
amount of variance accounted for is:
A. 0.50 * 0.50 = .25 =

25%
B. 0.50 / 0.50 = 1 =
100%
C. Sqrt(.50) = .7071 =
70%
T&P reflect trait-like individual differences in

emotional and cognitive biases that
A. First emerge early in life
B. Continue to evolve for many
years
C. Account for consistency in
behavior, inner experience,
and risk across time and
contexts. Can be relatively
simple (e.g., anxious distress)
or complex and multiply
determined (orderliness).
Excessive video game playing
D. Can be relatively simple
E. Can be complex and
multidimensional
F. All of the above
T&P are not different in kind (according to Shackman)

because they are both
A. Biological
B. Emotional
C. Cognitive
D. Somewhat
heritable
E. All of the above
What are the 3 fundamental dimensions of T&P?
A. N/NE
B. P/TA
C. E/PE
D. S/RE
E. C/SC
F. A, C, and E
G. A, B, and C
N/NE can be dissected into which 2 facet traits
A. Distress
(fear/anxiety)
and Irritation
(anger)
B. Guilt and Shame
Which statistical test is used to quantify

the continuity (temporal or test-retest stability) of
traits
A. Students t test
B. ANOVA
C. Correlation
T&P is
A. Fixed and
immutable
B. Moderately stable
(R = 0.4 to 0.6
over periods of
one to several
years)
C. Completely plastic
and malleable
Which features of modern culture tend to

magnify the impact of individual differences in
T&P, such as C/SC?
A. Longevity
B. Risk exposure (fast
food nation)
C. The relatively high
prevalance of
psychiatric disorders,
such as depression,
anxiety, and
substance abuse
D. All of the above
The Five Factor Model (FFM) is predicated on

the lexical hypothesis, the assumption that
the deep structure of T&P is embedded in our
natural language, waiting to be discovered.
What are some concerns with this
assumption?
A. Meaningful aspects of T&P may

not be captured by single word
adjectives (e.g., relationships
or processes). Key aspects of
T&P might be too complex for
single words, requiring
phrases, sentences, or even
whole paragraphs of words
B. No guarantee that words
(natural language) will permit
the expression of scientifically
crucial aspects of personality
C. Both
The FFM assumes that responses obtained

from untrained lay individuals (e.g., military
personnel, undergraduates) are an adequate
means of uncovering the core dimensions of
personality. What are potential concern with
this assumption?
A.
B.
C.
D.
Lay individuals are sloppy

and inconsistent in their use
of language (e.g.
aggressive, critical)
Untrained raters may not
have sufficiently
sophisticated mental models
of T&P
Untrained judges are more
likely to be biased or even to
lie
All of the above
Tomarken argued that biological

measures of T&P need to be
A. Reliable: Show
adequate internal
consistency reliability
B. Reliable: Show
adequate test-retest
stability (trait-like)
C. Reliable and Valid
Establishing the construct validity of a

measure requires that we demonstrate that it is
A.Sensitive to
some process,
such as fear
B. Specific to
some process
(fear & no other
process)
C. Sensitive and
Specific
he FFM was derived using factor analysis.

Factor analysis is a useful technique for
A. Reducing the
dimensionality of a
dataset
B. Compressing data
C. Identifying a relatively
small number of
factors that describe a
dataset
D. Creating new
questionnaires
E. All of the above
Can factor analysis be used to

objectively discover the nature of T&P?
A. Yes
B. No
In terms of discovery, potential

limitations of factor analysis include
A. Garbage In/Garbage Out;
Dependent on the kinds of inputs;
Cant identify factors that are not
sampled or represented in the data
B. Subjective decisions about the
number of factors to retain (degree
of acceptable lossiness); Splitter
or lumper
C. Requires the analyst to decide at
the outset whether dimensions are
independent or correlated (i.e.,
needs to pick the rotation
technique)
The FFM is largely based on factor analyses of

adjectives. Was the pool of words
A. representative of
the English
language
B. selected on the
basis of
preconceived
notions about the
importance and
understandability
of particular words?
Were the methods that were used to reduce

the ~400,000 words comprising the
unabridged dictionary to a more manageable
pool of adjectives (personality descriptors)
A. replicable,
objective, and
atheoretical
B. subjective,
idiosyncratic,
and
theoretically
biased?
The key take home point from

Blocks critique is that the FFM
A. Is a bunch of hooey
B. Reflects the
fundamental nature
of T&P
C. Is a convenient
short-hand, a
sometimes useful
fiction that begs for
additional research
Moffitt et al PNAS: Key results: Which

is true?
A. Kids with low C/SC are
prone to smoke, become
parents, and drop out of
school as teens
B. Teen snares explain the
negative adult outcomes
(reduced health, wealth,
public safety)
experienced by many kids
with low C/SC
C. Teen snares are only part
of the story.
D. All of the above
Establishing the construct validity of a

measure requires that we demonstrate that it is
A.Sensitive to
some process,
such as fear
B. Specific to
some process
(fear & no other
process)
C. Sensitive and
Specific
Which item would NOT be found on a

paper-and-pencil measure of N/NE?
A. Emotionally labile
(unstable)
B. Bothered by
change
C. Prone to sadness
D. Prone to anxiety
E. Blue or depressed
F. Punctual
While they tend to show good internal-consistency

reliability and test-retest stability, self-report measures of
T&P can be limited by biases and artifacts, including
A. Social desirability
(looking good)
B. Lying or
malingering
C. Mnemonic
distortions (e.g.,
peak-end rule)
D. All of the above
Behavior is guided by
A. Conscious processes
B. Automatic habits and
implicit attitudes that
lie outside of
awareness and which
opaque to
introspection, hence
not measureable using
standard paper-andpencil measures of T&P
C. Both conscious and
unconscious processes
Behavior is guided by
A. Conscious processes
B. Automatic habits and
implicit attitudes that
lie outside of
awareness and which
opaque to
introspection, hence
not measureable using
standard paper-andpencil measures of T&P
C. Both conscious and
unconscious processes
Which is true?
A. Amygdala lesions block the
conditioned fear response (SCR)
B. The Story We Tell Ourselves:
Hippocampal lesions block selfreported contingency learning
C. This double dissociation provides
direct evidence for separable
substrates and indicates the need for
using both ratings and other kinds of
measures (e.g., physiological)
D. All of the above
McNulty provided
evidence that
A. Implicit & explicit attitudes
toward spouses are uncorrelated,
suggesting that they reflect
distinct neural circuitry
B. Implicit attitudes (measured
behaviorally) predicted marital
satisfaction 4 years later
C. Whereas, explicit ratings of
attitudes toward ones spouse
did not
D. All of the above
There is considerable
evidence that
A. Trait-like differences in
T&P interact with traitrelevant cues to
produce states
B. Trait measures predict
state ratings
C. E/PE predicts pos affect
elicited by humorous
film clips; N/NE predicts
fear and anxiety elicited
by aversive film clips
D. All of the above
Traits predict
A. More intense
states in the
presence of
relevant cues
B. This reflects
heightened peak
activation in the
underlying neural
systems
C. Both
But, T&P also predicts

A. Motivated behavior: Approach
or avoid
B. Emotion regulation & recovery
following challenges
C. Anticipatory thoughts and
feelings (e.g., worry) before
challenges
D. All of the above; the common
denominator is the ABSENCE of
trait-relevant cues in the
immediate environment;
therefore, the T&P x Context
= States model is true but
incomplete
Moods, thoughts, and behavior are

determined by
A. The situation
B. T&P
C. Both
Longitudinal research studies
A. Provide strong evidence that

antecedants (childhood)
predict consequences
(adulthood), a precondition
for establishing causation
B. Complex, costly, and timeconsuming
C. Can not prove causation,
because they do not
manipulate the putative
cause of the outcome
D. All of the above
The key take home point from

Blocks critique is that the FFM
A. Is a bunch of hooey
B. Reflects the
fundamental nature
of T&P
C. Is a convenient
short-hand, a
sometimes useful
fiction that begs for
additional research
The Five Factor Model (FFM) is predicated on

the lexical hypothesis, the assumption that
the deep structure of T&P is embedded in our
natural language, waiting to be discovered.
What are some concerns with this
assumption?
A. Meaningful aspects of T&P

may not be captured by single
word
B. Key aspects of T&P might be
too complex for single words,
requiring phrases, sentences,
or even whole paragraphs of
words
C. No guarantee that words
(natural language) will permit
the expression of scientifically
crucial aspects of personality
D. All of the above
Are trait-like differences in T&P embodied

in the on-going, spontaneous activity of
the brain?
A.
B.
No, traits interact with

trait-relevant cues to
produce more transient
thoughts, feelings, and
behaviors (i.e., states)
Yes, individuals with
elevated N/NE
(dispositional anxiety)
show increased FDG
metabolism (indexed using
PET) and perfusion imaging
(ASL fMRI) in the
amygdala, even at rest.
Oftentimes, physiological measures, such as EEG, PET, and

functional MRI are collected "at rest" (i.e., when subjects are not
asked to perform any particular task). Are subjects necessarily in
an emotionally-neutral state of quiet quiescence?
A.
B.
Yes, they're quietly lying in

the scanner looking at a
fixation cross
No, not necessarily. Many
features of the scanning
procedures could
potentially elicit anxiety
(e.g., novelty, confined
conditions, absence of
normal freedom of
movement, claustrophobia,
noise stress, etc.)
Can we discern temperament &

personality when rewards and
punishments are absent (at rest)?
A.
B.
No, traits interact with

trait-relevant cues to
produce more transient
thoughts, feelings, and
behaviors (i.e., states)
Yes, research using EEG,
PET, and functional MRI
demonstrate that
differences in T&P are
associated with systematic
differences in the activity
and functional connectivity
of the brain in the absence
of explicit rewards and
punishments.
Is the brain ever really at

rest?
A.
Yes.
B.
No, although it only

comprises ~2% of the
adult body mass, the brain
consumes ~20% of the
body's oxygen and glucose
at rest. Importantly, this
consumption is only
modestly altered when
subjects are actively
engaged in performing
mental tasks.
in the serotonin-transporter
linked polymorphic region (5HTTLPR) on the SLC6A4 gene. In
particular, individuals with the
__________ allele tend to be
characterized by heightened
N/NE.
A.
B.
Short
Long
special kind of functional MRI

(arterial sping labeling or
perfusion imaging) to
demonstrate that individuals
with the short ("bad") allele of
the 5-HTTLPR (serotonin
transporter polymorphism) show:
A.
B.
Elevated amygdala
reactivity to threat-related
images.
Elevated activity
(perfusion) in the
amygdala and
hippocampus at rest.
Conventional functional MRI (blood

oxygenation level dependent signal) is
good for:
A.
Assessing differences in
activity, because it's in
arbitrary units that vary
from subject to subject
B.
Assessing trait-like
differences in resting
activity, because it's
calibrated to a real
physical scale.
Amygdala metabolism predicts individual

differences in N/NE (anxious temperament
or negative affectivity) in
A.
B.
C.
Young rhesus macaque

monkeys
Human adults
Both
dispositional anxiety that were

conducted in young monkeys by Ned
Kalin's lab. In these studies, the
monkeys are allowed to respond
naturally to various mild stressors
(e.g., novel testing cage, human
intruder's profile), anesthetized, and
then positioned in the PET scanner.
Activity
in the PET scanner reflects
A. The anesthetized brain.
Therefore, activity does not
reflect a reaction to the
scanner environment.
B.
Regions that were more

metabolically active and,
hence, took up more of the
radiolabeled glucose,
during the preceding 30-
can be used to quantify individual

differences in functional connectivity
(co-activation over time). In humans,
rs-fMRI is collected at rest. In
monkeys, it is typically collected
under light anesthesia. Unlike FDGPET, fMRI
measures of functional connectivity
acquired
under anesthesia
reflect
A. The anesthetized
brain.
Therefore, differences
functional connectivity
does not reflect a reaction
to the scanner
environment, they reflect
the brain's intrinsic
organization or
architecture.
B.
Regions that were more or
Anxious temperament (AT; increased freezing, increased levels of the stress

hormone cortisol, and less frequent coo vocalizations) in young monkeys shows
a number of parallels with _______________. Indeed, individual differences in AT
and __________ can be assayed using similar experimental procedures.
A.
Childhood behavioral
inhibition (BI)
B.
Behavioral Activation
System (BAS)
C.
Conscientiousness/Self-
Drew Fox and colleagues in the Kalin lab demonstrated

that amygdala metabolism predicted differences in
dispositional anxiety (anxious temperament) when it
was collected
A.
In stressful contexts (alone

in the novel testing cage,
human intruder)
B.
In more secure contexts

(home cage alone, home
cage with usual cagemate)
C.
Both stressful and secure

contexts
These results suggest that the "Traits x

Trait-Relevant Cues = States" model is
A.
B.
C.
True
False
True but incomplete
Individuals high in N/NE

tend to
A.
B.
C.
Show elevated reactions to

threat (bigger peak, slower
recovery)
Show chronically elevated
metabolism in regions of
the brain that help to
orchestrate states of
anxiety and arousal
Both
Trait-like differences in N/NE reflect [pick

the most correct & complete response]
A.
B.
C.
The amygdala
The amygdala and other regions
(e.g., the bed nucleus of the stria
terminalis (BNST), hippocampus,
and periaqueductal gray (PAG)).
Elevated metabolism in the
amygdala and other regions
(e.g., the bed nucleus of the stria
terminalis (BNST), hippocampus,
and periaqueductal gray (PAG))
as well as altered functional
connectivity between the
amygdala and prefrontal cortex
(PFC).
T&P potentially reflects

A.
Differences in the peak

response to perturbation
B.
Differences in the
threshold, rise time, peak
amplitude, and recovery to
baseline.
fundamental dimensions of T&P,

one based on sensitivity to
reward-predicting cues
('incentives'), the other based on
sensitivity to punishment or
threat-predicting cues. These
reflect differences in the BAS and
BIS, respectively. High-BAS
individuals
tend
A. Be more sociable,
socially to
B.
C.
dominant, and enjoy social

attention
Are predisposed to engage
in appetitively-motivated
(approach) behaviors.
Experience less anger when
their goals are thwarted.
In principle, high-BAS
individuals tend to
experience more intense
A.
"Wanting" related
emotional states
(excitement, joy, anger)
B.
"Liking" related emotional

states (contentment,
hedonic or sensual
pleasure)
BAS and BIS have been linked to

stable individual differences in
frontal EEG asymmetry. High-BIS
individuals tend to show ______,
whereas High-BAS individuals
tend to show ________ .
A.
B.
Right >> Left asymmetry

and Left >> Right
asymmetry.
Right << Left asymmetry
and Left << Right
asymmetry.
Pharmacological manipulations
(e.g., anti-anxiety drugs) and
neurofeedback manipulations
targeting frontal EEG asymmetry
don't just change the EEG, they
also change reactions to emotional
challenges.
This
suggests
that
A. The neural mechanisms that
underlie the scalp-recorded
EEG asymmetry make a
CAUSAL contribution to T&P.
B.
The neural mechanisms that

EEG asymmetry reflect a
CORRELATE of T&P
C.
The neural mechanisms that

EEG asymmetry reflect a
CONCOMITANT of T&P
Nicotine-deprived smokers anticipating a puff and

infants anticipating a reunion with their mother both
show
A.
L >> R frontal EEG

asymmetry, suggesting
that this biological
measure reflects appetitive
drive (wanting)
B.
L << R frontal EEG

asymmetry, suggesting
that this biological
measure reflects liking and
pleasure
Using daily diary techniques, Gable and

colleagues provided evidence that
differences in T&P reflect
A.
B.
C.
Differential reactivity to
motivationally-significant
daily events
Differential exposure to
motivationally-significant
daily events
Both
Converging with the results of the "resting" brain

activity studies, Gable's results suggest that T&P can
bias transient moods, feelings, and behaviors when
A.
B.
C.
Trait-relevant cues are

absent (or present)
Trait-relevant cues are
actively ignored
Both
Implicit/automatic and explicit

(declarative knowledge) processes can
A.
Be uncorrelated,
suggesting distinct neural
circuits
B. Guide behavior
C. Be disrupted by
circumscribed hippocampal
and orbitofrontal lesions,
respectively
D. A & B
E. A, B & C
Electrodermal activity (a.k.a.

EDA/SCR/GSR)
A.
Reflects changes in the

skin's resistance. Sweaty
palms (arousal) reduce the
skin's resistance,
increasing conductance.
B.
Is a measure of arousal and

can be amplified by
positive stress
(excitement), negative
stress (fear), and cognitive
challenges.
C.
Is valence-sensitive:
maximal when one is
experiencing a negative
emotional state,
intermediate for neutral
Extra Slides
Is T&P Impactful?
Is T&P Impactful? Yes!

1. Walt Mischel (1968) T&P only predicts ~10% behavior. Context is king.
2. Childhood C/SC predicts health, wealth, and public safety in early middle
age and this is mediated by teen snares
3. Childhood N/NE (BI) predicts psychopathology later in life (e.g., 3.4 risk
ratio for extreme BI vs. controls)
4. N/NE predicts a wide spectrum of mental and physical disorders
transdiag risk factor
5. Features of modern society accentuate the import of T&P
- Longevity Cumulative Impact
- Social fabric - public healthcare, public penal systems, public
education
- Increased exposure to certain lifestyle risks (sedentary, addictive
substances, retirement planning)
- Growing importance of substance abuse as well as mood and anxiety
disorders, as we have conquered other diseases; neuropsychiatric
How Should We Define T&P?
How Should We Define T&P?

Trait-like individual differences in emotion and
cognition that first emerge early in life (but
continue to evolve for many years) that
account for consistency in behavior, inner
experience, and risk across time and contexts
Are T & P Different in Kind?
Are T & P Different in Kind? No.

Classic view is that Childhood Temperament is
- innate, biological, endowed by nature/genes,
emotional
Classic view is that Adult Personality is
- plastic, environmental; reflective of nurture,
education,
and experience; more cognitive
My view is that T&P are implemented in the brain
and reflect a combination of genes/nature and
environment/nurture.
Simpler, less differentiated trait-like individual
differences (distress) become more complex over
the lifespan, in part reflecting the later maturation of
Spectrums or Types?
Spectrums or Types?
No compelling evidence for types (e.g.,
Type A), Jerry Kagan notwithstanding
Data indicates continuous individual
differences or spectra lacking discernible
zones of discontinuity (gaps or clusters)
How is T&P structured?
How is T&P structured?

Growing consensus that there are 3
broadband traits (E/PE, N/NE, and C/SC)
Little consensus about the narrow-band
facet scales
Broadband traits are probably too broad
Impedes the search for mechanistic
substrates; there is no gene or circuit for
punctuality
Fixed or Plastic?
Fixed or Plastic?
T&P traits are characterized by both continuity
(25% variance) and plasticity
If anything, more plasticity
Social relationships, reinforcements & roles have
a strong influence on the continuity of T&P
Individuals are not passive; they actively select
and
shape their environment in ways that reinforce
continuity
Your nature at birth is not your destiny, there is
Nature or Nurture?
Nature or Nurture?
T&P reflect the influence of both nature (genes; <50%)
and nurture (the environment; >50%)
Again, more plastic than was once thought
However, in many cases, environmental influences on
T&P in fact reflect the distal consequences of T&P on
physical (nighborhood, job) and social context (peers,
spouse) as well as life events (e.g., divorce); niche
building / G-E correlations
Nature and nurture should not be thought of as mutually
exclusive forces, as they often work together to influence
traits (G*E; G-E). Genes can get out of the skin;
Environment can get under the skin (epigenetics)
Causal pathways can be complex and recursive
What Are the Long-Term Prospects for

Understanding the Chain Connecting Genes to Brain to
T&P?
What Are the Long-Term Prospects for

Understanding the Chain Connecting Genes to Brain to
T&P?
Are Traits Good or Evil?
Are Traits Good or Evil? No!

No, normative variation in T&P probably
reflects the fact that traits are adaptive in
particular environments, contexts, or
cultures; (fit)
N/NE protective against danger
E/PE foraging, access to resources
such as mates, food
Is the FFM (Big 5) a Natural Kind?
Is the FFM (Big 5) a Natural Kind?

No!
Reflects the theoretical perspectives,

methods, and assumptions of key
investigators
Key assumptions underlying the 5 Factor

Model may not be warranted
- Single Words / Lexical Hypothesis
- Lay assessments and lay language
- Generic issues with single informants
and
introspective self-reports (e.g.,
artifacts,
biases, and fundamental
Are Biological Measures a Panacea?
Are Biological Measures a Panacea?

No!
To paraphrase John Cacioppo, Just
because youre measuring the brain (or
startle, or HR, GSR) doesnt mean you can
stop using your head
Still important to establish psychometric
properties, e.g., internal-consistency and
test-retest
Determining construct validity (functional
significance) is hardneed to establish
sensitivity (e.g., amyg is sensitive to fear
Is Neurogenetics a Panacea?
Is Neurogenetics a Panacea? No!

Aside from the issues raised by Kendlers Broken
Glass and Jet Mechanic metaphors, neurogenetics
confronts
-
Small effect sizes
Effect sizes can be increased at the expense of

mechanistic insight (e.g., multilocus profiles)
Massive combinatorial complexity
Problematic assumptions (e.g., that the genome

[DNA] is informative about protein expression in
the brain regions were excited about)
How are Traits & States Related? I
How are Traits & States Related? I

The traditional model going back to
Eysenck, Spielberger, Zuckerman, and
Kagan) is that traits are biological
diatheses that, in the presence of traitrelevant cues, lead to states
There is qrre and lab evidence for this
view, but it is surely incomplete
How are Traits & States Related? II

This model does not account for
1. PRE: Anticipatory affect in the absence of
cues
2. POST: Recovery-related affect in the
absence of cues
3. Motivation and instrumental behavior:
Traits can alter the probability of
encountering cues, which tends to regulate
emotional states
How are Traits & States Related? III

These phenotypic data are consistent with
growing evidence that the spontaneous,
ongoing activity of the brain predicts T&P
Chronic alterations in neural activity may, in
turn, help to explain differences in emotion
and cognition in the absence of trait-relevant
cues (e.g., why anxious individuals show
pervasive distress in the absence of threat)
Does T&P Simply Reflect

Differences in the Peak?
Does T&P Simply Reflect

Differences in the Peak? No!
No, other parameters are likely to be
important
Hi Trait e.g. N/NE
Lo Trait e.g. N/NE
Rise Time to Peak
Threshold
Peak Amplitude
Recovery Time
(Regulation/Decay)
Mood Spillover in the
ESM Lit.
What are some strategies for dissecting T&P

into simpler, mechanistically-important constituents?
What are some strategies for dissecting T&P

into simpler, mechanistically-important constituents?
Endophenotypes (Gottesman)
- causal, heritable, fixed, and simpler (not necessarily
bioll)
- bridge between genes and 1 or multiple phenotypes (T&P)
- T&P (e.g., BI) can serve as an endophenotype for Dx
- Some endos have been identified (e.g., P300 for
externalizing), but the links from the endo down to the genes
and up to the phenotype remain murky
Biomarkers
- all endos are biomarkers, but not all biomarkers are
endophenotypes
- again, the idea is to simplify
Cross-Species Comparisons (Borsook)
- difficult to establish causation in humans; need
mechanistic models
- animals do not suffer from human diseases
- identifying common brain circuits provides validation
How is T&P causally related to Dx?
How is T&P causally related to Dx?

To be honest, we do not yet really know
The most consistent evidence is for Common
Cause
But the Spectrum and Diathesis-Stress
models have nearly as much support
Depends on the Dx (e.g., D-S for substance
use)
N/NE is a Transdx Risk Factor. Why?
N/NE is a Transdx Risk Factor. Why?

The trait and the individual diagnoses
have much in common
- structural analyses indicate spectra not
silos
- high co-morbidity across Dxs
- overlapping Tx effects
- shared neural correlates (e.g., amyg)
- shared envtl liabilities (adversity, abuse)
- relatively strong genetic correlation
- common psychological phenotype
(intolerance of uncertainty, elevated NE,
etc.); common intermediate phenotype
(biomarker): amygdala
How Should We Dissect N/NE?

(Just Remember Pete & Paul!)
How Should We Dissect N/NE?

(Just Remember Pete & Paul!!)
1. Inflated estimates of threat (burglar, not
raccoon)
2. Elevated vigilance / threat bias (creaking
floorboards)
- Causal role; amygdala
3. Deficient safety learning and overgeneralization
(forgets alarm)
- Predicts 1st onset
4. Elevated threat avoidance (locks self in
bedroom); MCC?
5. Elevated reactivity (or deficient regulation of
Why Does the Amygdala Do So Much Heavy

Lifting in Theories of N/NE/Anxiety/BI?
Why Does the Amygdala Do So Much Heavy

Lifting in Theories of N/NE/Anxiety/BI?
What Are the Prospects for

Intervention?
What Are the Prospects for

Intervention?
Pretty good! Opportunity for growth &

positive change!
- T&P is more plastic than fixed
- Highly heritable traits are amenable to
intervention (e.g., height, IQ)
- Early intervention might prevent longterm cumulative damage (cf. BI) and
minimize evocative
and active G-E effects (make Mommy mad;
hang with delinquents; Teen Snares)
An integrative, multi-disciplinary
perspective on the science of T&P
When a scientist doesnt know the answer to a
problem, he is ignorant. When he has a hunch
as to what the result is, he is uncertain. And
when he is pretty damn sure of what the result
is going to be, he is still in some doubt
Scientific knowledge is a body of statements of
varying degrees of certaintysome most
unsure, some nearly sure, but none absolutely
certain.
Richard Feynman (1955), Nobel Laureate
An integrative, multi-disciplinary
perspective on the science of T&P
Science is not a body of facts established by experts, but a
set of methods for estimating and reducing uncertainty;
It is a process, at times messy or tedious, of grappling with
nature and our preconceived notions about how it works.
There are many, many fundamental questions about T&P
that remain unresolved.
Thats one of the things that make this class so fun! We
havent figured it out and there are many challenges that
remain for future research.

Shackman Psyc210 Module20 SemesterRecapAndFinalExamReview

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When a scientist doesnt know the answer to a

problem, he is ignorant. When he has a hunch as

PSYC 210: Temperament and

Where Did We Begin Our

Where Did We Begin Our

Where Did We Begin Our

Where Did We Begin Our

Use Science to Dispel Ignorance

Use Science to Dispel Ignorance

Use Science to Dispel Ignorance

Use Science to Dispel Ignorance

Use Science to Dispel Ignorance

Use Science to Dispel Ignorance

Use Science to Dispel Ignorance

Use Science to Dispel Ignorance

What did we actually learn?

What did we actually learn?

Statistical Tools and Concepts

Statistical Tools and Concepts

Brain Regions and Systems

Brain Regions and Systems

Methods and Measures

Methods and Measures

Famous and Not-So-Famous Scientists

Are temperament and personality

How many dimensions or types of

Where did these dimensions come from;

What exactly does it mean to be neurotic?

Is The Situation the primary determinant of

How stable are trait-like individual

How are traits related to emotional states?

How does T&P interact with cues, challenges, and

Does T&P reflect nature, nurture, or both?

Is depression just being really sad?

Is addiction just an excess of approaching highs and

Some Broad Take Home

T&P Are Important,

One important way in which temperament influences

T&P Are Important,

One important way in which temperament influences

T&P Are Important,

One important way in which temperament influences

I am really proud of you guys and all that you

Be Proud of Your New Knowledge and New Ways

Take Home Question

Take Home Question

Take Home Question

Take Home Question

Take Home Question

Based on fear conditioning studies in the

A. Amplified signs of anxiety

Real-time fMRI neurofeedback

Family, twin, and adoption studies (aka

Many or most individuals with diagnosable

T&P reflect trait-like individual differences in

A. First emerge in mid-life

Mechanistic studies in animal models

Are there pleasure centers in the

Individuals who show increased

fMRI signals in the ventral striatum are

Substance abuse disorders are associated

Which is the more correct

Which is FALSE: Height is

Substance abuse disorders reflect