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Psyc 362- Behavioral Neuroscience > Emotions, Aggression, and Stress > Flashcards

Emotions, Aggression, and Stress Flashcards

Final Exam

1
Q

What is an emotion?

A
  • Subjective mental state usually accompanied by distinctive behaviors, feelings, and involuntary physiological changes (ex. rapid heartbeat, tears, blush caused by autonomic nervous sytem)
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2
Q

What do emotions facilitate?

A

Social contact and learning

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3
Q

How many core emotions are there?

A

there are 6-8 core sets of emotions w various degrees of intensity

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4
Q

What are the high level of intensity emotions?

A

Ectasy, adoration, terror, amazement, grief, loathing, rage, and vigilance

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5
Q

What are the medium level of intensity emotions?

A

Joy, affection, fear, surprise, sadness, disgust, anger, expectation

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6
Q

What are the low level intensity of emotions?

A

Happiness, regard, apprehension, distraction, pensiveness, boredom, annoyance, alertness

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7
Q

How is emotion communicated?

A
  • through verbal communication (words, tone of voice)
  • and non-verbal communications (body language, facial expressions)
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8
Q

What is the purpose of facial expressions?

A

Facial expressions provide emphasis and context for verbal communication to your audience

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9
Q

Do people around the world agree on human emotions?

A
  • There are both biological and cultural influences but there is agreement about the meaning of most facial expressions
  • Happiness is the most agreed upon emotion
  • Non-literate isolated groups had trouble with disgust and surprise recognition
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10
Q

Individual variability

What percentage of infants had low and high reactivity?

A
  • Reactivity was measured in 4 month old infants
  • Low reactivity seen in around 40% of infants
  • High reactivity seen in around 20% of infants
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11
Q

Individual variability

What are high reactive children biased to become?

A
  • timid, shy, cautious in unfamiliar situations (risk averse)
  • greater risk for anxiety disorders
  • exaggerated amygdala response
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12
Q

Individual variability

What are low reactive children biased to become?

A

outgoing, spontaneous, and fearless

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13
Q

What is intra-cranial self stimulation?

A
  • A type of operant conditioning where stimulation of certain brain region may be reinforcing or aversive
  • Reinforcement may or may not correlate with subjective pleasure
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14
Q

How is the medial forebrain bundle related to emotions?

A
  • Positive emotion is elicited by stimulating the medial forebrain bundle (anials will work hard to recieve mild stimulation here)
  • The VTA area releases dopamine into the nucleus accumbens
  • Researchers have proposed that drugs of abuse are addictive because they activated these same neural circuits with an artificial intensity
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15
Q

Papez circuit-limbic system

What does stimulating the limbic system elicit?

A

negative emotion

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16
Q

Papez circuit/limbic system

What happens when you lesion an overactive amygdala?

A
  • increased social affiliation
  • decreased anxiety
  • increased confidence
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17
Q

What is the central amygdala a hub for?

A

anxiety, stress, fear, and addiction

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18
Q

What causes kluver-bucy syndrome and what are the symptoms?

A
  • Caused by lessions/removal of portions of temporal lobes (esp amygdala and hippocampus)
  • Symptoms include: dramatically lessened fear and aggression, blunted affect (decreased ability to express emotion), hyperorality, hypersexuality, and visual agnosia (inability to recognize or interpret visual info)
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19
Q

What were patient S.M’s symptoms?

A
  • developed fearlessness in childhood
  • outgoing, but few good friends
  • confronts risk
  • normal nervous system responses
  • unafraid of spiders/snakes
  • little social fear or sense of personal space
  • no (or very low) normal sympathetic nervous system response to nromally fear-evoking stimuli
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20
Q

What does the amygdala “low road” do?

A
  • direct projection from the thalamus to the amygdala
  • bypasses conscious processing and allows for immediate emotional reactions to stimuli
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21
Q

What does the amygdala “high road” do?

A
  • routes incoming info through sensory cortex, allowsing for processing that is slower, but is also conscious, fine-grained, and integrated with higher-level cognitive processes (like memory)
  • contributions from prefrontal cortex and anterior cingulate offer an additional level of fear conditioning called observational fear learning (when fear of potentially harmful stimuli is learned through social transmission)
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22
Q

What detects external threats?

A

the amygdala

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23
Q

What detects internal threats?

A

the brainstem

24
Q

Brain regions during sadness

A
  • anterior cingulate cortex activity increases
  • posterior cingulate corex activity decreases
  • dorsal pons activity increases
  • insula activity increases
25
Q

Brain regions activated during happiness

A
  • right posterior cingulate cortex activity increases
  • left insula activity increases
  • left anterior cingulate cortex activity decreases
26
Q

Brain regions activated by fear

A
  • midbrain activity increases
  • orbitofrontal region of prefrontal cortex activity decreases
27
Q

Anger brain regions

A
  • pons activity increases
  • left anterior cingulate cortex activity increases
28
Q

What happens during the initial response to stress?

A
  • The hypothalamus activates the sympathetic nervous system to stimulate many phsiological systems, including the adrenal medulla which releases norepinephrine, works quickly
  • Hypothalamus also stimulates the anterior pituitary to release hormones that drive the adrenal cortex to release cortisol, works slowly (known as Hypothalamus Pituitary Adrenal axis)
29
Q

How do norepinephrine and ephinephrine levels respond to stress?

A

both increase when stressed

30
Q

Autonomic Nervous System

A
  • Sympathetic: fight or flight, governed by norepinephrine
  • Parasympathetc: relaxation, governed by acetylcholine
  • Parasympathetic and sympathetic often oppose each other
31
Q

What does the adrenal cortex/adrenal gland secrete?

A

steriods, including glucocorticoids

32
Q

What is cortisol and what does it do?

A
  • Cortisol is a glucocorticoid hormone that prepares the body to deal with stress
  • increases blood glucose levels to energize you to respond to the situation you are in
  • Also promotes metabolism and suppresses inflammation
33
Q

What is positive about having early stressful experiences?

A

can allow for later resilience, known as stress immunization

34
Q

What happens if you have significant early life stress?

A
  • greater stress responses
  • learning deficits
  • long-lasting changes in brain steroid receptor expression, driven partly by epigenetic regulation (is where we get individual differences in babies’ reactivity)
35
Q

What does it mean to have a negative affect?

A
  • experience the world in negative terms
  • higher levels of distress, anxiety, and dissatisfaction
  • low subjective sense of wellbeing
36
Q

What increases risk for a negative affective disorder?

A
  • genetic risk: many genes contribute to susceptibility
  • chronic, lower grade stressors: increse risk for anxiety disorders/depression
37
Q

General adaptation to stress theory: Phase 1

A

Alarm reaction: body mobilizes to confront the threat

38
Q

General adaptation to stress theory: Phase 2

A
  • Resistance: body actively copes with the threat, has resistance
39
Q

General Adaptation to Stress Theory: Phase 3

A

Exhaustion: if the threat continues reserves are depleted, the body “gives up” and can’t do it anymore

40
Q

General adaptation to stress theory: What happens do to chronic stress?

A
  • chronic stress produces excess alarm and resistance
  • contributes to the development of negative affective disorders
41
Q

What biological markers show there is less adaptation to stress in negative affective disorders?

A
  • People with depression have higher plasma cortisol levels all of the time
  • DEX only momentarily suppresses plasma cortisol levels, then they go back to typical high levels
42
Q

What does DEX do?

A

suppresses cortisol in typically healthy individuals experiencing a stressful situation

43
Q

Generalized anxiety disorder

A

person is always very anxious, baseline is at an anxious level (chronic anxiety, exaggerated tension)

44
Q

OCD

A

recurrent unwanted thoughts (obsessions) and/or repetitive behaviors (compulsions)

45
Q

Panic disorder

A
  • person goes into panic mode much more frequently than healthy individuals
  • things that do not typically elicit a panic response will elicit a panic response
  • unexpected, repeated episodes of intense fear and physical symptoms
46
Q

Post traumatic stress disorder

A
  • memories of unpleasant events that produce same intense visceral arousal
  • people will have physiological response when placed in similar context to where the traumatic event occured
47
Q

Social anxiety disorder

A
  • overwhelming anxiety and excessive self-consciousness in everyday social situations
48
Q

What part of the brain is atrophied in individuals with PTSD?

A
  • the hippocampus
  • causal relationship… not sure if PTSD causes hippocampal atrophy or visa versa
49
Q

How is fear conditioning done?

A
  • Tone is associated with a mild electrical shock
  • Eventually tone alone will elicit a freezing response (along with raised BP)
  • If tone has a regular pattern, the animal will habituate
  • But, chronic unpredictable stressor (tone) will continue to elicit freezing
50
Q

Model of PTSD

A
  • Original trauma: activates the alarm stress systems and the amygdala
  • Subsequent stressors: produce heightened alarm stress response (sensitization)
  • This will trigger a traumatic memory via the amygdala
  • Over time, traumatic memory associations and physiological response are strengthened
51
Q

Alarm stress systems acute neurochemical responses:

A
  • Locus coeruleus (norepinephrine)
  • VTA (dopamine)
  • Endogenous opiods
  • Corticotropin-releasing hormone

Reciprocal interactions between these and the amygdala may facilitate the encoding and retrieval of traumatic memories

52
Q

Depression symptoms

A
  • Unhappy mood
  • loss of interests
  • loss of appetite and energy
  • difficulties with concentration
  • restless agitation
53
Q

Brain changes seen with depression

A
  • Greater brain activity in the PFC and amygdala that persists after depression period is over- electroconvulsive therapy can sometimes revert depression
  • Smaller hippocampus
  • Reduced monoamine (serotonin, dopamine, and norepinephrine) transmitter activity… why we use SSRIs
54
Q

What is comorbidity?

A
  • when two disease traits co-occur at a frequency that is higher than expected based upon the base rates of the two alone
  • MDD and GAD most common (58% cases are comorbid)
55
Q

Criticisms of Medical treatments of depression and anxiety

A
  • non-medical treatments (CBT) work
  • placebo effects
  • medications are not effective in some people
56
Q

Therapeutics for depression and anxiety

A
  • SNRIs (Serotonin-Norepinephrine Reuptake inhibitors)
  • Electroconvulsive therapy
  • Ketamine- NMDA receptor antagonist
  • CBT
57
Q

MAOs vs Tri/heterocyclics vs SSRIs

A
  • MAOs inhibit the enzyme monoamine oxidase that breaks down serotonin, dopamine, and norepinephrine
  • Cyclics inhibit reuptake of said neurotransmitters (sometimes all sometimes some)
  • SSRIs block reuptake of serotonin w little effect on dopamine and norepinephrine

Psyc 362- Behavioral Neuroscience (24 decks)

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