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Stress and the Brain > Exam #2 > Flashcards

Exam #2 Flashcards

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1
Q

Categories of Emotional Appraisals

Cognitive and Emotional Interactions beginning

A

1) Threat (Distress)

2) Challenge (Eustress)

3) Benign or Irrelevant

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2
Q

valence? activation?

1) Threat (Distress) vs Challenge (Eustress) Emotional Appraisal?

A

Threat (Distress):
- Stressor is dangerous or overwhelming
- Requires activation, negative valence (aversive)
- Sympathetic activation with large increase in cortisol (HPA axis)

Challenge (Eustress):
positive stress response
* Stressor may be engaging or rewarding
* Requires activation, positive valence (appetitive)
* Sympathetic activation with minor increase in cortisol

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3
Q

Benign or Irrelevant Emotional Appraisal?

A

it can be stressful to you, but not others
* Benign = “Stressor” is not stressful. May be harmless or even pleasant.
* Irrelevant = “Stressor” does not apply to you, even if it’s aversive to others.
* Does not require activation.
* Parasympathetic nervous system. Return to homeostasis.

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4
Q

Types of primary appraisals?

Primary (emotional) appraisal?

A
  • Immediate and first emotional appraisal (1-st reaction: is this a threat? - fear)
  • Influenced by personal relevance, cognitive beliefs, and behavioral commitments (goals)
  • Biased towards searching for threatening information.
  • Types of primary appraisals: Threat, Challenge, Benign, or Irrelevant
  • Fronto-limbic connections
  • Can be conscious or unconscious
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5
Q

questions to ask?

Secondary (emotional) appraisal?

A
  • Follows the primary appraisal (reaction to another reaction) or Re-interpretation of emotion (Your reaction to your reaction)
  • Involves cognitive evaluations of initial emotion and attempts to regulate emotional reactions
  • How to respond to or how to cope with the situation?
  • What will be required? What resources are available?
  • Can the stressor be minimized or avoided?
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6
Q

Implicit Appraisals: Unconscious emotional associations

A

1) Emotional appraisals do not have to be fully conscious
* Appraisals may be implicit
* Due to past experiences and conditioning

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7
Q

Implicit Appraisals: Classical conditioning?

A

1) Classical conditioning
* A stimulus that was initially neutral, gets paired with a stimulus that evokes an emotional response
* Later the stimulus that was neutral, now evokes that some emotional response

2) Classical conditioning does not require conscious awareness
* Individuals with severe amnesia can still learn from classical conditioning
* Can be conditioned while asleep
* Damage to hippocampus does not interfere with classical conditioning

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8
Q

Amygdala, which memory?

A
  • Best known for processing emotions
  • But…can also create “emotional memories”
  • Amygdala can create implicit memories (Which can remain unconscious)
  • Classical conditioning is implicit memory: The Amygdala (not the hippocampus) is required for classical conditioning
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9
Q

Coping Strategies: Problem-focused vs emotion-focused coping

A

1) Problem-focused coping:
* Coping based on trying to solve the problem causing stress
* Involves trying to understand the problem, devise a strategy to deal with it.
* Pros: May ”solve” the problem. Lessen, minimize, or avoid future stress.
* Cons: May be initially costly in time, energy, and resources.

2) Emotion-focused coping:
* Coping based on dealing with the emotional feeling of stress.
* Involves trying to limit the emotional reaction.
* May involve avoidance, denial, acceptance, venting, or blame.
* Pros: Initially less costly.
* Cons: The problem isn’t solved. Drains coping resources over the long-term.

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10
Q

“Gut” vs ‘‘Mental” feelings (which brain areas and appraisals)

A

Visceral or “Gut” feelings (aspects of emotions) - emotion regulation more associated with ventral PFC and ACC fronto-limbic connections - Primary appraisal.

“Mental” or cognitive aspects of emotions, emotional regulation (feelings) more associated with dorsal PFC and ACC fronto-limbic connections - Secondary Appraisal.
* Secondary appraisals may adjust the balance of “mental” vs “visceral” components

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11
Q

Brain Areas involved in Emotional Appraisals and Regulation (frontolimbic connections)

A
  • Frontal Areas —> prefrontal lobe (PFC), anterior cingulate cortex (ACC)
  • Limbic System —> Amygdala, hippocampus, hypothalamus
  • Connections between frontal areas and limbic areas (frontolimbic connections)
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12
Q

Amygdala Nucleii? Types and function?

A

Basolateral nuclei:
* learning “emotional” associations, classical conditioning

Central nuclei
* Regulates “fear” responses
* Connections to face (fearful facial expressions)
* Connections to hypothalamus (sympathetic activation… also CRF feedback)
* Connections to vagus nerve (feedback about sympathetic activation)
* Connections to brainstem (aminergic nuclei that influence attention, motivation, mood)
* The central nuclei of the amygdala plays a direct role in how our bodies respond to stress

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13
Q

LeDoux’s Low Road vs. High Road of Fear
connections? conscious vs non?

A

1) LeDoux’s Model of Fear Processing
* Amygdala can generate fear response consciously and unconsciously.

2) Low-road
* Connections from thalamus to amygdala
* Amygdala processes sensory info independent of cortex
* Fast, unconscious processing

3) High-road
* Sensory info processed by cortex prior to amygdala
* Slowe, conscious processing

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14
Q

connections and regulation

CRF Feedback System

A
  • Connections from brainstem back to frontal and limbic areas
  • This feedback system helps regulate emotional appraisal and responses
  • Particularly with stress that causes prolonged sympathetic activation
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15
Q

CRF Feedback System: Aminergic Nuclei

Cognitive and Emotional Interactions END

A

Aminergic Nuclei in the brainstem:

1) Ventral Tegmental Area

2) Raphe Nuclei

3) Locus Ceruleus

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16
Q

Ventral Tegmental Area

A
  • Dopamine ”circuit” (also connects to nucleus accumbens)
  • Regulates motivation and reward (related to addiction)
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17
Q

Raphe nuclei

A
  • Serotonin (sends signals between your nerve cells) “circuit”
  • Regulates mood (related to anxiety and depression)
18
Q

Locus ceruleus

A
  • Norepinephrine “circuit”
  • Regulates attention and arousal (related to sleep vs. waking)
19
Q

HSAM? regulated by? connects to? projections to?

Stress Sensitization begin

A

HSAM = Hypothalamus-> Sympathetic -> Adrenal Medulla
* Regulated by dorsal and ventral PVN
* Connects to brainstem
* Projections to organs of SNS
* Release of epinephrine and norepinephrine from medulla of adrenal gland

20
Q

HPAC? regulated by? connects to?

A

HPAC = Hypothalamus —> Pituitary —> Adrenal Cortex
* Regulated by medial PVN
* Connects to pituitary (release ACTH)
* Release of cortisol from the cortex of adrenal gland

21
Q

Epinephrine and Norepinephrine (common)

A
  • Hormones released by sympathetic activation
  • Increase release of stored energy (fat and sugar)
  • Increase blood pressure. Increase inflammation.
22
Q

Epinephrine vs Norepinephrine (differences)

A

Epinephrine:
* Greater activation of “beta” adrenergic receptors in the body.
* Bigger impact on heart rate and force of heart contractions (to increase blood pressure).
* Epi at the pituitary stimulates ACTH release —> increases cortisol
* Amygdala can monitor epi levels through beta-receptors on vagus nerve

Norepinephrine:
* Greater activation of “alpha” adrenergic receptors in the body
* Bigger impact on blood vessels (to increase blood pressure)
* Also, a major neurotransmitter that regulates attention (locus ceruleus)

23
Q

What’s cortisol? Traits?

A
  • Hormone of the HPA axis
  • A steroid hormone (made from cholesterol)
  • Glucocorticoids include cortisol (humans) and corticosterone(rats)
  • Cortisol has many, many effects in the body and in the brain (Cortisol can pass through the blood-brain barrier)
24
Q

Effects of Cortisol?

A
  • Stimulates catecholamine synthesis (make more epi, norepi, dopamine)
  • Sensitivity of aminergic receptors (increase response to epi and norepi)
  • Increase energy supply (burn carbs, releases fats)
  • Increase intensity of sensory stimulation (thalamus)
  • Enhance memory function (hippocampus activation)
  • Decrease inflammation (immune system)
25
Q

Circadian Rhythm of Cortisol Regulation? Which parts of brain?

A

Normal Cortisol Regulation:
1) Daily cycle. Peaks in the morning, decreases throughout day, lowest while asleep
2) Regulated by suprachiasmatic nucleus (SCN) of hypothalamus
* Connects to PVN of hypothalamus (control of HPA axis)
* Connects to pineal gland (to control release of melatonin)

26
Q

minor stressor on a day-to-day basis

A “normal” Stress Response (to a momentary stressor) ask!!

A

1) Sympathetic activation (HSAM):
* Autonomic —> direct control of heart, lungs, muscles, blood pressure
* Endocrine —> release epinephrine

2) Increase HPA axis (HPAC)
* Cortisol release occurs after brief delay (about 15 minutes)

3) Negative feedback loops turn off HPA axis
* Parvocellular neurons in the PVN (Controls normal level of cortisol secretion).
* Sensitive to low levels of cortisol. Turn off due to negative feedback.
* Cortisol returns to “normal” levels

(magnocellular don’t turn off easily, so cortisol levels get very high)

27
Q

Hormones in Harmony

A

1) HSAM and HPAC talk to each other and increase each other’s effects:
* HSAM —> release epi and norepi —> triggers activation of HPAC (short-term response)
* HPAC —> release cortisol —> makes body more responsive to epi and norepi (long-term response)

2) Extended activation of both can lead to stress sensitization

28
Q

Stress Hormones list?

A
29
Q

When CRF levels increase in Amygdala…

A
  • More activation of magnocellular (CRF-AVP) neurons in the PVN
  • More cortisol released…less negative feedback
30
Q

Amygdala involved in regulating?

A

1) Amygdala monitors HSAM and HPAC —> uses CRF to signal the PVN (“intense stress”)
2) PVN of hypothalamus:
* Activates magnocellular neurons (CRF-AVP neurons) —> way more ACTH –> way more cortisol
* Magnocellular neurons less responsive to negative feedback

31
Q

Sensitization to Stress (Amygdala?)

A

High levels of cortisol activate Type 2 (GR) cortisol receptors in amygdala:
* Type 2 can alter gene expression (Increases release of CRF with vasopressin):

1) Amygdala “remembers” associations with the stressor.

2) Amygdala has become sensitized. Similar stresses in the future will trigger bigger stress responses

  • Increased CRF in amygdala —> more ACTH and Cortisol release (increased stress reactivity)
  • Increased CRF in locus ceruleus (more epinephrine release) —> increased arousal and alertness (hypervigilance)
  • Stress-induced cortisol regulation allows cortisol levels to increase beyond “normal” levels
32
Q

Result of Stress Sensitization?

A

1) Increased reactivity:
* Bigger HPA response (HPAC) (more cortisol, less negative feedback)
* Bigger sympathetic response (HSAM) - More cortisol means the body makes more and is more sensitive to epi and norepi

2) Hypervigilance: increased arousal and alertness

33
Q

Hypervigilance? ask!!

A
  • Activation of CRF feedback system —> greater activation of the locus ceruleus.
  • Increased norepinephrine in the brain —> more attention and arousal.
  • Less attentional control (unable to change the focus of attention).
  • Useful for detecting threats in the environment.
34
Q

Individual vulnerability to Stress Sensitization

stress sensit. end

A

1) But, sensitization is long-lasting:
* May continue to have large stress responses even to mild stressors

2) Individual vulnerability:
* Hippocampus stronger negative feedback for HPA
* Helps “turn off” signals from the amygdala
* People with smaller hippocampus, more vulnerable to stress sensitization

35
Q

Dysregulation of stress responses linked to?

Blunted vs. Exaggerated Reactivity beginning

A

poor mental and physical health:
* Both exaggerated and blunted responses “unhealthy”
* Still unclear how or what types of stressors lead to blunted vs. exaggerated reactivity

36
Q

Exaggerated Reactivity?

A
  • May be triggered by traumatic stressful experiences.
  • More reactive stress responses. Weaker negative feedback system. (Stress response easily activated. Hard to turn off.)
  • More cortisol released. Bigger heart rate increase. (May be adaptive in threatening environments that require vigilance.)
  • More avoidance, less approach motivation.
  • Associated with Heart Disease, Hostility, trauma related anxiety (PTSD).
37
Q

Blunted reactivity?

A
  • May be caused by extended early life stress (like poverty or neglect)
  • Less reactive stress responses. Stronger negative feedback system - Stress response not easily activated. Turns off quickly.
  • Less cortisol released. Smaller heart rate increase - May be adaptive to protect body from allostatic load of high cortisol
  • More approach, less avoidance motivation
  • Associated with Alcoholism, Addiction, Depression, Obesity - Poor impulse control. More sensation seeking.
38
Q

baseline cortisol levels? stress reactivity?

Blunted Reactivity Research (2012)

A

No differences in baseline cortisol levels due to early life stress or gender
* On resting days, similar cortisol levels for men and women regardless of early life stress

Early life stress and gender predicted differences in stress reactivity:
* More early life stress —> less reactivity
* Women showed less reactivity
* Less cortisol change.
* Less heart rate change

39
Q

Early Life Stress predicted

Blunted Reactivity Research (focus on this)

A

Poor self-control
Early Life Stress predicted:
1) Less executive function
* More difficulty on Stroop Task

2) Less maturity
* Rated to have lower “mental age”
* “Act your age”

3) More impulsivity
* Less able to delay gratification

4) Larger BMI
* More likely to be overweight

5) Early Life Stress predicted:
* More antisocial behavior
* More neurotic personality traits
* Can be emotionally volatile, irritable
* More depression symptoms
* More novelty seeking
* Less behavioral control
* Less sociability

40
Q

Individual Differences

Level of Control over stress responses

A

1) Fronto-limbic (Level 1):
* Thoughts, Feelings, and Memories
* Frontal lobes (PFC and ACC), Amygdala, Nucleus Accumbens (dopamine system)
2) Hypothalamus-Brainstem (Level 2):
* Gain factors on autonomic and endocrine responses
* PVN, Locus Ceruleus, Raphe Nuclei, VTA (ventral tegmental area)
3) Peripheral Organs (Level 3):
* How the body responds
* Heart, lungs, stomach, kidneys

41
Q

Article #3 - “Cortisol induced impairments…” Conclusions

A

Trier Social Stress Test: Given 5 min to prepare a 5 min speech about a topic, then given the speech in front of a small audience (3 psychologists).

  • Working Memory (WM) most impaired immediately after TSST
  • Although the stress task did not evoke similar levels of stress in all participants…
  • ….Working memory was significantly impaired for those that were stressed (large increase in cortisol).
  • Cortisol levels alone did not predict lower working memory, only cortisol levels in response to stress - Cortisol levels were still elevated after recovery…. But sympathetic activation was back to normal
  • Both sympathetic activation and high cortisol levels (HPA) required to impact WM
42
Q

Article #4 - “Amygdala response…” Conclusions

A

(* Used prior fMRI data of amygdala activity while viewing negative images to predict PTSD symptoms after a terrorist attack * Greater amygdala activity to negative images predicted higher PTSD symptoms after a terrorist attack (Boston Marathon bombing).)
* Amygdala activity when reacting to negative images
* More activity —> more PTSD after bombing
* Hippocampus activity when regulating emotional reactions
* More activity —-> less PTSD after bombing
* Hippocampus activity was no longer correlated with PTSD symptoms after the bombing
* Amygdala activity was still strongly correlated with PTSD symptoms
* Helps show that PTSD symptoms in response to the bombing were best predicted by pre-existing amygdala reactivity
* Evidence that pre-existing differences in amygdala reactivity makes people more vulnerable to developing PTSD after a traumatic event (this evidence is rare)

Stress and the Brain (20 decks)

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