Exam #2 Flashcards
Categories of Emotional Appraisals
Cognitive and Emotional Interactions beginning
1) Threat (Distress)
2) Challenge (Eustress)
3) Benign or Irrelevant
valence? activation?
1) Threat (Distress) vs Challenge (Eustress) Emotional Appraisal?
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
Benign or Irrelevant Emotional Appraisal?
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.
Types of primary appraisals?
Primary (emotional) appraisal?
- 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
questions to ask?
Secondary (emotional) appraisal?
- 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?
Implicit Appraisals: Unconscious emotional associations
1) Emotional appraisals do not have to be fully conscious
* Appraisals may be implicit
* Due to past experiences and conditioning
Implicit Appraisals: Classical conditioning?
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
Amygdala, which memory?
- 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
Coping Strategies: Problem-focused vs emotion-focused coping
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.
“Gut” vs ‘‘Mental” feelings (which brain areas and appraisals)
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
Brain Areas involved in Emotional Appraisals and Regulation (frontolimbic connections)
- Frontal Areas —> prefrontal lobe (PFC), anterior cingulate cortex (ACC)
- Limbic System —> Amygdala, hippocampus, hypothalamus
- Connections between frontal areas and limbic areas (frontolimbic connections)
Amygdala Nucleii? Types and function?
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
LeDoux’s Low Road vs. High Road of Fear
connections? conscious vs non?
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
connections and regulation
CRF Feedback System
- 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
CRF Feedback System: Aminergic Nuclei
Cognitive and Emotional Interactions END
Aminergic Nuclei in the brainstem:
1) Ventral Tegmental Area
2) Raphe Nuclei
3) Locus Ceruleus
Ventral Tegmental Area
- Dopamine ”circuit” (also connects to nucleus accumbens)
- Regulates motivation and reward (related to addiction)
Raphe nuclei
- Serotonin (sends signals between your nerve cells) “circuit”
- Regulates mood (related to anxiety and depression)
Locus ceruleus
- Norepinephrine “circuit”
- Regulates attention and arousal (related to sleep vs. waking)
HSAM? regulated by? connects to? projections to?
Stress Sensitization begin
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
HPAC? regulated by? connects to?
HPAC = Hypothalamus —> Pituitary —> Adrenal Cortex
* Regulated by medial PVN
* Connects to pituitary (release ACTH)
* Release of cortisol from the cortex of adrenal gland
Epinephrine and Norepinephrine (common)
- Hormones released by sympathetic activation
- Increase release of stored energy (fat and sugar)
- Increase blood pressure. Increase inflammation.
Epinephrine vs Norepinephrine (differences)
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)
What’s cortisol? Traits?
- 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)
Effects of Cortisol?
- 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)
Circadian Rhythm of Cortisol Regulation? Which parts of brain?
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)
minor stressor on a day-to-day basis
A “normal” Stress Response (to a momentary stressor) ask!!
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)
Hormones in Harmony
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
Stress Hormones list?
When CRF levels increase in Amygdala…
- More activation of magnocellular (CRF-AVP) neurons in the PVN
- More cortisol released…less negative feedback
Amygdala involved in regulating?
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
Sensitization to Stress (Amygdala?)
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
Result of Stress Sensitization?
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
Hypervigilance? ask!!
- 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.
Individual vulnerability to Stress Sensitization
stress sensit. end
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
Dysregulation of stress responses linked to?
Blunted vs. Exaggerated Reactivity beginning
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
Exaggerated Reactivity?
- 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).
Blunted reactivity?
- 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.
baseline cortisol levels? stress reactivity?
Blunted Reactivity Research (2012)
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
Early Life Stress predicted
Blunted Reactivity Research (focus on this)
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
Individual Differences
Level of Control over stress responses
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
Article #3 - “Cortisol induced impairments…” Conclusions
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
Article #4 - “Amygdala response…” Conclusions
(* 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)
