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Stress and the Brain > Exam #3 > Flashcards

Exam #3 Flashcards

1
Q

What are genes? Function?

A

Genes - Sequences of DNA that code for proteins.
A gene is a blueprint for how to build a particular protein.

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2
Q

Sex-Linked Traits (sex chromosomes male vs female)

A
  • The sex chromosomes (X or Y)
  • Males = XY. Females = XX
  • Males have one X chromosome which comes from their mother
  • Females have two X chromosomes, one from mom. One from dad. In females, only one X chromosome is active in each cell of the body
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3
Q

Gene X Environment Interactions results (Caspi et al., 2002)

A

3) Measurements of adult social adjustment
* Antisocial personality, conduct disorder, prone to violence, criminal history

Results
* Interactions of low activity MAO and early life stress predicted poor social adjustment

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4
Q

MAO and Antisocial behavior

A

1) Childhood experiences of mistreatment were associated with high levels of antisocial behavior (in general)
2) Low activity MAO gene by itself was not linked to more antisocial behavior
3) But…individuals with the low activity MAO gene were more negatively impacted by experiences of mistreatment
* More antisocial behavior
* Genes + childhood stress was best predictor of adult antisocial behavior

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5
Q

Which gene? Serotonin transport and Depression

(Caspi et al., 2003)

A

Caspi et al, 2003 - Dunedin Cohort

1) Study of childhood maltreatment and adult symptoms of depression
* Long/long (l/l) vs. short/short (s/s) vs. short /long(s/l) alleles

2) Measures
* Childhood maltreatment between ages 3 -11
* Recent life stresses between ages 21 -26

3) Results
* Both childhood maltreatment and recent stresses interact with 5-HTT genes to predict symptoms of depression
* Individuals with two copies of the short serotonin transporter gene were more vulnerable to developing depressive symptoms
* Genes + childhood stress was best predictor of depression in adulthood

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6
Q

DNA Methylation

A

tag certain genes to be expressed (or not)
* A methyl group (CH3) added to DNA
* Methylation can deactivate (and sometimes activate) genetic expression
* Typically added to the cytosine in DNA (The C’s of the A, C, G, T)

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7
Q

Histone modification?

A

hide or expose genes by wrapping them around the histone
* Histones are proteins that DNA wraps around
* Histone deacetylase wraps the DNA more tightly which makes the gene inaccessible

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8
Q

Gene X Environment interactions also related to….

A

Individual differences, Exaggerated vs. Blunted Reactivity

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9
Q

Levine’s (1950) Study of Rat Stress: Early life stress in rats ALL CONSEQUENCES

A
  • Extended separations from mom
  • As adult rats —> more stress reactive
  • Bigger corticosterone increase in unfamiliar environments
  • Greater activation of the CRF system
  • Smaller hippocampus
  • Dopamine system altered. More likely to consume alcohol.
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10
Q

Levine’s (1950) Study of Rat Stress: Pups exposed to extended separations means?

A

Pups exposed to extended separations —> more stress-reactive as adults
* Control pups experienced normal amounts of maternal separation
* Some maternal separation is normal when moms forage for food

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11
Q

Stress-reactive rats when placed in unfamiliar environment?

A
  • Large increase in corticosterone when placed in novel environment
  • More fearful. Less exploration.
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12
Q

Effects of Early Life Stress on brain of rats

A

1) More hypervigilant. More reactive to stressors (stress-reactive rats).
2) More corticosterone release in response to stressors
3) More likely to drink water containing alcohol
* Control rats avoided alcohol

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13
Q

Benefits of a Nurturing Mother (ask professor if he’s going to ask beyond the study guide)

A
  • Extended grooming and licking from mom
  • As adult rats —> more stress-resistant
  • Less corticosterone in unfamiliar environments
  • Less activation of CRF system
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14
Q

Cross-fostering studies in rats

A

1) Pups of stress-reactive mothers “adopted” by stress-resistant moms
2) Pups that received high quality nurture became stress-resistant
* Even if they may have had genetic vulnerabilities to be stress-reactive

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15
Q

Epigenetic influences in rats?

A
  • The experience of receiving quality care did not change the genes
  • Changes in gene expression
  • Rats that received quality care increased the expression of genes related to serotonin production and decreased expression of CRF
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16
Q

Genetic Vulnerabilities: Bullying and Depression. Gender dif?

A
  • Bullying related to many mental health issues…, especially depression symptoms

Gender differences:
* Boys experience more physical forms of bullying which may peak in childhood
* Girls experience more social and emotional bullying that may peak during adolescence

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17
Q

Relational victimization?

A
  • Social and emotional forms of bullying
  • Involves being insults, ostracized, false rumors
  • Does not involve physical aggress or harm
  • Girls more likely to experience social/emotional bullying than physical
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18
Q

Study methods?

Internalizing vs. Externalizing symptoms

A

The twin that experienced more bullying between ages 7-9 had more “internalizing symptoms” than the twin that wasn’t bullied

1) Internalizing symptoms:
* Symptoms that primarily impact how the individual feels
* Feelings of sadness, anxiety, loneliness

2) Externalizing symptoms
* Symptoms that impact social interactions with others
* Aggression, disobedience, antisocial behavior

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19
Q

Which gene? transporter? function? Region? which forms?

SERT polymorphisms and depressive symptoms

A

Polymorphism of the serotonin transporter gene:
* 5-HTTLPR = is the main regulator of serotonin, a polymorphism in the promotor region of the serotonin transporter gene, Serotonin Transporter linked promoter region
* Area of gene that codes for a protein that moves serotonin in/out of the cell
* polymorphism = “different forms”
* The short-form and long-form of the serotonin transporter gene
* The short-form is less effective at making the transport protein (SERT)

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20
Q

Article #5: SERT polymorphisms and HPA axis

A

Women with two short SERT genes —> increased cortisol reactivity and delayed recovery to psychosocial stressor (mental math)

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21
Q

sources of individual differences

A

Many ways to be different
* Genes, Anatomy, Physiology, Stress reactivity, Stress recovery…

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22
Q

Temperament?

A
  • Individual differences in how infants respond to their environment
  • Aspects of “personality” present in newborns
23
Q

Main Dimensions of Temperament?

A

1) Negative Emotionality
- Fearfulness, irritability, emotional reactivity

2) Positive Emotionality
- Smiling, curious, social, approach motivated

3) Activity and attention
- Physical activity, regularity, attentional focus

24
Q

High Reactive Infants vs. Low Reactive Infants

A

High Reactive Infants:
* Inhibited to novelty
* Become quiet, vigilant, and avoidant in unfamiliar situations
* Greater activation of stress-responses systems
* Associated with negative emotionality (more likely to cry and fuss)

Low Reactive infants:
* Not inhibited to novelty
* Become curious, more likely to explore and engage with unfamiliar situation
* Decreased activation of stress-response systems
* Associated with positive emotionality

25
Q

Big 5 Personality traits

A

The Big 5 Personality Traits:
* Individuals may be high or low on each trait

1) Openness to Experience:
* Imaginative, open-minded, adventurous

2) Conscientiousness:
* Orderly, cautious, responsible

3) Extraversion
* Sociable, assertive, excitement seeking

4) Agreeableness:
* Trustworthy, helpful, cooperative, empathetic

5) Neuroticism:
- Emotionally volatile, prone to negative emotions like anxious, irritable, depressed

26
Q

Type A personalities?

A

“Type A” – competitive, aggressive, ambitious, impatient
* Highly organized, but also hostile and easily frustrated
* ‘Workaholics” that “play to win” and “focuses on the details”
* Greater risk of heart disease

27
Q

Individual Differences in Hostility: Methods (Everson et al. 1995)

A

1) Hypothesis:
* Trait levels of hostility will predict greater cardiovascular reactivity to stress

2) Participants:
* Men completed questionnaire measuring personality traits
* Divided into a high-hostile vs. Low-Hostile group

3) Task: Complete two difficult mental math tasks
* 1st Task: Under Neutral Conditions: First experimenter acts professionally
* 2nd Task: Under Harassing Conditions: A second experimenter is rude and disrespectful to participant

4) Dependent Measures
* Self-reported emotions
* Cardiovascular activity

28
Q

Individual Differences in Hostility.
Results: Self-Report

A
  • As expected, high hostile participants report being more upset (distress, tense, irritation) during the harassment condition - In comparison to the low hostile group
  • The high hostile group does not reported being more upset during the neutral condition
29
Q

Individual Differences in Hostility.
Results: Conclusions

A

1) High hostile subjects show hyper-reactive response to provocation (being treated rudely)

2) High hostile subjects also show largest decrease in cardiovascular activity during the neutral condition
* But, they don’t report being more or less upset (in comparison to low hostile)

3) Why the large decrease in the neutral condition?
* High hostile may have higher baseline level of irritability
* They start off with increased cardiovascular activity
* As if they expect to be insulted or annoyed
* So, show a relatively large decrease in CV when they calm down and habituate to a situation

30
Q

Hostile Attribution Bias

A
  • Tendency to view others as being intentionally insulting or demeaning towards you
  • Associated with growing up in a coercive home environment
31
Q

Adaptive Calibration Model? Types?

A
  • Sensitive - SRS healthy, appropriately responsive. Recovers easily.
  • Buffered – SRS partially blunted. Constant state of caution or readiness
  • Vigilant – Exaggerated SRS. May be antagonistic/hostile or withdrawn/anxious
  • Unemotional –SRS severely blunted. Minimal response to minor stressors. SRS may only be activated by severe stressors. “Cold-blooded” impulsive behavior
32
Q

Diathesis-Stress models?

A

Illness (mental or physical) due to combo of genetic vulnerability and life experience

33
Q

Cytokines?

A

messengers between immune system and nervous system

34
Q

Phagocytes?

A
  • Eat and destroy invaders. Shows their remains to lymphocytes
  • Release cytokines to communicate with other immune cells
35
Q

Microglia?

A

Microglial act as the brain’s immune response
Microglia cells act like phagocytes:
* Can “eat” pathogens and antigens
* Anti-inflammatory effects
* Can also release cytokines
* Pro-inflammatory effects

36
Q

Lymphocytes?

A
  • B-cells – Remember the invaders. Make anti-bodies to tag the invaders for destruction.
  • T-cells – Kill the invaders. Kill own cells that have been infected.
37
Q

Immune System cells?

A

Cytokines, Phagocytes, Lymphocytes: T-cells and B-cells, Microglia

38
Q

Innate Immune System vs. Adaptive Immune System

A
  • Innate – ready to fight any familiar invader.
  • Adaptive – learns how to fight new, unfamiliar invaders
39
Q

sympathetic, HPA, chronic stress

Hormonal effects?

A

1) Sympathetic: Epi and Norepi —> trigger inflammation. Enhances innate immune response
2) HPA: Cortisol —> reduces inflammation. Enhances the adaptive immune response
3) BUT… chronic stress limits cortisol ability to regulate immune system
* If cortisol is chronically high —> the anti-inflammatory signal gets lost in the background noise

40
Q

Dysregulated stress linked to?

A

Dysregulated stress linked to poor mental and physical health
* Most common health issues linked to HPA axis

41
Q

Glucocorticoid Cascade Hypothesis

A

Aging increases damaging health effects of stress

42
Q

signs of?

Telomere shortening

A

Signs of rapid aging at the cellular level

43
Q

Connections between physical and mental health

A
  • Inflammation both a cause and symptom of depression
  • Anti-depressants also reduce inflammation
44
Q

Tripartite Model of Anxiety and Depression

A
  • 1) General Distress, 2) Lack of Positive Affect, and 3) Anxious Arousal
  • Depression = General Distress and Lack of Positive Affect
  • Anxiety = General Distress and Anxious Arousal
45
Q

Dysregulated serotonin, dopamine and norepinephrine

A
  • Dysregulated serotonin = general distress (feel bad)
  • Dysregulated dopamine = lack of positive affect (anhedonia, nothing feels rewarding)
  • Dysregulated norepinephrine = anxious arousal (hypervigilance, feel “on edge”)
46
Q

Noradrenergic paradox?

A

Norepinephrine (Attention and Arousal) = “PAY ATTENTION”
- “Noradrenergic paradox” – anxiety linked to high and low levels of norepi

47
Q

Dopamine responsible for? Involved in?

A

Dopamine (Motivation and Reward) = “KEEP GOING”
* Involved in Desire (Anterior Nucleus Accumbens)
* And… Involved in Dread (Posterior Nucleus Accumbens)

48
Q

Serotonin responsible for? Function?

A

Serotonin (Mood/Affective bias ) = “WE GOT THIS, THIS AIN”T SO BAD”
* Least well understood. May function as an energy regulator
* Serotonin may signal that the animal has the resources to cope with a stressor
* Depleted serotonin signals deficient energy/resources (which amplifies negative emotions)

49
Q

Low Serotonin Hypothesis

A

Assumption was that depression was caused by low levels of serotonin in the brain (particularly in the PFC)
* Selective Serotonin Re-uptake inhibitors treat depression by increasing the amount of serotonin that remains active in the synapse

50
Q

Problems with the Low Serotonin Hypothesis

A

1) Therapeutic delay
* SSRI effects are immediate in synapses, but therapeutic benefit takes weeks
* Often feel worse before feeling better

2) Placebo Effects
* Anti-depressant drugs only slightly more effective than placebo effects

3) Reduced serotonin doesn’t trigger depressive symptoms
* Tryptophan depletion (thru diet or meds) reduces serotonin levels
* Tryptophan depletion not associated with depressive symptoms

Mechanism of action (increased or decreased re-uptake may work)

51
Q

What are the types of anti-depressants work?

A
  • SSRIs – selective serotonin reuptake inhibitors
  • SNRIs – serotonin and norepinephrine reuptake inhibitors
  • NDRI – norepinephrine and dopamine reuptake inhibitors
  • ”Broad spectrum” – alter serotonin, norepinephrine, and dopamine
52
Q

Effectiveness of anti-depressants due to brain’s?

A

Effectiveness of anti-depressants due to brain’s compensatory mechanisms:
* How brain compensates more important than specific mechanism of drug
* Meds alter neurotransmitter activity. Brain compensates for the change.

Brain adapts to re-balance effects of serotonin, dopamine, and norepinephrine

53
Q

Negative feedback systems of drugs

A
  • If drug increases amount of neurotransmitter, the brain could make fewer receptors
  • If drug blocks a receptor, brain could make more neurotransmitter, etc…

Stress and the Brain (20 decks)

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