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Year 2 Brain and Behaviour > Stress (Laura) > Flashcards

Stress (Laura) Flashcards

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1
Q

What is a stressor biologically

A
  • A stimulus/event that causes a disturbance to homeostasis
  • Activates the brain’s alert system that leads to the release of the stress hormone cortisol
  • Fight or flight
  • Once disturbance dealt with the stress system returns to normal
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2
Q

Psychologically speaking what is a stressor

A
  • A stimulus/event that is a threat challenge, demand to the individual that is not physical
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3
Q

What is the stress response?

A

Represents an integrated reaction to stressors, broadly defined as real or perceived threats to homeostasis or well-being

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4
Q

What is the hypothalamic-pituitary adrenal (HPA) axis

A
  • HPA activation is the hallmark of the stress response
  • Activation of the HPA axis is the primary hormonal response to a stressor
  • Mobilises energy reserves insuring an organism can respond to an actual stressor or anticipated threat.
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5
Q

HPA axis pathway

A
  1. When hypothalamus is activated it releases corticotropin releasing hormone (CRH)
  2. CRH activates the anterior pituitary
  3. Anterior pituitary releases adrenocorticotropin releasing hormone (ACTH)
  4. ACTH is detected by the adrenal cortex
  5. Adrenal cortex releases cortisol
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6
Q

How does the hypothalamus become activated?

A
  • Signals (visceral afferents) from all over the body are received by brainstem noradrenergic neurons
  • These then stimulate (innervate) the paraventricular nucleus (PVN) of the hypothalamus
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7
Q

What is the output of the HPA axis

A 
GR = glucocorticoid receptors 
MR = mineralocorticoid receptor
  • GR mediate mobilisation of energy stores (liver, fat, muscle), inflammation and neural function
  • MR important for basal circadian and ultradian rhythms
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8
Q

How does the stress response shut down

A

Involves 2 processes:

  1. Passive steroid ‘clearance’
  2. Negative feedback
  • GR binding in the PVN leads to endocannabinoid release and eventual reduction in ‘drive’ to CRH neurons
  • GR and MR in ventral hippocampus and pre-frontal cortex
  • When these detect cortisol they activate the glutamergic projections to GABAergic PVN projecting neurons (inhibitory pathway)
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9
Q

What is chronic stress?

A
  • Chronic stress is the result of repeated or prolonged exposure to a stressor
  • Its hallmark is the chronic central ‘drive’ to the neurons controlling the stress response
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10
Q

What is allostasis?

A

The adaptive process that maintains homeostasis through the production of mediators such as adrenalin, cortisol and other chemical messengers

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11
Q

What is allostatic load?

A

Mediators of the stress response promote adaptation in the aftermath of acute stress, but they also contribute the wear and tear on the body and brain that results from being ‘stressed out’.

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12
Q

Examples of chronic stress as a cumulative process

A
  • Adrenal cortex frequently (but not always) increases in size and becomes more sensitive to ACTH meaning that cortisol responses to stressors are amplified
  • Glucocorticoid-sensitive immune organs (e.g. thymus) undergo cell death and involution
    0 Loss of glucocorticoid feedback control of the HPA axis, associated with decreased GR in regions such as the hippocampus and prefrontal cortex (as well as the PVN)
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13
Q

What is habituation to a ‘homotypic’ stressor?

A
  • Repeated exposure to the same stressor results in decreasing cortisol response over time
  • Despite reduced response, organism is still undergoing repeated stress
  • Decrement in HPA drive requires the MR
  • Paraventricular thalamic nucleus (PVT) is crucial to this process
  • Some degree of habituation is evident following exposure to varying (heterotypic) stressors
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14
Q

What is facilitation?

A
  • HPA axis stress response to a new stressor is either maintained or increased
  • Exposure to stressor 1 facilitates the cortisol response to a stressor 2
  • Overall faster onset of cortisol release and higher peak cortisol levels
  • Facilitation involves circuits connecting with the PVT
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15
Q

How do facilitation and habituation work in conjunction with the severity of the stressor?

A

Habituation:

  • Responses to very ‘severe’ stressors do not reduce
  • Possibly not worth the ‘cost’ to adapt to the stressor

Facilitation:
- If either of two stimuli are sufficiently intense, facilitation will override the feedback inhibition

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16
Q

Selye’s general adaptation syndrome (GAS)

A
  • Father of stress research
  • First person to use word stress in the context of ‘nonspecific response of the body to any demand’
  • Suggests a universal and similar response to a range of stimuli
17
Q

Henry (1992) Perceptions of control and stress

A
  • Specific perceptions of control result in different patterns of neuroendocrine activation

Easy to handle situation –> active coping response –> sense of control –> release of noradrenaline

  • Testosterone rises with success

Not easy to handle situation –> more passive coping mode –> behaviour less assured –> loss of control –> adrenaline rises

  • Less certainty = growing distress = adrenocorticotropic hormone and cortisol levels rise
18
Q

Perceptions of control and stress animal example (Van Holst’s tree shrews)

A
  • Male tree shrews competing for dominance in a large cage
  • The control was animal living alone without challenge

3 roles the shrew could be:

  1. Dominant - has full access and control
  2. Submissive - only emerges to eat when the coast is clear
  3. Sub-dominant - (prepared to fight) occasionally tries his luck but can retreat to nesting box
19
Q

Perceptions of control and stress animal example (Van Holst’s tree shrews): Results

A
  • 8-12 day confrontation period
  • Cortisol and corticosterone of the defeated submissive nearly doubled
  • No change in others
  • Tyrosine hydroxylase (norepinephrine synthesis) elevated in subdominant
  • No change in the relaxed dominant or in the submissive
  • Testosterone elevated only in dominant animal
20
Q

Prenatal stress and adult offspring (Rats)

Barbazanges, Piazza, Le Moal and Maccari (1996)

A
  • Hippocampal type I and type II corticosteroid receptors in male adult rats submitted to prenatal stress are born
  • MOTHERS:n either intact corticosterone secretion or blocked by adrenalectomy with substitutive corticosterone therapy
  • Intact: decrease in type I hippocampal corticosteroid receptors observed in prenatally stressed adultsa
21
Q

Dutch hunger winter (1944)

A
  • Extreme stress from starvation
  • <1000 cal/day in pregnancy
  • Early gestational exposure: Normal birth weight, increased risk of obesity and cardiovascular disease
  • Mid-gestational exposure: Low birth weight, reduced renal function
  • Late gestational exposure: Low birth weight, smaller throughout life –> lower obesity rates
22
Q

Postnatal stress and ageing

Brunson et al (2005)

A
  • Affects of early exposure to stress may not be evident until later life
  • Rat mothers and pups exposed to 2 different environments, harsh or comfortable
  • Stress effects evident after early stress but gone by 12 months
  • Mothers limited in nesting material spend less time nursing and more time off their pups
  • AT 4-5 months of age, both early-life stress (n=8) and control rats (n=11) require progressively less time to find a hidden platform in the Morris water-maze test
  • By 12 months of age, early-life rats require significantly longer time
  • Reduction intotal dendritic length and in dendritic aborization in the early-stress group
23
Q

Early life stress in humans

Gunnar, Morison, Chisholm and Schnuder (2001)

A
  • 6-12 year olds
  • RO = those who had spent at least 8 months of first years of life in romanian orphanage
  • EA = early adopted (<4 months)
  • CB = canadian born raised by family of origin
  • Measured cortisol
  • RO had higher cortisol levels
  • Could not isolate mechanism as multiple risk factors possible, including gross privation of basic needs and exposure to infectious agents
24
Q

What is PSS?

A
  • Psychosocial short stature
  • First described by Talbot over sixty years ago
  • “Abuse dwarfism” and “psychosocial dwarfism”
  • Beyond infancy failure to grow as a results of psychosocial circumstances
25
Q

What is HSS?

A
  • Excessive eating not motivated by hunger but is a maladaptive hypothalamic response to negative emotions but BMI is normal
  • Growth failure is reversible when the child is removed to a nurturing environment
26
Q

What is the PSS mechanism?

A
  • Growth hormone (GH) insufficiency (hypothalamic in origin)
  • Do not respond to GH without psychosocial intervention
  • Two lesions in hypothalamic-pituitary-growth axis which are reversible
  • Cortisol abnormalities not characteristic
  • Some discussion of ACTH decreased but only in few. cases.
27
Q

What are social determinants of health?

A
  • The health gradient: higher social position = better health
  • Not just comparing top with bottom but every step down the social hierarchy there is a step down in health
28
Q

Candidate stressors of health

A

Often but not always linked to lower socio-economic status:

  • Perceived financial strain
  • Job security
  • Low control and monotony at work
  • Stressful life events and poor social networks
  • Low self esteem
    Fatalism
29
Q

How are racism and health related?

A
  • Health outcomes are distributed unequally among diverse ethnic groups
  • Substantial heterogeneity in health outcomes
  • Puerto Ricans demonstrate particularly poor health whereas Cubans show better health
  • Racial and ethnic discrimination have been explored as potential causes for health inequalities
30
Q

Racism as a determinant of health study

Paradies et al (2015)

A
  • Meta-analysis
  • 233 studies reported in 333 articles
  • These studies were published between 1983 and 2013
  • Racism was associated with poorer mental health, including depression, anxiety, psychological stress and various other outcomes
  • Racism was also associated with poorer general health
  • Racism was also associated with poorer physical health
  • Age, sex, birthplace and education level did not moderate the effects of racism on health
31
Q

Racism as a determinant of health study: 5 mechanisms that underpin racism and health

Paradies et al (2015)

A
  1. Reduced access to employment, housing and education and/or increased exposure to risk factors
  2. Adverse cognitive/emotional process and associated psychopathology
  3. Allostatic load and concomitant patho-physiological processes
  4. Diminished participation in healthy behaviours (e.g. sleep and exercise) and/or increased engagement in unhealthy behaviours (e.g. alcohol consumption) either directly as stress coping, or indirectly, via reduced self-regulation
  5. Physical injury as a result of racially-motivated violence

Year 2 Brain and Behaviour (4 decks)

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