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Psychology & Neuroscience of Affective Disorders > The neurobiological aspects of stress > Flashcards

The neurobiological aspects of stress Flashcards

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1
Q

What are stress responses?

A

Physiological and behavioural responses arising

  • in response to anything that threatens the homeostasis of the organism
  • in an attempt to reinstate equilibrium

e.g. fight, flight or freeze

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2
Q

What causes stress?

A

Any circumstances that either

  • threaten individual’s well-being
  • or that the individual perceives as threatening to their well-being
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3
Q

To whom has the concept of stress been attributed?

A

Hans Selye

- Australian-Canadian endocrinologist of Hungarian origin

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4
Q

For what has Hans Selye been nominated the Nobel Prize between 1949-1953?

A

Nominated for Nobel Prize 17 times for his:

  • work on endocrinology and adaptation syndrome
  • contributions to the isolation of steroid hormones
  • formulation of stress reactions
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5
Q

What was Hans Selye’s experiment on stress responses (1974)?

A

> Neurochemical experiment
- rats were injected with new ovarian extract

> Environmental experiment
- rats were placed on roof in winter, others in boiler room, others subjected to forced exercise or surgical procedures

-> changes observed were a general response to the different types of stress rats were subjected to

=> Selye called it the “general adaptation syndrome”
= stress response, producing stress hormones

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6
Q

What are glucocorticoids?

A

Stress hormones
- glucose + cortex + steroid

  • regulate glucose metabolism
  • synthesised in adrenal cortex
  • classified as steroid chemical structure
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7
Q

What mediates the action of glucocorticoids?

A

2 types of corticosteroid receptors:

  • Mineralocorticoid receptors (MR)
  • classical glucocorticoid receptors (GR)
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8
Q

What characterises mineralocorticoid receptors (MRs)?

A
  • High affinity for endogenous glucocorticoids

- Activated by low basal cortisol concentrations

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9
Q

What characterises glucocorticoid receptors (GRs)?

A

They are ligand-activated nuclear transcriptions factors

  • Low affinity for endogenous glucocorticoids
  • Activated by high cortisol concentrations
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10
Q

How do glucocorticoids regulate gene transcription?

A

Stress -> adrenal cortex -> high cortisol concentrations
-> activates GRs

  • Upon ligand binding from cortisol, GR residing in cytoplasm, in association with chaperone proteins, translocates in nucleus
  • Binds to glucocorticoid response elements (GREs) present on DNA
  • > regulates gene transcription
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11
Q

How does the hypothalamus-pituitary-adrenal (HPA) axis produce cortisol?

A

> Paraventricular nucleus (PVN) o hypothalamus secretes corticotropin-releasing hormone/factor (CRH/CRF) and arginine-vasopressin (AVP)

> CRH and AVP stimulate secretion of adrenocorticotropic hormone (ACTH) from pituitary gland

> ACTH travels to adrenal glands (adrenal cortex, above kidneys) to promote synthesis and release of cortisol

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12
Q

What is the role of cortisol?

A

> Enables body to maintain adequate and steady blood sugar levels

  • by releasing stored glucose from liver for energy
  • causing suppression of immune system

> Cortisol is part of endocrine system
- acts in different ways in neurotransmitters of nervous system

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13
Q

What is the consequence of excessive levels of circulating cortisol?

A

Negative feedback regulation

  • feedback inhibition of secretion of adrenocorticotropic hormone (ACTH) from pituitary glands and corticotropin-releasing-hormone (CRH) from hypothalamus
  • > decreasing cortisol production
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14
Q

What is the negative feedback regulation of cortisol?

A

Excessive levels of circulating cortisol signal the brain to regulate cortisol production

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15
Q

What is the endocrine system made of?

A

Hormones, glands and receptors

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16
Q

How does the endocrine system work?

A

Stimulus -> endocrine cells release hormones into blood vessels

-> hormone-induced response at protein or genetic level

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17
Q

What characterises the transmissions in the endocrine system?

A

Chemical impulses transported by blood

- slow

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18
Q

What characterises endocrine responses and effects?

A
  • Involuntary responses

- Slow and short or long lived effects

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19
Q

What is the nervous system made of?

A

Neurones

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20
Q

How does the nervous system work?

A

Stimulus -> neuronal cell receives signal from dendrites

  • signal travels along axon
  • neuronal responses in synapses
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21
Q

What characterises the transmissions in the nervous system?

A

Neurotransmission

  • electrical impulses transmitted by neurons
  • rapid
22
Q

What characterises neuronal responses and effects?

A
  • Voluntary or involuntary responses

- Fast and short lived effects

23
Q

What is the role action of the endocrine and nervous systems in normal conditions?

A

Maintain constant internal environment, while being able to respond and adapt to external events

24
Q

What is the Recent Life Changes Questionnaire (RLCQ)?

A

Tool to assess stress levels by taking into account the presence or perception of recent life events

  • uses a list of most common sources of stress as evaluation tool
  • includes 5 categories:
25
Q

How is the Recent Life Changes Questionnaire (RLCQ) composed?

A

> Uses a list of most common sources of stress as evaluation tool

> Includes 5 categories:

  • Work
  • Home and Family
  • Health
  • Personal and Social
  • Financial

> Scoring:

  • score each event according to severity using Life Change Units (LCUs)
  • add up all LCUs to get final score

> Individual reaction to stress is key factor

26
Q

What characterises the acute stress response?

A
  • Increased blood pressure and blood flow to the brain
  • Faster breathing
  • Slower digestion
  • Increased perspiration
  • Increased levels of cortisol in saliva
  • Increased muscle tension
  • > mobilisation of glucose and other energy molecules to fuel muscles for fight-or-flight response
  • > focuses aspects of memory and cognition, sharpening detection of sensations and increasing alertness
27
Q

What are the effects of chronic stress?

A
  • Digestive problems
  • Increased stomach acidity levels
  • Increased cholesterol and fatty acids
  • Increased levels of blood pressure and blood sugar
  • Menstrual cycle irregularities in women
  • Reduced sperm count and testosterone levels in men
  • Increased chances of developing infections (weakened immune system)
  • When severe, can lead to depression
28
Q

What did Kendler and colleagues find about the vulnerability factors in the relationship between stressful life events and depression?

A

> 7500 twins from population based sample

> Overall increase in stress levels

> Individuals with low levels of neuroticism were much less sensitive to depressogenic effects of adversity
vs. those with high levels of neuroticism

29
Q

What are the observed effects of high glucocorticoid levels in animal studies?

A
  • Depression-like behaviour
  • Decreased neurogenesis
  • Monoamine dysfunction
  • Impaired synaptic plasticity
  • Reduced volume of hippocampus

Same changes are thought to be present in brains of depressed patients

30
Q

What are the effects of high glucocorticoid levels in humans?

A

> When treated with synthetic glucocorticoids, might lead to:

  • development of manic symptoms at start of treatment
  • development of depressive symptoms after few weeks of treatment

> Patients with Cushing’s syndrome (chronic hypercorticolism) demonstrate high rates of depression

31
Q

When are synthetic glucocorticoids used?

A

To treat many inflammatory conditions and autoimmune diseases

32
Q

What is the action of the hypothalamic-pituitary-adrenal (HPA) axis under normal conditions?

A

Negative feedback regulation of HPA axis

-> feedback inhibition stops production of cortisol

33
Q

What is glucocorticoid resistance?

A

Reduced cortisol effects, believed to be related to impaired function of glucocorticoid receptor (GR)

34
Q

What could cause a failure in the function of the glucocorticoid receptors (GRs), hypothesised in depression?

A

Reduced glucocorticoid binding to the GR
OR reduced GR expression

  • > increased levels of cortisol don’t send feedback to brain, to stop secretion corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH)
  • > cortisol synthesis and release continues
35
Q

In which cases has the alteration of the hypothalamic-pituitary-adrenal (HPA) axis been observed?

A

> HPA hyperactivity and hypercorticolism
- associated with MDD and depression with melancholic features (unreactive mood)

> HPA hyperactivity and hypocorticolism
- associated with atypical depression (reactive mood)

36
Q

How are stress effects neurobiologically evaluated in animals?

A
  • Blood samples

- Brain samples

37
Q

How are stress effects neurobiologically evaluated in humans?

A
  • Blood
  • Urine
  • Saliva
  • Hair
  • Stem cells
38
Q

How do corticoids affect neurogenesis in rodents?

A

> Corticosterone:

  • negatively affects hippocampal neurogenesis
  • increased corticosterone -> decreased neurogenesis

> Adrenal steroids:

  • regulate both proliferation and differentiation of new neurons in dentate gyrus
  • adrenalectomy (removal of adrenal glands) -> no corticosterone -> increased neurogenesis
39
Q

What is corticosterone?

A

Main glucocorticoid in rodents

- affects hippocampal neurogenesis

40
Q

What did Tanapat and colleagues (2021) find on the relationship between psychological stress and neurogenesis?

A

> When rats were exposed to fox door:
- decreased number of proliferating cells in dentate gyrus (dependent on stress-induced rise in adrenal hormones)

  • increased levels of circulating corticosterone
  • decreased number of new granule cells was transient
  • > did not cause permanent damage

> When rats subjected to adrenalectomy:
- no suppression of cell proliferation was found

41
Q

What was the novel theory of Jacobs and colleagues on neurogenesis and depression (2000)?

A

Altered rates of neurogenesis in adult hippocampus might underlie the development of major depression or hinder one’s recovery from it

  • stress + raised glucocorticoids
  • > decreased neurogenesis and increased depression
  • exercise + antidepressants
  • > increased neurogenesis and decreased depression

=> high cortisol levels and adversity are risks for depression, whilst exercise and antidepressants hasten recovery in humans

42
Q

What is the novel cellular pathway revealed by Wohleb and colleagues (2018) which contributes to the pathophysiology of stress-induced disorders?

A

Stress-induced signalling between neurons and microglia

> Mice intermittently exposed to stressful conditions
= chronic unpredictable stress

-> Increased messenger RNA levels of colony stimulating factor 1 (CSF1)

-> Changes in microglia corresponded with reduced dendritic spine density on pyramidal neurons in layer 1 lf medial PFC
= reduction in synaptic connections in PFC (associated with major depression in clinical studies)

-> When preventing neurons from producing CSF1 by viral knockdown, mice exposed to chronic stress DID NOT develop symptoms of anxiety or depression

=> Interrupting stress-induced signalling between neurons and microglia might be an effective treatment for anxiety and depression

43
Q

What did Anacker and colleagues (2013) show about the effects of high cortisol levels using a clinically relevant model of human hippocampal progenitor cells?

A
  • In cells treated with high doses of cortisol: reduction in neurogenesis
  • Cells stained for BrdU showed reduction in Dcx-positive neuroblasts (doublecortin) and MAP2-positive neurons (microtubule-associated protein) = growth factors
44
Q

What are the effects of antidepressants on glucocorticoid receptors shown (Anacker et al., 2011)?

A

Using dexamethasone: synthetic glucocorticoid specific GR-agonist

  • demaxethasone decreased number of MAP2-positive neurons by 27%
  • decreased Dcx-positive (Doublecortin) neuroblasts by 25%
  • co-treatment of cells with selective serotonin reuptake inhibitor sertraline and demaxethasone abolished the reduction of MAP2- and Dcx-positive cells
45
Q

What is the cortisol awakening response (CAR)?

A

Sharp increase of cortisol at awakening, for 35 minutes

46
Q

What has been found on the cortisol circadian rhythm?

A

> Cortisol awakening response showed unique associations with range of lifestyle factors and psychological traits
(often different from those observed over remainder of day)

> High cortisol awakening response may be indicative of an increased biological vulnerability for depression

47
Q

What is the condition for collecting saliva samples to measure cortisol levels?

A

Participants must refrain from eating, smoking, drinking or brushing teeth, 15 minutes prior to collection

48
Q

What is the limit of saliva samples for measuring cortisol levels?

A

Saliva samples only allow for single measurements, reflecting short-term levels of cortisol

49
Q

How can long-term levels of cortisol be measured?

A

With urine or hair samples

50
Q

What is the importance of measuring the long-term levels of cortisol in the aetiology of chronic diseases?

A

Cumulative effect of frequent HPA axis activation may be associated with maladaptive effects of the organism

51
Q

What has been observed on cortisol in postnatal depression (Taylor et al., 2009)?

A
  • Non-depressed postnatally women showed pattern of cortisol secretion over the day similar to non-perinatal controls
  • Depressed women showed significantly higher cortisol levels at awakening and no increase 30 minutes later

=> lack of morning cortisol rise in depressed women group is similar to that reported for PTSD and chronic fatigue syndrome
- may reflect a response in vulnerable women to marked cortisol withdrawal that occurs after delivery

52
Q

What did Weger and colleagues find on the vulnerable phenotypes for stress-induced depression (2018)?

A
  • Highly anxious individuals show behavioural alterations and more reactive physiological stress responses
  • Molecular variations (due either to genetic or epigenetic factors) in key neurobiological systems (e.g. NT systems and HPA axis) might define high anxiety trait in people
  • Only in combination with suboptimal environmental conditions does high anxiety trait provide a vulnerability phenotype for development of psychopathology (anxiety disorders, depression)
  • > It is not stress that kills us but our reaction to it

Psychology & Neuroscience of Affective Disorders (16 decks)

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