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Scientific Foundations > Neuroendocrinology and Stress > Flashcards

Neuroendocrinology and Stress Flashcards

1
Q

The brain is key in the _________________ and ____________ to potential stressors

A

Interpretation
Response

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2
Q

What are the consequences of short-term, everyday stress?

A

▪️ Altered brain function
▪️ Adaptation to environmental challenges

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3
Q

What are the consequences of long-term stress?

A

▪️ Mal-adaptation
▪️ Psychiatric disorders

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4
Q

What are the key messengers for communication between the endocrine systems and the nervous system?

A

▪️ Hormones
▪️ Neurotransmitters

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5
Q

What are the key messengers used for communication between the immune system and the nervous/endocrine system?

A

Cytokines

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6
Q

What is the pituitary gland?

A

The master gland - produces hormones that control for many different processes, sending signals to other organs and glands to regulate function and homeostasis

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7
Q

What are the main pituitary hormones?

A

▪️ TSH
▪️ ACTH
▪️ FSH and LH
▪️ Growth hormone
▪️ Prolactin
▪️ Endorphins

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8
Q

What are hormones?

A

Chemical messengers, produced by glands, that are transported via blood to target organs to coordinate physiology and behaviour

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9
Q

What activities are regulated by hormones?

A

▪️ Digestion
▪️ Metabolism
▪️ Growth and development
▪️ Reproduction
▪️ Maintenance of body temperature
▪️ Cognitive function and mood etc

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10
Q

How do hormones relate to the circadian rhythm?

A

Secretion and action usually follows it
▪️ Follows the particular needs of the body at a particular time of day
▪️ Not always secreted in the same way throughout the day

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11
Q

How does transmission in the nervous system differ to the endocrine system?

A

▪️ Neurotransmitters
▪️ Rapid and brief duration
▪️ “wired”
▪️ Anatomical proximity

(Hormones as slower, have longer action, can go anywhere in the body)

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12
Q

What condition first led to the appreciation of psychiatric problems in patients with endocrine disorders?

A

Cushing’s syndrome:
▪️ Increased glucocorticoid secretion
▪️ Depression, irritability, loss of recent memory

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13
Q

How does stress relate to psychosis?

A

▪️ Stressful events associated with onset
▪️ Vulnerability stress model
▪️ Childhood trauma as a risk factor

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14
Q

How does stress relate to depression?

A

Adverse experience, especially during childhood, associated with significant increase in risk

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15
Q

What is the Hypothalamus-Pituitary-Adrenal (HPA) Axis?

A

In response to stress:
▪️ CRF stimulates pituitary gland to produce ACTH
▪️ ACTH stimulates adrenal gland to produce cortisol
▪️ Cortisol induces physiological changes supporting fight or flight response
▪️ Negative feedback loop - cortisol can feedback to pituitary and hypothalamus when too much to stop production

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16
Q

What are the two main types of corticosteroid receptor?

A

▪️ Mineralocorticoid receptor (type I/MR)
▪️ Glucocorticoid receptor (type II/GR)

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17
Q

What does the mineralocorticoid receptor do?

A

▪️ Binds endogenous glucocorticoids (e.g., cortisol) with HIGH AFFINITY (thus good even when levels are low)
▪️ Leads to regulation of circadian fluctuations of these hormones

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18
Q

What does the glucocorticoid receptor do?

A

▪️ Binds to endogenous glucocorticoids with LOWER AFFINITY
▪️ Leads to regulation of the response to stress when levels of glucocorticoids are high enough

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19
Q

What needs to detach from corticosteroid receptors before they can be activated?

A

HSP complex

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20
Q

What happens if the HSP complex does not detach from the corticosteroid receptor?

A

▪️ Translocation to the nucleus cannot occur
▪️ Receptors don’t get activated despite potentially very high levels of cortisol

21
Q

Why might individuals with depression have increased levels of cortisol?

A

▪️ GR receptors not working properly
▪️ No negative feedback to the PG/HT to stop cortisol production

(Glucocorticoid resistance due to high levels)

22
Q

How can you test for overproduction of cortisol/glucocorticoid resistance?

A

Dexamethasone Suppression Test

▪️ Potent synthetic glucocorticoid
▪️ Activates negative feedback, suppressing cortisol production in non-depressed people
▪️ If depressed/high cortisol, will have no effect staying high throughout the day, indicating negative feedback isn’t working

23
Q

What can the low dose dexamethasone suppression test be used for?

A

Differentiating healthy individuals from those who produce too much cortisol

24
Q

What can the high dose dexamethasone suppression test be used for?

A

Determining whether the abnormality is in the pituitary gland (i.e., Cushing’s disease)

25
Q

Are HPA axis abnormalities as consequence of depression?

A

Possibly but there is also evidence that is PRECEDES depression, increasing risk of developing it

26
Q

What are the consequences of sustained increased cortisol levels?

A

▪️ HPA axis alterations correlate with impaired cognitive function in depression
▪️ More common and more pronounced in severely depressed patients with melancholic and/or psychotic features
▪️ Damaging to brain and neurogenesis?

27
Q

How does chronic stress affect neuroplasticity in rats?

A

▪️ Dendrites become shorter in CA3 (hippocampus)
▪️ BUT reversible within several weeks

28
Q

Why might HPA axis dysfunction increase risk or psychosis?

A

Glucocorticoids increase dopaminergic activity in the mesolimbic system

29
Q

What stress/HPA-related changes are evident in both depression and psychosis?

A

▪️ Enlarged pituitary gland
▪️ Cortisol hypersecretion
▪️ Dexamethasone non-suppression

BUT not as consistent in psychosis - greater heterogeneity?

30
Q

How does treatment with antipsychotics affect cortisol levels in FEP?

A

It decreases it to the level of healthy controls throughout the day

BUT does not appear to normalise cortisol awakening response (less of a natural increase on awakening)

31
Q

What is the relationship between cortisol levels and hippocampal volume in FEP?

A

Moderate negative relationship

Increased cortisol = decreased left hippocampal volume

32
Q

How does cortisol response to Social Stress Test differ in depression and psychosis from healthy controls?

A

▪️ No difference in cortisol peak response in depression
▪️ Lower peak response in psychosis - blunted?

33
Q

How does HPA axis activity differ in psychosis to controls?

A

▪️ Increased cortisol during the day
▪️ Decreased awakening cortisol
▪️ Decreased cortisol response to stress

34
Q

How does HPA axis activity differ in depression to controls?

A

▪️ Increased cortisol during the day
▪️ Increased/equal awakening cortisol
▪️ Equal cortisol response to stress

35
Q

Can cortisol activity predict response to treatment for FEP?

A

Possibly - non responders had lowest cortisol awakening response

36
Q

What is the immune system?

A

▪️ Host defence system
▪️ Protects against disease
▪️ Distinguished pathogens from own healthy tissue

37
Q

How does psychological stress impact wound healing?

A

Disrupts immune function thus impairing wound healing

Study found mouth wound 3 days before exam healed ~40% slower than during summer holiday

38
Q

How does the HPA axis affect inflammation and immune response?

A

▪️ Modulates release of cytokines
▪️ Cytokines alter monoamine metabolism, increased excitotoxicity, and decrease production of trophic factors
▪️ Cortisol = immunosuppressant

39
Q

What is the relationship between depression and immune activation?

A

Patients show raised inflammatory markers (proinflammatory cytokines), even before development of depression
(e.g., TNF-alpha, IL-6)

Glucocorticoid resistance due to high levels so cortisol doesn’t suppress as it should

40
Q

Is there increased inflammation in psychosis?

A

Yes - elevated levels of pro-inflammatory cytokines (IL1-beta, IL-6, TFG-beta) in both schizophrenia and FEP

41
Q

How does stress affect inflammation in psychosis?

A

▪️ Significantly increased levels of TNF-alpha, CRP, and IL-6 in those with childhood trauma
▪️ Significantly increased levels of C reactive protein in those with sexual abuse

42
Q

What is interleukin-6?

A

One of the main inflammatory cytokines in the brain, marking inflammation

43
Q

How does inflammation relate to hippocampal volume in FEP?

A

Greater inflammation (greater IL-6 expression) = smaller HC volume at onset of psychosis

(significant but weak negative correlation)

44
Q

Can inflammation predict treatment response in FEP?

A

▪️ Non responders has significantly elevated IL-6
▪️ Responders still elevated compared to controls but not by a lot

(Similar in depression!)

45
Q

What is the main issues with anti-inflammatory treatments for psychiatric disorders?

A

▪️ A certain degree of inflammation may be beneficial and neuroprotective
▪️ Should we only target those with increased inflammation?

46
Q

What did the trial of infliximab (TNF-alpha antagonist) for treatment resistant depression find?

A

▪️ Placebo better overall
▪️ Those with higher levels of CROP had most benefit
▪️ Thus may only be beneficial to those with inflammation, may be harmful otherwise?

47
Q

What did the MINDEP clinical trial investigate?

A

Minocycline in addition to antidepressant for treatment-resistant depression

48
Q

What is minocycline and why was it chosen for the MINDEP trial?

A

It is a tetracycline antibiotic that can cross the BBB

49
Q

What did the MINDEP trial find?

A

▪️ Overall no difference to placebo
▪️ BUT when divided by baseline CRP, those with higher baseline inflammation showed significant improvement in symptoms

(Important to understand threshold for treatment benefit e.g., CRP >3? )

Scientific Foundations (27 decks)

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