Week 4-Endocrinology Flashcards by Meg A

What are the 6 Hypothalamic releasing and Inhibitory hormones?

Thyrotropin-releasing hormone (TRH)
Gonadotropin-releasing hormone (GnRH)
Growth hormone-releasing hormone (GHRH)
Growth hormone-inhibitory hormone = somatostatin
Prolactin-inhibiting hormone (PIH)
Corticotropin-releasing hormone (CRH from paraventricular nucleus)

Tends to tell hormones to do something (aka hormones telling other hormones)

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What’s the function of TRH?

It stimulates the secretion of thyroid-stimulating hormone in the pituitary gland.

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What’s the function of GnRH?

Stimulates the secretion of luteinising and follicle-stimulating hormones in the anterior pituitary

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What’s the function of GHRH?

Stimulates the secretion of growth hormones in the anterior pituitary

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What’s the function of Somatostatin?

Inhibits the secretion of the growth hormone in the anterior pituitary

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What’s the function of PIH?

Inhibits the secretion of prolactin in the anterior pituitary

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What’s the function of CRH?

Stimulates the secretion of the adrenocorticotropic hormone in the anterior pituitary (key for the HPA access)

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What’s the simplistic process of the HPA axis?

Hypothalamus -> releasing factor –> anterior pituitary -> ACTH (through blood) –> Adrenal cortex -> Cortisol

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What are the 5 main anterior pituitary hormones?

Growth hormone (somatotropin) GH
Thyroid stimulating hormone TSH
Follicle-stimulating hormone FSH
Luteinizing hormone LH

5.Adrenocorticotropic hormone ACTH

These hormones have a more direct effect with actions to the body

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What is the function of GH?

To stimulate body growth, cell multiplication & differentiation.

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What is the function of TSH?

To stimulate the secretion of thyroid hormones.

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What’s the function of FSH?

To stimulate the development of ovarian follicles & spermatogenesis in the testis.

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What’s the function of LH?

To cause ovulation and stimulate the corpus luteum; to stimulate the secretion of estrogen & progesterone in ovaries; to stimulate testosterone in the testes.

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What’s the function of ACTH?

To stimulate the secretion of glucocorticoids & androgens in the adrenal cortex.

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Where is cortisol released?

In the adrenal cortex just at the top of the kidneys (medulla=centre layer + cortex=outer layer)

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What are the 3 Ways in which HPA Axis Activity is regulated?

Diurnal rhythm (our energy is mobilised with sugar entering our body early into the day and decreasing by end of night)
Negative feedback
Stress

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Where does cortisol go?

-Almost every cell in the body has cortisol receptors

-Up to 95% of secreted cortisol is bound to large proteins e.g., globulin and albumin) & carried in the body through the blood

-Unbound cortisol can freely enter all tissues, passing through the parotid gland into the saliva and through the kidney into the urine (it goes through so many places)

-Unbound cortisol can cross the blood-brain barrier (this is how we know cortisol affects behaviour including the fact that there are cortisol receptors in areas of the brain)

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How is the amygdala involved in cortisol?

-Has glucocorticoid receptors

-Acute (1 day) & chronic (10 days) administration of corticosterone caused prolongation of dendrites (makes us more sensitive to receiving info from our neurones=sensitising our emotional response in the amygdala) in the basolateral nucleus of the amygdala in rodents (Mitra & Sapolsky, 2008) (means we know it responds to cortisol)

-Similarly, acute (1 day) & chronic (10 days) immobilisation stress (can’t move) in rats caused an increase in the number of dendritic spines in the basolateral amygdala after 10 days in rodents (Mitra et al., 2005) (has same response as study above)

How is the hippocampus involved in cortisol?

-Has glucocorticoid receptors

Glucocorticoids affects the hippocampus in neurotoxic ways (Lupien & McEwen, 1997, McEwen, 1999):
-Decreased neuronal firing
-Further decreases in neuronal excitability later (have a harder time firing)
-Impaired neurogenesis in the dentate gyrus of the hippocampus, which projects to the amygdala
-Loss of neurons, shrinkage of neuronal bodies & retraction of dendrites (these effects are reversible) in CA1-3 regions (key to learning and memory in the hippocampus)

What did Uno et al., (1989) find concerning the hippocampus and cortisol in monkeys?

-Suggested there’s a hierarchy with subordinate monkeys and dominant monkeys (looked at the subordinates)

-Neurones had shrunk there was fewer of them

-Concluded this stress was causing the neurotoxicity to the hippocampus

-Also found the adrenal glands were enlarged and were outputting a lot of cortisol (as this is where it’s released)

How is the Pre-frontal cortex involved in cortisol?

-Has an abundance of glucocorticoid receptors

-Activity in the ventral medial PFC decreased during acute stress in healthy people, correlating with cortisol increases (Sinha et al., 2016) (concluded cortisol is involved in the decreased activity)

-Daily injections of corticosterone for 3 weeks or 10 min/day stress caused shortening of dendrites in PFC pyramidal neurons in rodents (Brown et al., 2005)

-amygdala=prolonging of dendrites
-hippocampus=neurotoxic effects
-PFC=shortening of dendrites

How does cortisol modify behaviour?

-Emotional regulation is impaired (amygdala)

-Complex effects on memory, disrupting memory formation but sharpening memory consolidation and retrieval (hippocampus)

-Cognitive deficits in learning and decision-making & slow extinction of fearful memories (PFC)

-Observed rodents & people after long-term exposure to corticosterone/cortisol & stress, suggesting evolutionary-based functions and processes during stress

How does cortisol work in a negative feedback loop?

The hippocampus, amygdala, PFC sends signals back to the hypothalamus e.g., ‘we have enough cortisol you can down-regulate and produce less CRH’

What are 4 ways cortisol samples can be collected?

Blood
Saliva (1 and 2 reflects activity in the past 10-60 minutes)
Urine (Reflects activity in the past 24 hours)
Hair (reflects activity in the past few months)

What are the 5 ways to assess cortisol?

Single sample: 1. Overnight cortisol Multiple samples: 2. Total cortisol concentration over the day (area under the curve, aka AUC) 3. Diurnal cortisol rhythm 4. Cortisol awakening response (CAR) 5. Cortisol reactivity & recovery

What's overnight cortisol?

-Urine sample -Provides a measure of non-stimulated level of cortisol activity (aka cortisol NOT in response to a stressor just general levels) -Greater overnight cortisol is associated with increased mortality risk & declines in cognitive and physical function (Seeman et al., 2001)

What's Total Cortisol Concentration Over the Day (Area Under the Curve, AUC)?

-Saliva or blood samples, < 2 samples per day, < at least 3 days -Provides a daily measure of cortisol activity with more precision than overnight cortisol

What's the Diurnal Cortisol Rhythm?

-Saliva or blood samples, < 2 samples per day, < a least 3 days -Provides a measure of changes in cortisol activity throughout the day

What did Bower et al., 2005 find with cortisol and fatigue?

-Those without fatigue have cortisol levels decline throughout the day whereas those with fatigue had their levels still elevated during the evening -Diurnal cortisol rhythm

What did Knight et al, 2010 find with cortisol and depression?

-People with depression have blunted levels of cortisol and less of a slope than those without -Diurnal cortisol rhythm

What's Cortisol Awakening Response (CAR)?

-Saliva or blood samples, < 2 on day, 1 immediately after waking (before getting out of bed), 1 30-45 min post-waking -Unbound cortisol levels increase by 50-75% within the first 30 minutes post-walking -"Blunted" or "exaggerated" rise may be associated with psychopathology

What did Rohleder et al., 2004 find with cort response and PTSD?

Found blunted cortisol awakening response with people in PTSD

What did Adam et al., 2010 find with awakening cort response predicting onset of major depression?

Exaggerated cortisol awakening response in those with depression compared to those without

What's Cortisol Reactivity & Recovery?

-Saliva or blood samples, < 3 on day, 1 pre-stress, 1 20 min post-stress (peak), < 1 15-20 min after peak (to see how someones cortisol levels returns to normal after peak) -Best to conduct studies in late afternoon to minimise diurnal rhythm influence/have lower baseline -Cortisol increases in response to certain types of stress

What did Dickerson and Kemeny (2004) find with acute stress and cortisol?

-Largest stress with cortisol is public speaking or uncontrollable cognitive task -Next was public speaking WITHOUT cognitive task -Uncontrollability and social threat are the biggest stressors eliciting a cortisol response (which aligns evolutionary wise) -Small gender differences in this study (men took longer to recover from stress)

What did Creswell et al., 2005 find with self-affirmation buffering cortisol reactivity to acute stress?

-Blunted reactivity to the stressor if doing self-affirmations (i.e., lowered stress can be regulated with kindness)

What did Bower et al., 2005 find with cortisol reactivity and fatigue?

People with fatigue have a lower reactivity response

How does a low-dose dexamethasone suppression test inform about the strength of HPA negative feedback?

Dexamethasone (a potent, synthetic glucocorticoid) is applied, & the cortisol level is recorded. If HPA negative feedback works, cortisol levels would decrease -Poor HPA feedback could be a result of Cushing's disease or stress as an example

What's the definition of pain?

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage (International Association for the Study of Pain, 1994)

What's Stress-Induced Analgesia?

-Based on the observation on Col. Henry Beecher (1946) on soldiers sustaining major injuries in combat zones of WW2 -73% of wounded soldiers did not require any morphine -"Stress-induced analgesia is a built-in mammalian pain suppression response that occurs during or following exposure to a fearful or stressful stimulus" (Butler & Finn, 2009)

What's the basic scheme of stress-induced analgesia?

1. Stress 2. Cortisol secretion (through the HPA axis activity) 3. Binds to receptors in the brain 4. Brain regions responding to cortisol stimulate the endogenous opioid system (provides relief from pain) 5. the endogenous opioid system suppresses incoming afferent pain impulses by inhibiting the spinal cord neurons via descending spinal tract

What did Van Uum et al., 2008 find with elevated levels of stress & hair cortisol in chronic pain patients?

-Patients with chronic pain are perceiving more stress and have elevated levels of cortisol in their hair -This shows cortisol activity levels have been high the past month

What evidence shows that cortisol levels are often found to be elevated in chronic pain patients?

1. Fibromyalgia syndrome patients (Crofford et al., 2004) 2. Burning mouth syndrome (Amenabar et al., 2008) 3. Temporomandibular disorder (Korszun et al., 2002)