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Chapter 11: Stress > Flashcards


Chapter 11: Stress Flashcards

1
Q

What is Stress?

A

Stress is a state of threatened homeostasis or disruption in homeostatic balance

The thing responsible for the imbalance is the stressor.
Can be environmental, physiological, psychosocial.

The body’s response to the imbalance is the stress-response.
Suite of physiological and behavioral responses that help to reestablish homeostasis.
Non-specific i.e. all stressors elicit a similar stress response

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2
Q

The body’s response to imbalance?

A

The body’s response to the imbalance is the stress-response.

Suite of physiological & behavioral responses that help to reestablish homeostasis.

Non-specific, i.e. all stressors elicit a similar stress response

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3
Q

The Stress Response:

General Systems

A

1) SYMPATHETIC NERVOUS SYSTEM
2) HYPOTHALAMIC-PITUITARY-ADRENAL AXIS
3) OTHER BRAIN-DERIVED HORMONES

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4
Q

Sympathetic Nervous System

A

Projections to virtually every organ in body where norepinephrine (NE) released

Adrenal medulla secretes epinephrine (aka adrenaline) and norepinephrine (NE)

“Fight or flight”: low priority systems shut down; blood & oxygen sent to the most necessary parts of the body.

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5
Q

HPA AXIS

A

Involved in Stress Response

The paraventricular Hypothalamus (PVN) releases corticotrophin-releasing hormone (CRH), which affects the anterior pituitary

The anterior Pituitary releases tropic hormone: ACTH

In response to ACTH, the Adrenal glands release cortisol or corticosterone (CORT)

CORT influences many neurons in the brain, increasing the release of several neurotransmitters

Amygdala also stimulates CRH release in the PVN

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6
Q

ACTH

A

Adrenocorticotropic hormone, also known as corticotropin

Tropic hormone.

Produced and Released by Anterior Pituitary

An important component of the hypothalamic-pituitary-adrenal (HPA) axis and is often produced in response to biological stress (along with its precursor corticotropin-releasing hormone from the hypothalamus).

A polypeptide hormone produced and secreted by the anterior pituitary gland.

Its principal effects are increased production & release of cortisol by the cortex of the adrenal gland.

ACTH is also related to the circadian rhythm in many organisms.

Cushing’s disease, Addison’s disease.

A polypeptide hormone produced and secreted by the anterior pituitary gland.
Primary adrenal insufficiency, called Addison’s disease, occurs when adrenal gland production of cortisol is chronically deficient, resulting in chronically elevated ACTH levels.
When a pituitary tumor is the cause of elevated ACTH (from the anterior pituitary) this is known as Cushing’s disease and the signs & symptoms of the excess cortisol (hypercortisolism) is known as Cushing’s syndrome.
Conversely, deficiency of ACTH is a cause of secondary adrenal insufficiency, often as a result of hypopituitarism.

In addition to its endogenous role, ACTH is used clinically as a diagnostic agent in assessing adrenal function.

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7
Q

CORT

A

Adrenal glands release cortisol or corticosterone (CORT) in response to ACTH

CORT influences many neurons in the brain, increasing the release of several neurotransmitters

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8
Q

Amygdala stimulates the release of _____ in the ____.

A

Amygdala stimulates the release of Corticotrophin-Releasing Hormone (CRH) in the Paraventricular Hypothalamus (PVN).

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9
Q

Other hormones involved in the stress response:

A

Posterior pituitary: vasopressin

Anterior pituitary: β-endorphin, prolactin

Pancreas: glucagon

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10
Q

Hormonal Changes in Humans in Response to Social Stressors

A

10% Increase in passengers caused high epinephrine recreation… high stress

Levels of epinephrine and norepinephrine speak at graduate exams, showing the stress response students have to exams.

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11
Q

Cortisol concentrations are altered by the stress of parachute jumps

A

pre-jump: baseline

Right before jump: super high
Right after jump: even higher

Cortisol before & after was decreased until 5 days after initial jump.

11 days, a little increased cortisol before & after.

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12
Q

The stress response:

Acute vs. Chronic

A

In the short term, the stress response produces adaptive changes that help the animal cope with emergency situations

Ideally, the stress response is initiated by stressful stimuli and then is deactivated shortly after.

If the stress response is activated too long, too frequently (i.e. chronic stress), or if is not activated for a physiological reason (i.e. psychological and social stressors), the stress response can be maladaptive and can endanger health.

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13
Q

Chronic Stress Has Systemic Effects:

Brain

A

Dendritic Atrophy

Enhanced Benzodiazepine Tone

Impaired Neurogenesis & Synaptic Plasticity.

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14
Q

Chronic Stress Has Systemic Effects:

Heart

A

Basal Hypertension

Sluggish Response to Stress

Sluggish Recovery from Stress

Pathogenic Cholesterol Profile

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15
Q

Chronic Stress Has Systemic Effects:

Ovary

A

Decreased Levels of Gonadal Hormones

Increased Risk of Anovulation and Miscarriage

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16
Q

Chronic Stress Has Systemic Effects:

Testis

A

Testicular Atrophy

Decreased Levels of Gonadal Axis Hormones

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17
Q

Chronic Stress Has Systemic Effects:

Adrenal Gland

A

Elevated Basal Levels of Glucocorticoids

Sluggish Response to Stress

Sluggish Recovery from Stress

Feedback Resistance

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18
Q

Chronic Stress Has Systemic Effects:

Immune System

A

Basal Immunosuppression

Decreased Immune Responsiveness to Challenges.

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19
Q

Metabolic Stress Response

A

2 metabolic responses to stress which increase glucose in the blood stream to provide energy:

1) Prevent energy storage via glucagon inhibition of insulin secretion from pancreas

2) Release of energy store via increased secretion of glucocorticoids, catecholamines (i.e. NE and E), glucagon
Lipolysis (triglycerides into fatty acids)
Glycogenolysis (glycogen into glucose)
Proteolysis (proteins into amino acids)
Gluconeogenesis (fatty acids and amino acids into glucose)

Pathological consequence:
Lack of energy reserves leads to myopathy (muscle loss), weakness and fatigue

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20
Q

Prevent energy storage via glucagon inhibition of insulin secretion from pancreas

A

Metabolic stress response.

The body prevents energy storage, promotes energy release by making the pancreas stop releasing insulin.

Glucagon inhibits insulin release.

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21
Q

Release of energy store via increased secretion of glucocorticoids, catecholamines (i.e. NE and E), glucagon

A

Metabolic stress response.

The body promotes energy release by secreting more Glucocorticoids, Catecholamines (i.e. NE and E), and Glucagon

Lipolysis (triglycerides into fatty acids)

Glycogenolysis (glycogen into glucose)

Proteolysis (proteins into amino acids)

Gluconeogenesis (fatty acids and amino acids into glucose)

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22
Q

Gluconeogenesis

A

Process by which fatty acids and amino acids are changed into glucose

Metabolic stress response.

Gluconeogenesis (GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as pyruvate, lactate, glycerol, and glucogenic amino acids.

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23
Q

Lipolysis

A

triglycerides are broken down into into fatty acids

Metabolic stress response.

the breakdown of lipids.

Involves hydrolysis of triglycerides into glycerol and free fatty acids.

The following hormones induce lipolysis:
epinephrine, norepinephrine, ghrelin, growth hormone, testosterone, and cortisol.

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24
Q

Proteolysis

A

The breakdown of proteins into smaller polypeptides or amino acids.

Metabolic stress response.

Uncatalysed, the hydrolysis of peptide bonds is extremely slow, taking hundreds of years.

Proteolysis is typically catalysed by cellular enzymes called proteases, but may also occur by intra-molecular digestion.

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25
Q

The following hormones induce lipolysis:

A

epinephrine, norepinephrine, ghrelin, growth hormone, testosterone, and cortisol.

Metabolic stress response.

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26
Q

Glycogenolysis

A

glycogen breaks down into glucose

Metabolic stress response.

Glycogenolysis is the breakdown of glycogen (n) to glucose-6-phosphate and glycogen (n-1).

Glycogen branches are catabolized by the sequential removal of glucose monomers via phosphorolysis, by the enzyme glycogen phosphorylase.

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27
Q

Pathological Consequences of Metabolic Stress Response.

A

Lack of energy reserves leads to myopathy (muscle loss), weakness, and fatigue

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28
Q

Cardiovascular Stress Response

A

Increase Cardiovascular Tone:
Stimulation of SNS: Increased heart rate, blood pressure, decreased blood flow to some organs (i.e. digestive tract)
Increased Secretion of Vasopressin: Increased blood volume and blood pressure

Pathological Consequence:
Chronic hypertension damages heart muscle, weakens blood vessel walls, promotes deposition of cholesterol, and the formation of plaques.
Over time, could lead to heart attack and stroke.

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29
Q

Increase Cardiovascular Tone:

A

Stimulation of SNS:
Increased heart rate, blood pressure, decreased blood flow to some organs (i.e. digestive tract)

Increased Secretion of Vasopressin:
Increased blood volume and blood pressure

Cardiovascular Stress Response

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30
Q

Gastrointestinal Stress Response

A

Inhibition of GI tract:
primarily mediated by shift from parasympathetic to sympathetic tone

Pathological consequence:
Gastric ulcers: stress makes the stomach more vulnerable to certain damaging bacteria which increase inflammation and compromise the ability of cells lining the walls of the stomach to defend themselves against acid

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31
Q

GI tract:

Stress and the Microbiome

A

We are colonized by billions of bacteria, many are protective

Stress changes makeup of this microbiome

Bacteria can signal to the brain: Make serotonin, hormones like testosterone

Changes in gut microbes could possibly lead to increased stress-related behavior (anxiety, depression)

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32
Q

Reproductive Stress Response

A

Inhibition of Reproduction:

  1. Hypothalamus: CRH and β-endorphin inhibit GnRH
  2. Pituitary: GC & Prolactin cause reduced responsiveness to GnRH, which causes decreased LH & FSH release
  3. Gonads: GC decreases sensitivity to LH

In females: secretion of E & P and the release of an egg less likely and reduces chances that a fertilized egg will implant into the uterine wall

In males: decreased T secretion and sperm production

Pathological consequence:
Anovulation, infertility, impotency, loss of libido

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33
Q

Luteinizing Hormone (LH) is important for ________.

A

LH is important for the production of hormones

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34
Q

The Hypothalamus’ CRH and β-endorphin inhibit ______

A

The Hypothalamus’ CRH and β-endorphin inhibit GnRH

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35
Q

GnRH

A

Gonadotropin-releasing hormone (GnRH)

Also known as follicle-stimulating hormone–releasing hormone (FSH-RH), luteinizing hormone–releasing hormone (LHRH), gonadoliberin, luliberin in its endogenous form, gonadorelin (INN) in its pharmaceutical form

A releasing hormone responsible for the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the Anterior Pituitary.

GnRH is a tropic peptide hormone synthesized and released from GnRH neurons within the hypothalamus.

The peptide belongs to gonadotropin-releasing hormone family.

It constitutes the initial step in the hypothalamic–pituitary–gonadal axis.

36
Q

Increased Cardiovascular and Cardiopulmonary Tone are damaging.

A

Prolonged stress has been linked to the development of high blood pressure (hypertension), and other cardiovascular problems.

37
Q

Stress elevates the levels of several hormones, but suppresses other hormones such as ______ and ______.

A

Stress elevates the levels of several hormones, but suppresses other hormones such as testosterone and progesterone.

This can eventually lead to suppression of ovulation, impotency, and loss of libido.

38
Q

Stress elevates the levels of several hormones, but suppresses other hormones such as testosterone and progesterone.

This can eventually lead to suppression of ____, ____, and _____.

A

Stress elevates the levels of several hormones, but suppresses other hormones such as testosterone and progesterone. This can eventually lead to suppression of ovulation, impotency, and loss of libido.

39
Q

Acute stress mobilizes internal energy stores, which is highly adaptive.

A

However, prolonged stress can lead to fatigue and muscle wasting.

40
Q

The temporary suppression of immune responses makes sense because the stress response demands a rapid mobilization of energy.

A

Immune responses extend longer than the immediacy of a demanding situation would require.

41
Q

Long-term stress is believed to cause oxidative damage in the brain, which may contribute to neural degeneration.

A

Prolonged stress can cause the altered cognition and sensory thresholds, as well as accelerated neural degeneration during aging.

42
Q

Psychogenic dwarfism can be caused by extremely stressful situations, such as being locked in a closet, living in a war zone, etc.

A

Bone decalcification and dwarfism can be consequences of extreme childhood stress.

Children in such traumatizing situations may lag years behind the normal growth rate.

43
Q

Chronic stress may lead to the formation of ____ in the digestive system.

A

Chronic stress may lead to the formation of gastric ulcers.

44
Q

THE LOGIC OF THE STRESS RESPONSE

A
  1. There is a need for immediate energy/ energy storage is prevented
    - > increase glucose in blood stream.

glucocorticoids prevent glucose uptake by cells

glucagon mobilizes stored glycogen

Insulin is inhibited (no glucose storage)

-> oxygen must be delivered to muscles and other cells

Breathing rate increases (sympathetic NS)

Heart-rate increases (sympathetic NS)

Blood pressure increases (sympathetic NS + vasopressin)

Water is retained to increase blood volume (vasopressin)

  1. Anabolic Processes are inhibited (why waste energy on processes important tomorrow?)
    - > digestion is curtailed
    - > reproductive processes are inhibited
    - > immune system inhibited
    - > suppression of inflammation
    - > no pain perception “stress induced analgesia”
45
Q

Consequences of a prolonged stress response on growth:

A 
Inhibition of Growth: 
Increased somatostatin (GH-inhibiting hormone) release from hypothalamus

Pathological consequence: Young–> psychosocial dwarfism (Kaspar Hauser syndrome)
Adults–> growth & repair processes

46
Q

somatostatin

A

a hormone secreted in the pancreas and pituitary gland that inhibits gastric secretion and somatotropin release.

A polypeptide hormone that is mainly produced in the hypothalamus.

Inhibits the secretion of various other hormones, including somatotropin, glucagon, insulin, TSH, and gastrin.

47
Q

Differences between all the “G” hormones

A

Gonadotropin-releasing hormone (GnRH):
A decapeptide hormone from the hypothalamus that regulates FSH & LH release from the Anterior Pituitary. Stress chapter.

Growth hormone (GH)
A protein hormone that stimulates somatic (body) growth.
GH, however, does not directly induce skeletal growth; it stimulates the production of growth-regulating substances (somatomedins) by the liver, kidneys, etc.
Somatomedins cause bone to take up sulfates, leading to growth.
GH and somatomedins also stimulate protein synthesis.

Growth hormone-inhibiting hormone (GHIH):
A peptide hormone secreted from the hypothalamus thatreduces the secretion of growth hormone by the anterior pituitary gland.

Growth hormone-releasing hormone (GHRH):
A polypeptide hormone that is released from the arcuate nucleus of hypothalamus that provokes the secretion of growth hormone from the anterior pituitary gland.

48
Q

Stress Response & Analgesia

A

Stress-induced analgesia (pain reduction): B-endorphin

Pathological consequence: ???

  • Maybe blunted pleasure responses if long-term exposure leads to receptor desensitization.
  • Maybe risk for drug abuse
49
Q

Pancreas

A

A composite gland with both endocrine & exocrine functions.

In humans, the pancreas is located within the curve of the duodenum behind the stomach and liver, and secretes digestive enzymes (exocrine function), insulin, glucagon, and somatostatin (endocrine function), as well as bicarbonate.

50
Q

Immune Function

A

Acutely, Glucocorticoids enhance some aspects of immune function (e.g. trafficking of immune cells to skin where injury might occur) but inhibit other aspects of immune function (e.g. inflammatory response)

Pathological consequence:
Sustained inhibition of inflammatory response may make it more difficult for body to heal itself after injury.
Sustained suppression of the immune system increases vulnerability to infections because GCs suppress lymphocytes

51
Q

Glucocorticoids (GCs)

A

Glucocorticoids (GCs) are a class of steroid hormones which bind to the glucocorticoid receptor (GR), that is present in almost every vertebrate animal cell.

The name glucocorticoid (glucose + cortex + steroid) derives from its role in the regulation of the metabolism of glucose, its synthesis in the adrenal cortex, and its steroidal structure. Another synonym is glucocorticosteroid.

GCs are part of the feedback mechanism in the immune system which reduce certain aspects of immune function, such as reduction of inflammation.

They are used in medicine to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis.
GCs have many diverse (pleiotropic) effects, including potentially harmful side effects, and as a result are rarely sold over the counter. They also interfere with some of the abnormal mechanisms in cancer cells, so they are used in high doses to treat cancer.

GCs cause their effects by binding to the glucocorticoid receptor (GR). The activated GR complex, in turn, up-regulates the expression of anti-inflammatory proteins in the nucleus (a process known as transactivation) and represses the expression of proinflammatory proteins in the cytosol by preventing the translocation of other transcription factors from the cytosol into the nucleus (transrepression).

Glucocorticoids are distinguished from mineralocorticoids and sex steroids by their specific receptors, target cells, and effects.
Glucocorticoids are chiefly produced in the zona fasciculata of the adrenal cortex.

Cortisol (or hydrocortisone) is the most important human glucocorticoid. It is essential for life, and it regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions.
Various synthetic glucocorticoids are available; these are used either as replacement therapy in glucocorticoid deficiency or to suppress the immune system.

52
Q

The Hippocampus and Termination of Stress Response

A

Hippocampus (and prefrontal cortex too)….

has dense concentration of glucocorticoid receptors (GRs)

participates in negative feedback regulation of the HPA axis

When Hippocampus binds cortisol, it leads to inhibition of CRH release from PVN

Prefrontal cortex does this too

PVN and pituitary also directly sensitive to GCs

53
Q

When Hippocampus binds cortisol, it leads to inhibition of ______ release from ______

A

When Hippocampus binds cortisol, it leads to inhibition of CRH release from PVN

54
Q

The Stressed Hippocampus:

Acute vs. Chronic

A

Acute stress:
Improves memory
Enhances long term potentiation (LTP)

Chronic stress:
Impairs LTP.
Shrinks dendrites.
Causes loss of dendritic spines
Reduces adult neurogenesis 
Impairs memory
Increases anxiety & depression (both regulated by hippocampus)
These effects of chronic stress are due to glucocorticoids
55
Q

The Stressed Amygdala

A

Chronic stress:
Increased dendrites and dendritic spines.
Amygdala becomes hyperactive (leads to anxiety, fear, etc).
Increased anxiety & depression.
These effects of chronic stress are due to glucocorticoids.
Connection between amygdala, hippocampus, and prefrontal cortex important for fear, anxiety, and PTSD

56
Q

Factors that affect stress responsiveness

A 
Pre-natal Environment
Post-natal Environment
Social Support
Prior Experience 
Age
Sex
Psychological variables
57
Q

Prenatal Environment and Stress

A

Offspring of mothers stressed during pregnancy…

  1. Had impaired negative feedback of the HPA axis, which increases basal CORT levels.
  2. Due to deceased hippocampal glucocorticoid receptors in the offspring.
  3. Adrenalectomy of the mother prevents the elevated stress response in offspring
58
Q

Prenatally stressed human infants:

A 
Reduced birth weight
Developmental delays
Attentional deficits
Hyper-anxiety
Impaired social behaviors
Impaired stress coping strategies as adults
May increase incidence of schizophrenia

In the Netherlands, there was increased incidence of schizophrenia in individuals who were in utero during German invasion

59
Q

Postnatal Environment

A

Short-term, mild stressors improve response to stress as adults, i.e. stress immunization

But…

Long-term moderate to severe stressors impair response to stress as adults

60
Q

Early stressful experiences affect reactions to stress:

Stress-IMMUNIZED Offspring

A

More Maternal Care
More adaptive pups

Decreased HPA response to stress

Increased Hippocampal GR

61
Q

Early stressful experiences affect reactions to stress
later in life

Stress-SUSCEPTIBLE Offspring

A

Prolonged Maternal Separation

  • —> Decreased LG-ABN
  • —> Increased HPA response to stress + Decreased Hippocampal GR
62
Q

LG-ABN

A

licking/grooming and arched-back nursing

63
Q

Early stressful experiences affect reactions to stress later in life:
Children & Orphanages

A

Children who were adopted from the orphanages before 8 months of age were able to develop stress coping ability almost as well as regular children.

Once the child was older that * months, it was harder to rescue the affects of having lived in the orphanage. Their baseline cortisol levels were higher.

64
Q

Postnatal Environment (humans)

Ace Study:

A

Adverse early childhood experiences linked to stress related disorders, drug/alcohol abuse, cancer, cardiovascular disease, early death

True of low SES families too

Many more stressors

The ACE Score test

65
Q

Epigenetics

A

Heritable changes in phenotype or gene expression caused by mechanisms other than changes in the underlying DNA sequence

These changes may last for multiple generations despite the fact that there is no change in the underlying DNA sequence of the organism

Non-genetic-factors cause the organism’s genes to behave (i.e. “express themselves”) differently

66
Q

Epigenetic Mechanisms

A

1) Methylation state:
- methylation silences genes
- demethylation of a gene leads to protein expression

2) Chromatin structure:
DNA in eukaryotic cells is wrapped around proteins called histones (DNA + histones = chromatin)

Compactness of the histones in a particular region of chromatin determines how readily transcription factors access promoters in the DNA

Variety of processes can alter chromatin structure including acetylation which decreases the binding of histones to DNA thereby increasing access of transcription factors to promoters

67
Q

Methylation

A

methylation silences genes

de-methylation of a gene leads to protein expression

Epigenetic Mechanism

68
Q

Chromatin structure:

A

DNA in eukaryotic cells is wrapped around proteins called histones

DNA + histones = chromatin

Compactness of the histones in a particular region of chromatin determines how readily transcription factors access promoters in the DNA

Variety of processes can alter chromatin structure, including acetylation which decreases the binding of histones to DNA thereby increasing access of transcription factors to promoters

69
Q

chromatin

A

DNA + histones = chromatin

70
Q

acetylation

A

Alters chromatin structure by decreasing the binding of histones to DNA, thereby increasing access of transcription factors to promoters

Acetylation of the lysine residues at the N terminus of histone proteins removes positive charges, thereby reducing the affinity between histones and DNA.

This makes RNA polymerase and transcription factors easier to access the promoter region.

Therefore, in most cases, histone acetylation enhances transcription while histone deacetylation represses transcription.

71
Q

Epigenetic influences of maternal behavior on stress offspring

A

Stress leads to decreased glucocorticoid receptor expression in hippocampus

less negative feedback on HPA axis

more stress responsive

72
Q

Epigenetic influences of maternal behavior on stress offspring

A

Early life stress leads to decreased methylation of vasopressin promoter in hypothalamus, which leads to:

  1. Increased vasopressin in response to stress
  2. Bigger HPA axis response to stress throughout life
73
Q

Early life stress leads to _____ of vasopressin promoter in _____.

A

Early life stress leads to decreased methylation of vasopressin promoter in the hypothalamus.

74
Q

Epigenetics in humans

A

Brains of suicide victims revealed same epigenetic change in expression of the GR but only in those victims that had a history of being abused or neglected as children

Implication: early abuse modified expression of genes, making people less able to handle stress and thus more likely to become depressed and commit suicide

75
Q

Social Factors:

Vervet monkeys

A

Most studies show that dominant animals have lower CORT than subordinate animals, particularly with social unrest.

Example: Vervet monkeys in captivity

Form social hierarchy where dominants constantly harass subordinates

Subordinate animals died at younger age and exhibited signs of chronic stress including enlarged adrenal glands, ulcers, and neural degeneration in the hippocampus

76
Q

The relationship between dominance and Glucocorticoids doesn’t hold true for all species….

A

In African hunting dogs, subordinates have the lowest CORT and the dominants have the highest CORT

77
Q

Sustained suppression of the immune system increases vulnerability to infections because…..

A

Glucocorticoids suppress lymphocytes.

78
Q

Social support serves as a “stress buffer”

A

Social support has many beneficial effects on various aspects health and well being:
Mice who live alone before heart attack or stroke experience more neurological damage and more harmful inflammation as compared to mice housed with partners.

In humans, social support has been shown to accelerate and improve recovery from a variety of illnesses including cancer, stroke, heart disease.

79
Q

Previous Experiences Can Modify Stress Responses

A

Repeated experience can desensitize response to stress

80
Q

Repeated experience can also sensitize response to stress

A

….

81
Q

Whether sensitization or desensitization occurs depends mostly on 2 factors…

A

Type of stressor:
Mild stressors desensitize.
Strong stressers sensitize.

Same stressor repeated leads to desensitization while changing stressor (i.e. chronic mild unpredictable stress) sensitizes.

82
Q

Age and Stress

A

HPA axis tends to become less sensitive to negative feedback regulation as individuals age, resulting in higher glucocorticoid levels after stress.

More age –> greater susceptibility to stress

83
Q

Sex Differences in Stress

A

Rodents:
Females higher basal and stress-induced CORT.
Activational—> ovariectomy removes these sex diffs, E2 treatment restores.
Higher glucose utilization in females than in males following stress, esp. in hippocampus, hypothalamus, amygdala

Humans:
Females higher basal and stress-induced CORT.
Females have higher ACE scores on average.
Females higher likelihood of stress-related disorders.

84
Q

Psychological variables that affect stress responsiveness

A

Control
Predictability
Outlet for Frustration

85
Q

Controllability

A

“Yoked Control” design is a popular way to assess the effects of controllable vs. uncontrollable stressors

Animal 1 receives a shock but can turn it off by turning the barrel

Animal 2 receives same duration shock as Animal 1 but can not turn the shock off

Results:
Animal 2 has higher CORT and more ulcers than Animal 1 even though the animals were exposed to exactly the same duration of shocks.
The only difference was that Animal 1 could control the stressor whereas Animal 2 could not.

86
Q

Predictability

A

“Yoked Control” design is also used to assess the effects of predictable versus unpredictable stressors

Flashing light notifies animal 1 that shock is coming.

Animal 2 receives same duration shock. But there is no light, so the animal never knows when to expect shock.

Results:
Animal 2 has higher CORT and more ulcers than Animal 1 even though the animals were exposed to exactly the same duration of shocks.
Only difference was that Animal 1 could predict onset of shock and Animal 2 couldn’t.

87
Q

Outlets for Frustration

A

The ability to engage in displacement behavior (i.e. having an “outlet”) can ameliorate the effects of stress

Example: chewing on wooden stick or attacking another rat

In humans: hobbies, exercise, meditation

Child Development (19 decks)

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