Lect 17. Integrative Bio

Q: What types of environmental changes can act as stressors for organisms?

Stressors are environmental factors that challenge homeostasis. Examples include:

Unpredictable stressors

• Predators

• Injury or infection

• Habitat loss or fragmentation

• Human disturbance

• Pollution

• Invasive species

• Extreme weather

• Global climate change

Predictable environmental changes

• Day/night rhythms

• Seasons

• Tidal cycles

• Lunar cycles

• Rainy vs dry seasons

Predictable changes allow organisms to prepare in advance, while unpredictable changes trigger stress responses.

Q: What is the difference between regulated and facultative responses to environmental change?

Regulated changes

• Occur in anticipation of predictable events

• Include changes in morphology, physiology, or behavior

Examples:

• Seasonal breeding

• Migration

• Molting

Rapid facultative changes

• Occur during or after unexpected events

• Often involve stress physiology

Examples:

• Predator escape

• Injury responses

• Acute stress reactions

Q: What is the Principle of Allocation?

Organisms have limited energy, so they cannot maximize all life processes simultaneously.

Energy must be allocated among:

• Growth

• Reproduction

• Immune function

• Predator avoidance

• Foraging

• Maintenance/homeostasis

Trade-offs determine survival and reproductive success.

Q: What is the Barrel Model (Weiner 1992)?

The Barrel Model illustrates that organisms must balance competing physiological demands because energy is limited.

Life functions compete for the same energy resources, so increasing investment in one function reduces energy available for others.

Q: What is allostasis?

Allostasis is the process of achieving stability through physiological change.

Unlike homeostasis (maintaining constant internal conditions), allostasis allows set points to shift depending on environmental conditions.

Example:

• Seasonal hormone changes

• Stress hormone increases during emergencies

Q: What are the three energy components used in the allostasis framework?

EE (Existence Energy)

• Energy required for basic homeostasis

• Example: maintaining body temperature

EI (Energy Intake Cost)

• Energy needed to find, process, and assimilate food

EG (Energy Gain)

• Energy available in the environment

Stress occurs when:

Energy demand > energy available

Q: What is Perturbation Resistance Potential (PRP)?

PRP is the capacity of an organism to cope with environmental disturbances.

It depends on:

• Available energy reserves

• Environmental conditions

• Life-history stage

Higher PRP = greater ability to withstand stressors.

Q: What is the Emergency Life History Stage (ELHS)?

ELHS occurs when environmental conditions are severe and organisms temporarily abandon normal activities to survive.

Examples:

• Stop reproduction

• Stop territorial defense

• Reduce activity

• Focus on survival

Once conditions improve, organisms return to their normal life-history stage.

Q: What is a stressor?

A stressor is any stimulus that disrupts homeostasis and activates the stress response system.

Examples:

• Predation threat

• Food shortage

• Disease

• Temperature extremes

• Social conflict

Q: What is the difference between acute and chronic stress?

Acute stress

• Short-term

• Adaptive

• Helps survival

Examples:

• Predator attack

• Sudden injury

Chronic stress

• Long-term exposure

• Can be harmful

• Causes physiological damage

Examples:

• Persistent food shortage

• Long-term habitat disturbance

Q: What system controls the first phase of the stress response?

The Autonomic Nervous System (ANS), specifically the sympathetic nervous system.

This activates the fight-or-flight response.

Q: Which hormones are released during Phase 1 of the stress response?

Catecholamines:

• Epinephrine (adrenaline)

• Norepinephrine (noradrenaline)

• Dopamine

These hormones are released from the adrenal medulla.

Less than 1 min

Q: Why do catecholamines act very quickly?

Because they:

• Are stored in vesicles

• Are released by neurons

• Use existing proteins and signaling pathways

• Are linked to the sympathetic nervous system

Response time: seconds to <1 minute

Q: What physiological effects do catecholamines cause?

Catecholamines prepare the body for fight or flight:

• Increased blood flow to muscles

• Increased heart rate

• Increased airflow to lungs

• Suppressed digestion

• Increased alertness

• Release of glucose and fats

• Inhibition of insulin

• Increased glucagon

• Release of β-endorphins (pain reduction)

Q: What does HPA axis stand for?

Hypothalamus
Pituitary
Adrenal axis

It regulates the endocrine stress response.

Q: What hormone cascade activates the HPA axis?

• Hypothalamus

  • Releases CRH (Corticotropin Releasing Hormone)

• Anterior Pituitary

  • Releases ACTH (Adrenocorticotropic Hormone)

• Adrenal Cortex

  • Releases glucocorticoids → Cortisol, Corticosterone

Q: What are the main glucocorticoids?

Cortisol

• Found in fish and mammals

Corticosterone

• Found in birds, reptiles, amphibians, rodents

These hormones regulate metabolism during stress.

• people think corticosterone and HPA is only funcctional for stres; NOT TRUE. Durng daily life without stressful events. hugher in morning

Q: Why can glucocorticoids cross cell membranes?

Because they are steroid hormones, which are lipid-soluble.

They diffuse across cell membranes to reach intracellular receptors. Mineralocorticoid receptor (MR)

Glucocorticoid receptor (GR)

Q: Why can glucocorticoids NOT be stored in cells?

Steroid hormones must be synthesized on demand, because:

• They diffuse through membranes

• They cannot be stored in vesicles

Q: What protein transports glucocorticoids in the blood?

Corticosteroid Binding Globulin (CBG)

Produced in the liver.

Functions:

• Transport glucocorticoids

• Extend hormone half-life

Q: What is the Free Hormone Hypothesis?

Only unbound (free) hormone can:

• Enter tissues

• Bind receptors

• Produce biological effects

Bound hormone is inactive.

Q: What is the Reservoir Hypothesis?

Bound hormones act as a reserve pool.

When needed:

• Binding proteins release hormone

• Hormone becomes biologically active

Q: What are the two main glucocorticoid receptors?

1. MR (Mineralocorticoid Receptor)

2. GR (Glucocorticoid Receptor)

They differ in affinity and function.

Q: How do MR and GR receptors differ?

MR

• High affinity

• Activated at low hormone levels

• Active during baseline conditions

GR

• Lower affinity

• Activated during high stress hormone levels

• Controls stress responses

Q: What role do MR receptors play?

MR receptors regulate:

• Circadian glucocorticoid rhythms

• Baseline hormone regulation

• Brain stress regulation

They are mostly active under normal conditions.

Q: What role do GR receptors play?

GR receptors regulate:

• Stress response

• Gene expression changes during stress

• Metabolic adjustments

They are activated when glucocorticoids rise during stress.

Q: Why can't all glucocorticoid effects be genomic?

Some glucocorticoid effects occur within seconds to minutes, which is too fast for gene transcription.

Therefore, some effects occur through membrane receptors and non-genomic pathways.

Q: What do 11β-HSD enzymes do?

They activate or deactivate cortisol before receptor binding.

Two types:

11β-HSD1

• Converts inactive cortisone → cortisol

11β-HSD2

• Converts cortisol → cortisone (inactive)

Q: Why is cortisol deactivated in the kidney?

To allow aldosterone to bind mineralocorticoid receptors.

Otherwise cortisol would activate them.

Why can eating large amounts of licorice cause hypertension?

Licorice inhibits 11β-HSD2, preventing cortisol deactivation.

Result:

• Cortisol activates mineralocorticoid receptors

• Increased Na⁺ and water reabsorption

• Increased blood volume

• High blood pressure

Q: How do glucocorticoids affect metabolism?

They increase available energy by:

• Protein breakdown (muscle catabolism)

• Gluconeogenesis (glucose production)

• Fat breakdown

This provides fuel during stress.

Q: How does stress affect reproduction?

Stress generally suppresses reproduction.

It can:

• Delay breeding

• Reduce reproductive hormones

• Cause abandonment of breeding attempts

Q: How do stress hormones suppress reproduction?

They:

• Inhibit GnRH release

• Reduce gonadotropin secretion

• Lower testosterone production

• Reduce LH receptor activity

Q: How is the HPA axis regulated by negative feedback?

High glucocorticoid levels:

1. Inhibit CRH release from hypothalamus

2. Inhibit ACTH release from pituitary

3. Reduce pituitary sensitivity to CRH

This prevents excessive hormone production

Q: How can extreme climatic events affect organisms?

Direct effects:

• Mortality (heat waves, cold snaps)

• Nest flooding

• Dehydration

Indirect effects:

• Reduced feeding success

• Lower chick provisioning

• Changes in breeding timing

• Fewer offspring

Q: How does the stress response change seasonally?

HPA axis sensitivity varies across the year.

Typically:

• Peaks before breeding

• Decreases during breeding

This prevents stress responses from interrupting reproduction.

Q: Why might the stress response be suppressed during molt?

High glucocorticoids damage feather quality.

Therefore, organisms reduce stress responses during molt to avoid feather defects (fault bars).

why is it that you’re able to run faster or something in a stressful situation

Adrenal Medulla-

Catecholamines

• increase heart ratee → oxygen to muscles

• increase ventilation

• increase vasocotriction of specific region such as skin (bring more volume of air)

• decrease digestion

• increase glucagon

• glucose released from muscle and liver

• β-endorphin, an endogenous opiate and may

  contribute to analgesia; that is, it may decrease the

  perception of pain → allow you to escape

why do you remember traumatic events so easily

• stimulus to amygdala: center of fear

• stimulus to hippocampus: memory

• useful for learning in evolutionary sense

Droughts &

Heat waves

Dehydration: Behavioral strategies

- Lower MR? (Tieleman et al. 2002)

- Lower LH

- Lower STI response

- Camels: adjustments in plasma renin-

angiostensin-aldosterone but not in CORT

- Spadefoot toad: facultative metamorphosis

• environmentally induced, reversible, or selectable developmental pathway in amphibians—primarily salamanders and newts—where individuals can either transform into terrestrial adults or retain larval characteristics

Perturbation Resistance Potential: draw graph and short explanation

difference between the amount of energy that an individual needs to perform all the normal activities and the amount of energy available in the environment

• varitations related to life history stages and environemnt changes

Potential explanations for

Seasonal modulation of the adrenocortical stress

response

1. The Energy Mobilization Hypothesis: corticosteroid concentrations

will be highest during energetically costly times of the year  metabolic

role of CORT

2. The Behavioral Hypothesis. Life-history stage expressing (or not)

CORT-mediated behaviors.

3. The preparative Hypothesis: Seasonal peaks in corticosteroid

concentrations provide better preparation for periods when adverse

conditions are more common.

4. The brood value Hp: Brood value is high  greater resistance

potential to acute stressors and the adrenocortical response is mitigated

core/hub of HPA axis

perceive what is going on in the conditions outside of the body and those conditions could be individual stae, environmental, abiotic

• inform hpa axis and respond by mobilizing energy

• modulator of metabolism

• what is “master of masters”????