Exam 2 PSY 438

Important Forebrain Structures

Thalamus: Sensory processing, movement. Relay station for incoming information (sends and receives info from cerebral cortex)

Hypothalamus (~almond shape and size)

◦ Learning, memory, motivation, regulation of body temperature, hunger, thirst, sexual drives, circadian rhythms, etc.,

◦ Helps regulate two key stress communication systems: autonomic nervous system and endocrine system

Pituitary (~pea size)

◦ “master gland”

◦ Plays key role in regulating metabolism, growth, reproduction

◦ Regulates other endocrine glands in body and body organs through release of hormones from brain into bloodstream

Limbic system:

• Motivation, emotion, memory

Amygdala – involved in assessment of emotional valence/significance of incoming sensory & other info

Hippocampus – involved in memory formation, storage, and retrieval

What was the finding of the study discussed in class that examined amygdala activity and carotid intra-medial thickness (atherosclerosis in the carotid artery)? ***not sure if I’ll include this

measured:

• Amygdala activity: How strongly the amygdala responded to angry and fearful facial expressions.

• Carotid intima-media thickness (IMT): The thickness of the inner layers of the carotid artery wall, which is an early marker of atherosclerosis.

• Greater amygdala activity was associated with greater carotid artery wall thickness.

Higher amygdala reactivity to threats → Associated with thicker carotid artery walls →

Greater indication of early atherosclerosis

Explain the significance of the findings of the study of individuals about to undergo medical board examination. ***not sure if I’ll include this

Compared activity of PFC during an attentional task (rodent studies)

• During exam prep period, participants had significantly higher Perceived Stress Scoure scores (M=17.7) compared to non-test controls (M=11.1), no difference between test-takers and controls during non-stress period following the exam

• Poorer task performance + observed reductions in functional connectivity in PFC in test takers compared to controls

Differences in performance and functional connectivity not observed in low stress period (thus reversible)

Fast + Slow Communication Tracks to Amygdala (recognize)

Fast (Unconscious) - to thalamus, then directly to amygdala

• Fast and automatic: Reacts before you consciously understand the threat.

• Less accurate: The brain makes a quick judgment with limited information.

• Purpose: Helps you respond to potential danger immediately.

Slow- to thalamus, then visual cortex, then amygdala

• Slower and more detailed: The brain analyzes what you're seeing.

• More accurate: Helps determine whether the threat is real.

• Purpose: Allows you to evaluate the situation and adjust your emotional response.

Immune System Primary Functions

1. Identify “self” from “non-self” (or non-normal self)

2. Destroy and/or remove non-self (or non-normal self)

“Non-Self” or “Non-Normal Self” Targets

Invading pathogens: disease-causing micro-organism, such as a virus or bacteria

• Virus: nucleic acids enclosed in a protein coat; cannot reproduce without a host cell

• Bacteria: single-celled micro-organisms self-equipped with machinery for their own survival/reproduction

➢Antigen: unique, complex molecule that triggers an (acquired/specific) immune response

Cancerous cells: identifying and destroying abnormal cancerous cells in the body

Damaged or worn-out cells: injury or disease

Non-Immunologic Defenses

• Skin forms protective barrier

• Destroyed by bodily secretions or other mechanisms (e.g., mucous, mechanical reactions like coughing)

• If not destroyed: immune system…

Carried to spleen via bloodstream,

Lodging in tissues → lymphatic vessels/nodes,

Gastrointestinal (GI) or respiratory tract, lodging in lymphoid organs

Two Major Classes of Immune Defense

1. Innate, non-specific (phagocytes, NK cells)

• first line of defense, relatively fast (hours)

• non-specific ‘killers’

2. Acquired, specific (T and B lymphocytes)

• second line of defense, slower (days)

• Immune processes are carried out by white blood cells (WBCs)

• Polymorphonuclear granulocytes – eosinophils, neutrophils, basophils (50-75%)

• T and B lymphocytes (20-40%)

• Monocytes/Macrophages (2-8%)

Phagocytic cells (specialized WBCs)

• Include macrophages, neutrophils, and eosinophils

• Non-specific “killers” of non-self/foreign material; degraded by digestive enzymes of lysosomes in cell

• Macrophages also operate as antigen-presenting cells to support adaptive immune functions (T & B-call activity)

Natural killer (NK) cells.  (won’t need to write these out but be able to recall them)

• destroy virus-infected and tumor cells

• release chemical that breaks down cell membrane of infected/damaged cell

Complement system

• system of plasma proteins which can destroy bacteria, viruses

• binding of proteins punches a hole in membrane of invader

Innate (nonspecific) immunity quick sheet

Defense	Main Function	Memory Trick
NK Cells	Kill infected or abnormal body cells	Kill
Phagocytes	Engulf and digest invaders	Eat
Complement	Mark invaders, promote inflammation, or create holes	Assist & Attack

Adaptive (or Acquired) Immunity.  (won’t need to write these out but be able to recall them)

T cells (lymphocytes)

• helper T-cell (CD4+)

• help B-cells/macrophages

• cytotoxic, killer T cells (CD8+ kill virus-infected and mutated cells)

• cell-mediated immunity

B cells (lymphocytes)

• release antibodies (Ab)

• specific antibody-antigen match

• encounter antigen → proliferate

• humoral immunity

Cytokines: Immune Messengers

Cytokines: signaling proteins produced by activated cells (immune and non-immune cells)

• Play key role in inflammatory and other immune responses (Activate immune cells, Promote inflammation, Signal the brain, Regulate immune responses)

• Multiple sources, targets, and functions

• Specificity of actions affected by cell receptors, other cytokines, hormones, etc.

• Hundreds have been identified thus far

Cytokines are released by many different cells, especially immune cells, including:

• Macrophages: Release cytokines when they detect an infection.

• T cells: Release cytokines to coordinate immune responses.

• Natural Killer (NK) cells: Release cytokines that help activate other immune cells.

Cytokine Signal route

1. Macrophage detects bacteria → 2. Macrophage releases cytokines → 3. Cytokines signal other cells → 4. Immune response increases, and the brain may trigger sickness symptoms

Inflammation

• Goal: bring immune cells to site of injury/infection, destroy/inactivate foreign invaders, prep for tissue repair

• Vasodilation

• Increased vascular permeability (So Tissue repair can begin)

• Influx of immune cells (e.g., phagocytes)

• Destruction of non-self (e.g., bacteria)

What happens during a local inflammatory response

For example, when you get a small cut on your finger.

1. Injury or infection occurs

Damaged cells and immune cells release inflammatory chemicals, including cytokines and histamine.

2. Blood vessels widen (vasodilation)

More blood flows to the injured area, causing redness and warmth.

3. Blood vessels become more permeable

Fluid and proteins move into surrounding tissue, causing swelling.

4. White blood cells arrive

Neutrophils and macrophages help destroy pathogens and clear damaged cells.

5. Healing begins

Inflammation decreases as the threat is controlled and tissue repair progresses.

Characteristic	Why it happens
Redness	Increased blood flow
Heat	Increased blood flow
Swelling	Fluid leaks into tissues
Pain	Inflammatory chemicals and swelling stimulate nerves

Acute phase response route

1. Virus enters the body → 2. Immune cells release cytokines → 3. Cytokines signal the brain and liver → 4. Fever, fatigue, loss of appetite, and immune changes occur

Advantages and disadvantages of inflammation with respect to our health and well-being.   

Good: Acute inflammation is a fast- acting, adaptive response designed to remove offending agent and initiate healing

Bad: Chronic inflammation can promote the development and progression of disease

Inflammation implicated in the etiology and progression of major killers:

1. Heart Disease 2. Cancer 3. Stroke 4. Respiratory disease

Inflammation and Other Diseases: Autoimmune Diseases, Allergy, Asthma, Inflammatory Bowel Disease, Osteoarthritis

Atherosclerosis

Atherosclerosis:

• hardening of the arteries

• lipid/cholesterol deposits – plaques

• leads to reduced blood flow

• Cause and consequence of hypertension

• plaques can rupture – clot (thrombis)

• coronary artery/heart disease (CAD/CHD): can lead to heart attack

• cerebrovascular disease (CVD): can lead to stroke

The Progress of Atherosclerosis

1. Damage or dysfunction of the artery's inner lining (endothelium): This allows cholesterol-containing particles, especially LDL, to accumulate in the artery wall.

2. Inflammation begins: Immune cells enter the artery wall and respond to the accumulated cholesterol.

3. Plaque forms: Macrophages take up cholesterol and become foam cells. Fatty deposits and scar-like tissue gradually build up.

4. Artery narrows: Growing plaque can restrict blood flow.

5. Plaque may rupture: A blood clot can form over the damaged plaque, potentially blocking blood flow suddenly.

How does Atherosclerosis cause blood clots, heart attacks, and strokes?

Health Event	What Happens
Blood clot (thrombus)	Plaque ruptures or erodes, exposing material that activates platelets and clotting.
Heart attack	A clot blocks blood flow through a coronary artery, depriving heart muscle of oxygen.
Ischemic stroke	A clot blocks an artery supplying the brain, depriving brain tissue of oxygen.

What is the role of inflammation in Atherosclerosis

• Early stages: Inflammation attracts immune cells to the artery wall, contributing to plaque formation.

• Progression: Chronic inflammation helps plaques grow and can damage the artery wall.

• Plaque rupture: Inflammatory cells release substances that weaken the protective fibrous cap covering the plaque.

• Heart attacks and strokes: If a vulnerable plaque ruptures, blood clots can form and suddenly block blood flow.

Role of inflammation: Chronic inflammation promotes plaque buildup, growth, and instability, increasing the risk of clot formation.

Key Inflammatory Components of Atherosclerosis

Damaged endothelial cells attract macrophages into inner layer of vessel

• Macrophages and smooth muscle cells eat lipid/oxidized LDL – develop into foam cells – upregulate inflammatory activity

• Arterial damage also activates local inflammatory response

• Local inflammatory response contributes to weakening of plaque – rupture leads to clot, stroke, heart attack

Therapeutics target LDL (e.g., statins) and anti- inflammatory pathways (e.g., statins, proinflammatory cytokine blockers)

Cardiovascular System

Transport system: deliver oxygen and food to cells; remove wastes and carbon dioxide

• Main components: heart, lungs, blood, blood vessels

• Pulmonary (lung), cardiac (heart) and systemic (body) circulation

GOALS:

*pump blood into arteries to provide cells with needed nutrients worldwide pump blood into lungs to be oxygenated and remove waste (CO2)

*pump blood to filter organs - liver and kidneys – to remove wastes)

Cardiovascular system terms

• Arteries - blood vessels responsible for carrying oxygen-rich blood away from the heart to the body

• Veins - blood vessels that carry oxygen-poor blood from the body back to the heart for reoxygenation

• Venous return – strength of blood flow back to the heart via veins

• Arterioles - small blood vessels that connect arteries and capillaries

• Capillaries – smallest blood vessels in our body!

Cardiovascular system: symp vs. parasymp

Cardiovascular Effect	Sympathetic	Parasympathetic
Heart rate	↑ Increases	↓ Decreases
Heart contraction strength	↑ Increases	Little direct effect on ventricular contraction
Blood pressure	Generally ↑	May ↓
Blood vessels	Constricts many vessels; some dilate	Minimal direct effect on most vessels
Main purpose	Prepare for action	Conserve energy

ANS Regulation of Cardiovascular Activity

Hybrid Nervous-Endocrine Sympathetic-Adrenal-Medullary (SAM) Axis

Disease Spotlight: Hypertension

BP = systolic (pressure in arteries when heart beats and fills them with blood) /

diastolic (pressure in the arteries when the heart relaxes between contractions)

~95% “essential hypertension” (no specific identifiable cause)

~5% “secondary hypertension” (due to other diseases)

Hypertension is a risk factor for: atherosclerosis, heart attack, stroke (leading cause of stroke), kidney failure, vision problems, “Silent killer”, Over half of adults age 65 and over have hypertension

Reactivity hypothesis

Exaggerated or prolonged cardiovascular reactivity to psychological stressors can promote the development of cardiovascular disease

• i.e., those with greater stress responses or who experience cardiovascular responses over prolonged periods (the chronically stress) will be more likely to develop cardiovascular health conditions

Meta-analyses of many prospective studies indicate that greater cardiovascular stress reactivity OR slower recovery to a lab stressor predicted greater risk of future:

• high blood pressure

• atherosclerosis

• cardiac events

• cardiac and all-cause mortality

Autonomic Imbalance

Under resting conditions, the parasympathetic branch of the nervous system (PNS) maintains inhibitory control on the heart (i.e., keeps heart rate down)

• Communication via vagus nerve (main parasympathetic nerve)

• The PNS via the vagus also regulates variability in heart rate (i.e., its up and down activity) – this is referred to as heart rate variability (HRV)

• Greater HRV = healthier function

• Thayer and Lane (2007) provide a comprehensive overview of the routes through which the PNS, particularly through regulation of HRV, might influence cardiovascular health outcomes

PNS – downregulates HR, enhances HRV

SNS – elevates HR

Autonomic imbalance occurs when one branch, typically SNS, dominates.

Indicators of autonomic imbalance:

• greater resting HR (suggests greater SNS control of heart)

• less HR recovery following stress (suggests PNS unable to inhibit HR when stress is over)

• lower HRV (suggests PNS is less able to up or down regulate activity)

Thayer and Lane review evidence that the prefrontal cortex plays an important inhibitory role on the SNS and upregulation of PNS

• But conditions of threat/stress can lead to hypoactive frontal cortex – less inhibition

• Key objective is to identify the mental states/processes that enhance this inhibitory control

Understand the model by Boehm and colleagues describing potential relationships between positive psychological well-being, stress, health behaviors, and disease risk (including cardiovascular disease).

This figure explains how positive psychological well-being, stress, and health behaviors influence your risk of developing cardiovascular disease (heart and blood vessel disease) throughout your life.

The main idea is that positive psychological well-being can protect your heart, while chronic stress can increase your risk of heart disease.

1. Positive Psychological Well-Being

• Decrease stress (−).

• Increase restorative processes (+), which support health and recovery.

• Decrease deteriorative processes (−), which can harm health over time.

2. Stress

• Increased blood pressure.

• Greater inflammation.

• Prolonged activation of stress hormones.

• Unhealthy changes in sleep and behavior.

3. Restorative vs. Deteriorative Processes (Blue Arrow)

The blue arrow represents the balance between health behaviors and physiological functioning that support health versus those that contribute to disease.

4. Cardiovascular Disease

• More restorative processes → Lower cardiovascular disease risk (−).

• More deteriorative processes → Higher cardiovascular disease risk (+).

5. Social Environment and Age

Experiences and behaviors can accumulate over time and affect cardiovascular health later in life.

Functional View of Emotions

The functional view of emotions suggests that emotions serve a purpose: they help us adapt to our environment, respond to situations (short-lived), and survive.

• psychological functions: alter attention, direct behavior, activate relative associative memory networks

• physiological functions: organize responses of biological regulatory systems to support adaptive response.

Fear

Fear is considered a basic emotion because it is universal, biologically based, and important for survival.

What adaptive challenge triggers fear?:

The adaptive challenge is perceived danger or a threat to survival.

What is fear designed to do?

Fear is designed to protect us by preparing the mind and body to respond to danger.

It helps us: Detect threats, React quickly, Increase physiological arousal, Learn from danger.

• amygdala: fear detection. organizes sensory info and info from other areas of the brain (frontal cortex)

• sends info to other areas of the brain that organize behavioral and physiological responses, such as the hypothalamus which organizes endocrine and NS responses

The 3 key features/characteristics of a basic emotion. 

• distinct - you can distinguish the behavior/physiology of one basic emotion from another. v dif in the brain.

• hard wired - circuity for emotion hard wired in the nervous system. somewhere in the brain that causes the emotion

• functional - provides adaptive solution to a survival relevant problem. must be useful; survival advantage.

What system in the brain plays a key role in emotional experience and its downstream consequences?  This system in the brain includes the brain area which organizes our fear response.

• The limbic system is a group of interconnected brain structures involved in emotions, motivation, memory, and physiological responses.

  It helps us experience emotions and influences how our bodies and behaviors respond to them.

• organizes nervous and endocrine system activity to direct downstream physiological activity in the peripheral body (ex. cardiovascular, immune)

Important Structures of the Limbic System

Brain Structure	Main Function
Amygdala	Detects threats and helps organize fear responses.
Hypothalamus	Controls physiological responses, including heart rate, stress hormones, and autonomic activity.
Hippocampus	Helps form memories and connects emotions to experiences.

Example: Seeing Something Scary

Imagine you're walking outside and see a snake.

1. Amygdala: Helps detect the threat and organize your fear response.

2. Hypothalamus: Helps activate the sympathetic nervous system, increasing heart rate and preparing your body for action.

3. Hippocampus: Helps you remember the experience and its context.

Is there strong support for distinct profiles of physiological activity for specific emotions (e.g., for fear vs. anger)? 

• is there evidence for emotion-specific physiology?

• mixed for autonomic NS activity

  • decent support for specific patterns of activity for positive vs. negative emotions

  • less clear for specific emotions, but some support (ex. distinct patterns for anger vs. fear)

• less data regarding specific patterns of endocrine activity

  • some hints of specificity in studies of specific threats ( ex. social threats)

  • don’t know which comes first

Are emotions always adaptive?  Describe four characteristics that affect the adaptive value of an emotion.  

Emotions are not always adaptive. Although emotions evolved to help us survive and respond to situations, they can sometimes be maladaptive, aka it is inappropriate for the situation or causes more problems than it solves.

different forms of affect (emotion, mood, affective temperament) typically differentiated by:

• time/duration

• cognitive characteristics

• antecedents

• universality. emotional can look different on everyone

• developmental considerations

Major Depressive Disorder

• depressed mood (sad or empty)

• loss of interest or pleasure in activities

• significant weight change or change in appetite

• insomnia or hypersomnia nearly every day

• fatigue or loss of energy

• feelings of worthlessness

• diminished ability to think/concentrate

• recurrent thoughts of death/suicidal ideation

occurring together during a 2 week period most of the day, enarly every day

change from previous functioning

detrimental to functioning

Risk factors for depression

• genetic

• biochemical (5-HT, NE)

• personality (low self esteem, pessimistic, poor coping strategies)

• stress (abuse, neglect, exposure to violence, poverty, etc.)

• diease/illness

• 
  

• 80-90% of affected respond well to treatment (pharmaceutical, psychotherapy, or combo)

depression in young adults and older adults

young adults:

• highest prevalence of MDD

• also high rates of subclinical depression (almost meet diag. criteria)

• 45% of students report feeling so depressed at some time in the last year that they have trouble functioning

• 20% diagnosed/being treated

• ¼ experience a depressive episode by age 24

older adults:

• prevalence estimates range from 8-20% of community residing older adults

• impairs physical, mental, and social functioning

• increased risk of and or exacerbates course of many diseases (heart dis, cancer)

• highest in the oldest-old (80+) and often undertreated.

depression breaks the heart

high prevalence of comorbid (at the same time) depression and heart disease

depression associated with:

• increased risk of heart disease development

• increased risk of cardiac events and mortality in those with existing CHD

Inflammation-induced depression

proinflammatory cytokines induce sickness behavior

• fatigue

• sleepiness

• irritability

• loss of appetite

• cognitive impairment

• reduced activity/social

• 
  

• proinflammatory cytokines can reach the brain to active a sickness behavior response and fever through these pathways:

  1. travel through blood (cross the blood brain barrier)

  2. via stimulation of the vagus nerve. stimulates internal organs.

  evidence from experimental manipulations

  • injection of IL-1, IL-6, TNF-a cause people to have sick behavior, even if they are not sick.

  • blockage of cytokine activity reduces/eliminates sick behaviors.

cytokine induced negative mood in typhoid vaccine recipients

the vaccinated group felt worse and worse emotionally

vaccine caused an immune response and released proinflammatory cytokine IL-6

IL-6 increase associated with negative mood increase

when people are susceptible to low mood and they get sick, they could end up doing worse than others

anger in/out/control

anger: irritation, rage, annoyance, fury

anger out: tendency to express anger towards individuals or objects through physical or verbal aggression

anger in: tendency to suppress angry feelings. rumination, frustration

anger control: ability to control outward expression of anger. more in, less out.

anger and wound healing

Simply expressing anger or suppressing it was not significantly associated with healing speed. The important factor was anger regulation.

difficulty regulating anger is associated with slower wound healing, supporting a connection between emotions, stress, and immune-related processes; endocrine system, specifically the HPA axis (hypothalamic-pituitary-adrenal axis).

The researchers measured cortisol, a stress hormone released through HPA-axis activity.

anger control strategies

cognitive reappraisal: manage your emotional reactions, think about what your partner is saying objectively and analytically, maintain a neutral mood

emotional suppression: control your facial expressions, muscles, etc, so no one can recognize what you might be feeling

control: no specific directions

the suppression group experienced the most anger

the most HRV was from the reappraisal group = more effective peripheral NS regulation of heart activity

anger and physiology

anger is the only emotion that has physiological constancy.

HR, BP, Stress reaction and others all go up

emotion/affect and immunity

short-term experience of emotions:

• if positive may be immunoenhancing

• if negative may be immunosuppressing

however, better to express negative emotions that suppress them

• suppression of negative emotions typically associated with poorer immune functioning

• can create stress

long term mood (ex. depression and anxiety) - generally associated with poorer immune function and a pro-inflammatory state

Happiness, Stress, and Physical Health Study

• People in the lower three happiness quintiles were significantly happier on their leisure day (weekend) than on a workday.

• People in the top two happiness quintiles reported similarly high happiness levels on both workdays and weekends.

• 
  

  Biological measure	Relationship with happiness
  Cortisol	More happiness → Lower cortisol
  Heart rate	More happiness → Lower heart rate in men
  Blood pressure	No significant relationship in the original 2005 study
  Blood pressure at follow-up	More happiness → Lower systolic blood pressure

esearchers exposed participants to stressful mental tasks and measured changes in fibrinogen.

They found:

• Less happy participants: Larger increases in fibrinogen after stress.

• Happier participants: Smaller increases in fibrinogen after stress.

This suggests happier individuals experienced a reduced inflammatory/clotting-related response to acute stress.

Importantly, baseline fibrinogen levels were not significantly related to happiness. The difference was in how fibrinogen responded to stress.

 the “undoing effect” and “stress buffering” hypotheses

the “undoing effect”: positive emotions speed physiological (cardiovascular) recovery from stress. recover faster after experiencing stress or negative emotions

positive affect can provide a “stress buffering” function. reduce the intensity of our negative emotional and physiological responses when stress occurs

Chopsticks experiment

neutral face, standard smile, or Duchenne smile

Greater HR recovery in the smiling groups, especially the Duchenne group

• support for hypothesis that positive affect can help “undo” or “buffer'“ physiological effects of stress

• however null findings have also been observed