PSY 340 - EXAM 3

ch 9, 10, 11

Allostasis

Body’s anticipatory adjustments that change set points depending on circumstances (stress, time of day, etc.)

Basal metabolism

Energy required to maintain body temperature.

Consumes 2/3–½ of energy intake.

Ectothermic Animals

Body temperature = environment temperature.

Behavioral regulation (basking, shade, burrowing)

Endothermic Animals

Maintain constant internal temperature regardless of environment.

Heat generated ∝ body mass

Heat lost ∝ surface area

Physiological Responses (to cool down)

Dilate blood vessels

Sweat/pant (eccrine & apocrine glands)

Evaporation cools body

Physiological Responses (to warm up)

Constrict blood vessels

Shivering

Fluff fur (increase insulation)

Pros/Cons of Consistent Body Temp

Pros: Stable environment for protein function, Enables rapid muscle contractions, & Supports high metabolism

Cons: Requires constant fuel and Reproductive cells require cooler temperature (testes outside body)

Brain Regulation of Temp

Preoptic Area/Anterior Hypothalamus (POA/AH)

Integrates signals from: Skin temperature receptors, Organ receptors, & Brain temperature (self-monitoring)

Controls: Shivering, Sweating, Heart rate, Metabolism, Blood flow changes

Damage → severely impaired temperature regulation.

Fever

A temporary increase in the body’s set point.

Triggered by infection → leukocytes release cytokines → stimulate vagus nerve → hypothalamus raises temperature

Danger: above 39.25C, life-threatening 41C

Water importance

70% of body = water

Necessary for blood pressure maintenance

Too much → stomach distension; excretion

Too little → vasopressin released → kidneys conserve water

Osmotic Thirst

Trigger: High solute concentration outside cells (after salty foods)

• Water leaves cells → cells shrink → osmotic receptors detect imbalance.

Mechanism: Osmotic pressure pulls water across cell membranes to restore balance.

Hypovolemic Thirst

Trigger: Loss of blood volume (bleeding, sweating, diarrhea), detected by baroreceptors.

Hormones involved:

• Vasopressin (ADH): conserves water

• Angiotensin II: constricts blood vessels; triggers drinking

• Aldosterone: retains sodium

Behavioral outcome: Craving for salty water → “Sodium-Specific Hunger”

Circumventricular Organs

These areas have weak BBB so they can monitor blood solutes:

• OVLT (Organum Vasculosum Laminae Terminalis)

• SFO (Subfornical Organ)

They send signals to:

• Paraventricular nucleus (controls ADH)

• Supraoptic nucleus (ADH release)

• Lateral preoptic area (drinking behavior)

Synergistic Effects

When baroreceptors + angiotensin II are activated together —> The urge to drink is MUCH stronger

Combined effect > sum of parts (2+2 = 6 instead of 4)

Saliva

breaks carbs

Stomach

stores foods, digests proteins

Duodenum

first to absorb nutrients

Small Intestine

primary absorption

Large intestine

absorbs water & minerals

Food Preference & Flavor

Smell, Taste, Texture, Temperature, Spiciness

most ppl Prefer sweet, Avoid bitter, Salt & sour okay in moderation

Conditioned Taste Aversion

an adaptive learning where an organism develops a strong aversion to a specific food or taste after associating its consumption with subsequent illness or nausea

Stomach Signals

Vagus nerve → stomach stretch → satiety

Splanchnic nerve → nutrient content → satiety especially when vagus damaged

Duodenum Signals

Distention → satiety

Fat → releases OEA

All food → releases CCK, which:

• Closes sphincter

• Stimulates vagus nerve

• Signals satiety

Glucose

Main energy source; excess → glycogen & fat

Insulin

From pancreas

Helps glucose enter cells

Acts as satiety hormone in brain

Glucagon

From pancreas

Converts glycogen → glucose

Dysregulation: High insulin

Most glucose stored → little available

Hunger returns quickly

Leads to overeating + weight gain

Dysregulation: Low insulin (diabetes)

Glucose stays in blood

Cells starve → excessive eating

Glucose excreted in urine → weight loss

Long-term Hormonal Control: Leptin

Released by fat cells → measures long-term fat reserves

Low leptin → hunger

High leptin → increased activity (but not always decreased hunger)

Obesity

Leptin insensitivity

Rare cases: cannot produce leptin (genetic)

Hypothalamic Control of Hunger (Arcuate Nucleus)

Hunger-sensitive neurons stimulated by: taste input, ghrelin

Satiety-sensitive neurons stimulated by: CCK, glucose, insulin, leptin, GLP-1

Hypothalamic Control of Hunger (Paraventricular Nucleus)

Receives satiety signals → releases melanocortin

Receives hunger signals (NPY, AgRP, GABA)

Damage → large meals (can’t stop eating)

Hypothalamic Control of Hunger (Lateral Hypothalamus)

Releases orexin → increases persistence in seeking food

Increases taste responsiveness and insulin release

Damage = anorexia-like refusal to eat or drink

Hypothalamic Control of Hunger (Ventromedial Hypothalamus)

Damage → Frequent meals, Weight gain, High stomach motility

Excess insulin production → increased fat storage

Why we overeat

Eating with others

Emotional eating

Highly pleasant tasting foods

“Low fat” labels

Variety effect → Sensory Specific Satiety (we eat more when many flavors available)

Heritability of Obesity

Change 0.4-0.7/1.0

Genes: Melanocortin gene variations, Prader–Willi syndrome (supported by twin study)

Environment matters (EX: Pima Tribe → obesity due to genetic + high-calorie environment)

Obesity Treatment options

Exercise

Reduce calories & soft drinks

Appetite suppressant drugs

GLP-1 agonists

Bariatric surgery: Gastric bypass, Gastric banding, & Intragastric balloon

Bulimia Nervosa

Cycle of dieting → binge eating

Sometimes purging

Mostly women

Biological features: low CCK, high ghrelin

Similar to addiction: Higher D3 receptors, Withdrawal symptoms

Anorexia Nervosa

90–95% female

Extreme weight loss, excessive exercise

Fear of weight gain

Altered dopamine activity

New treatment hypothesis: adjust temperature regulation

Chromosomal Sex

Determined at conception by sperm (X or Y)

SRY gene on Y chromosome activates testis development

Gonadal Sex

Gonads become testes (if SRY present) or ovaries (if absent)

Phenotypic Sex

Internal ducts (Wolffian vs Müllerian)

External genitalia

Determined by hormones released from gonads.

Before Week 6-7 of Pregnancy

Embryo is sexually indifferent.

Both Wolffian ducts (male) and Müllerian ducts (female) are present.

If SRY gene is present

Gonads → testes

Testes release:

• Testosterone → develops Wolffian ducts

• MIH (Müllerian Inhibiting Hormone) → degenerates Müllerian ducts

If SRY gene is absent

Gonads → ovaries

Müllerian ducts → uterus, oviducts

Low testosterone → clitoris + labia

Wolffian ducts degenerate

Steroid hormones

Function: Bind to membrane receptors, Activate proteins, Bind to nuclear receptors → alter gene expression

Androgen (testosterone)

steroid hormone higher in males

Estrogens (estradiol)

steroid hormone higher in females

Progesterone

steroid hormone that prepares uterus, mainly in females

Cortisol

steroid hormone that’s not sex-specific

Activating Effects of Sex hormones

Temporary

Occur at any time in life

hormonal effects on sexual arousal or behavior

Organizing effects of sex hormones

Long-lasting structural changes

Occur during sensitive periods:

• Prenatal first trimester

• Puberty

Organizing effects on genital development

Testosterone

• High → male external genitalia

• Low → female external genitalia

Estradiol

• Critical for internal female reproductive organs

• Not essential for external female development

Influences later sexual behavior in females

Developmental Timeline

Week 6: hormone-independent

Weeks 7–8: testes form → androgens rise

Week 15 onward: genital masculinization continues

Female development occurs when hormone exposure is low

Female Genital Differentiation

XX, no SRY

Müllerian ducts → ovaries, uterus

Low testosterone → clitoris, labia

Wolffian ducts regress

Male Genital Differentiation

XY, SRY present

Testes produce testosterone + MIH

Testosterone → Wolffian ducts → vas deferens, seminal vesicles

MIH → Müllerian ducts degenerate

External genitalia masculinize; testes descend

Hormonal Masculinization

Alpha-fetoprotein binds estradiol → prevents it from masculinizing females

Testosterone in males enters brain → converted to estradiol → masculinizes the hypothalamus

Brain Areas with Sex Differences

Medial preoptic area (MPOA)

Ventromedial nucleus

Arcuate nucleus & AVPV

Sexually Dimorphic Nucleus (SDN)

Because changes are local, humans do not have fully male- or female-typical brains

Sex Differences in Play

Low prenatal testosterone in boys (due to phthalates) → more atypical toy choices

Prenatal testosterone increases male-typical play in girls

Activating Effects of Sex Hormones in Males

Testosterone → nitric oxide → activates MPOA → ↑ dopamine release

Low testosterone → reduced sexual activity

Nitric oxide release needed for erection

Menstrual Cycle

Hypothalamus ↔ pituitary ↔ ovaries

Beginning: Follicle-stimulating hormone → follicle growth

Periovulatory Period (~Day 14): Follicle produces estradiol, Surge in FSH + LH, Ovulation occurs

End: LH, FSH, estradiol, progesterone decline

Birth Control Pills

Contain estrogen + progesterone

Prevent FSH/LH surge → no ovulation

Thicken cervix

Prevent implantation

Related to changes in sexual desire

Do not protect against STDs

Sexual Interest in Females

Nipple erection → oxytocin

Periovulatory phase

high sexual activity in females

Luteal/menstruation

the second half of the menstrual cycle that begins after ovulation and ends with the start of menstruation if no pregnancy occurs

prolactin

hormone involved in milk production

Oxytocin

hormone involved in bonding & maternal behaviors

Estradiol

hormone involved in increasing Medial Preoptic Area sensitivity

Medial Preoptic Area

brain region controlling instinctual social behaviors like maternal care (parenting) and sexual motivation/behavior

Vasopressin

hormone involved in bonding, olfactory recognition (especially in males)

Natural selection (Evolutionary Psychology of Mating)

traits increasing survival —> passed on

Sexual Selection (Evolutionary Psychology of Mating)

Male competition

Female choice

Mating Preferences (Evolutionary Psychology of Mating)

Males → more partners, prefer younger mate

Females → prefer good odor, good provider

Jealousy (Evolutionary Psychology of Mating)

Men more distressed by sexual infidelity

Women more distressed by emotional infidelity

Intersexes

Mixture of male + female anatomy

Causes:

• Mutation of SRY

• Congenital adrenal hyperplasia (CAH)

• Androgen insensitivity

• Prenatal exposure to testosterone blockers (alcohol, marijuana, phthalates)

Sexual Orientation influences

Childhood gender-typical behaviors

Prenatal stress

Prenatal testosterone exposure

Older brother effect (the number of older brothers a man has increases the probability that he will be homosexual)

Brain Differences in Sexual Orientation

Hemispheres:

• Hetero men: Right > Left

• Hetero women: symmetrical

• Gay men: intermediate

Anterior Commissure & SCN

• Larger in women and Homosexual men compared to heterosexual men

Interstitial Nucleus 3 (INAH-3 / SDN):

• Larger in heterosexual males

• Smaller in heterosexual females

• Gay men show female-typical size

Basic Biological States

Paul Ekman

Emotions are biologically innate

Universal facial expressions (anger, fear, disgust, happiness, sadness, surprise)

Specific categories of emotion exist

Predictive Conceptual Construction

Lisa Feldman Barrett

Emotions are constructed by the brain

Brain predicts what is happening using prior experience

Emotion is a mental category, not a fixed biological state

LeDoux’s Model

Overlap Theory

Biological circuits respond

Conscious interpretation produces the feeling of emotion

Components of Emotion

1. Cognition – interpretation, judgment

2. Feeling – autonomic nervous system arousal

3. Action – behavioral response (EX: facial expression)

Evidence that ANS arousal isn’t necessary for emotion

Pure Autonomic Failure → people still feel emotion but less intensely

Right somatosensory cortex damage → weak emotional experience

Prefrontal cortex damage → poor decision-making despite emotional arousal

Facial Feedback Hypothesis

changing facial expression changes emotional feeling

EX:

• Botox limits facial movement → weaker emotional experience

• Möbius syndrome → limited facial expression → reduced feedback

Reinforcement Sensitivity Theory

explains individual differences in personality based on sensitivity to reward and punishment

Hemispheric Contributions to Emotions (Behavioral Activation System)

Left frontal/temporal lobe

Moderate arousal

Approach behaviors

Linked with happiness, anger, reward-seeking

Hemispheric Contributions to Emotions (Behavioral Inhibition System)

Right frontal lobe

Increased attention/arousal

Inhibits action

Linked with fear, anxiety, avoidance

Functions of Emotion

1. Act adaptively

2. Make quick decisions

3. Use past experience to anticipate outcomes

4. Make moral decisions (Individuals with prefrontal cortex damage make poor moral decisions because they fail to anticipate consequences)

Attack & Escape Behaviors

Triggered by pain or threat

Anger & fear are physiologically related

Both associated with increased activity in corticomedullar amygdala

Environmental Causes on Violent Tendencies

Lead exposure

Childhood violence

Bad neighborhoods

Prenatal smoking

Gene × Environment Interaction on Violent Tendencies

MAOA enzyme levels matter

Low MAOA + severe childhood maltreatment → highest aggression risk

Adopted children show influences from biological and adoptive parents

Neurochemistry of Aggression (Dual Hormone Hypothesis)

High testosterone

Low cortisol

Neurochemistry of Aggression (Triple Threat Hypothesis)

High testosterone

Low cortisol

Low serotonin

Neurochemistry of Aggression (Serotonin Turnover)

Measured via 5-HIAA

Low 5-HIAA → high aggression, impulsivity

Startle Reflex

Extremely fast defense response to external stimuli

Amygdala Damage Leads to…

No learned fear

Trouble recognizing emotional expressions

Rating all faces as equally trustworthy

EX: Urbach–Wiethe disease → amygdala atrophy

Toxoplasma gondii

Parasite reduces fear in rodents by damaging amygdala

Fear Generalization

Controlled by bed nucleus of the stria terminalis (BNST)

BNST handles long-term anxiety, while amygdala handles immediate fear

PTSD Symptoms

Flashbacks

Nightmares

Avoidance

Enhanced startle

PTSD Risk Factors

Smaller hippocampus

Low cortisol → difficult to regulate stress

Anxiety Disorder Key Neurotransmitters

CCK – increases anxiety

Orexin – increases wakefulness & anxiety

GABA – inhibitory; reduces anxiety