PSYC 106 Final

Exocrine glands

secrete stuff locally, sweat, saliva, breast milk (through ducts)

Endocrine glands

secrete hormones into the blood.

• Hormones are carried in blood to organs of the body where they influence cell activity

• hormnes hae global and long lastin

Hormones

hormones have global and long lasting effects.

Global since they are carried in the blood to organs in the body

Neurotransmitters

have lova, short lived effects

Hormones that are also neurotransmitters

Adrenaline = epinephrine

• but we call it adrenaline when it is released as a hormone from the adrenal gland. We call it epinephrine when it's

  released as a neurotransmitter for neuro communication

Noradrenaline = norepinephrine

Hypothalamus & Pituitary Gland

Hypothalamus releases hormones (e.g., gonadotropin-releasing hormone) into the pituitary gland, and then.... The pituitary releases hormones (e.g., FSH and LH) into the bloodstream, which travel to other endocrine glands (e.g., ovaries in females), and then... The other endocrine glands (e.g., ovaries in females) release hormones into the bloodstream (e.g., Estradiol), which then affect cell functioning through the body

Two major types of hormones

• Steroid hormones

• Non-Steroid Hormones

Steroid Hormones

• diffuse across the cell membrane

• attach to receptors in the cytoplasm

• receptor-hormone complex enters nucleus

• triggers gene expression

  • very long lasting effects (days)

Non-Steroid Hormones

Ex: adrenaline and noradrenaline

• attach to receptor on cell membrane

• activate 2nd messenger system inside cell

• alters metabolism of cell (e.g., breakdown of glycogen to glucose)

  → effects last for minutes or hours

Two Main Types of Steroid Hormones

• cortisol

• sex hormones

cortisol

produced and secreted by the adrenaline cortex

Sex hormones

produced and secreted by the Gonads (i.e., Ovaries and Testes),

but also a bit from the Adrenal Cortex

Two Main Types of Sex Hormones

1) Androgens

e.g., Testosterone (TTT) (higher levels in males)

2) Estrogens

e.g., Estradiol (higher levels in females)

Aromatase

enzyme much higher concentration in females than males gonads which is why females have more estrogen than male

Gonads

endocrine glands that are part of the reproductive organ

1. secrete sex hormones

2. produce/release gametes

Female gonads

Ovaries

1. secrete hormone estradiol (a type of estrogen)

2. produce (and release) ovum(egg) which is the female gamete

(All eggs present at birth)

Male Gonads

Testes (in human called testicales)

1. Secrete hormone TTT (a type of Androgen)

2. produce and release sperm (male gamete)

Adrenal cortex (in both females and males)

produces and secretes some TTT, referred to as “Adrenal Androgens”

....relevant to Puberty and Gender Phenotype Anomalie

Genitalia

non-endocrine parts of the reproductive organs (have external and internal structures)

Genetic Genderm (genotype)

XX vs. XY This is fixed s gonads are based on genetics

• determines the outcome of the Gonads (Male vs. Female

• the Y chromosome contains the gene to form the TESTES (male gonads) At 7 weeks prenatal (in humans), if have Y chromosome → TESTES

If there s no Y chromosome → ovaries

Gender Phenotype

how an organ/organism “appears”

• Organizing” Effects of Sex Hormones in Utero determine the outcome of the Genitalia (Male vs. Female)

• Early in fetal development both males and females genitalia appear female-like

• Later in fetal development TTT in utero (released by the Testes in Male Fetus) “Masculinizes” the Genitalia → male genetalia develops

• Ovaries in Female fetus secrete Estradiol

  • But most importantly...... without TTT, the genitalia continue to be Female Genitalia

    This is the “default”

Gender Phenotype Anomalies

When sex hormones are atypical in utero

1. Female Masculinization

2. Testicular Feminization

Female Masculinization

GENETIC FEMALE, XX

But exposure of the fetus to TTT in utero:

A) Adrenal Cortex gland (mother or fetus):

-> excess of TTT

B) anti-miscarriage drug -> mimics TTT

2) Testicular Feminization (“Androgen insensitivity syndrome”, from a gene mutation)

Genitalia are intermediate (but have female gonads, i.e., ovaries)

These people are usually made into phenotypic females (and are sometimes infertile

Testicular Feminization

GENETIC MALE (XY)

But insensitive to TTT in utero (and always), because lacking (or dysfunctional) TTT receptors, so TTT cannot activate genes inside cells.

• Genitalia (and general appearance) are female (but have male gonads, i.e., testes, that are small and do not descend)

And their estradiol (which is not counterbalanced by TTT) later leads to formation of breast

Puberty

sexual maturation ~ 12 – 14 years

• TT & Estradiol start being produced AGAIN by the Testes and Ovaries, respectively because the Hypothalamus starts to release Gonadotropin Releasing Hormone

Effects of Sex Hormones at Puberty

Gonads

• Testes (secrete TTT) -> continual sperm production

• Ovaries (secrete Estradiol) -> Menstrual (reproductive) cycle = releasing of egg (“ovulation”) and preparation of uterus for fertilized egg (progesterone)

Effects of Sex Hormones on Gender Phenotype

Secondary Gender Characteristics

• Estradiol (less known about): broader hips, breast development

• TTT: a bunch of things

Effects of TTT at Puberty and beyond

Adrenal Androgens (e.g., TTT) are released from Adrenal Cortex

in BOTH males and female

• TTT is much higher in males

Effects of TTT on Gender Phenotype:

A) Physical features

• Body hair (facial, pubic, underarm)

• Voice deepening

• Bones and Muscles growth/strength

B) Behaviors

* Sex drive (i.e., “libido”) Estradiol

* Rough and tumble (aggressive) behavior

Effects of Sex Hormones on Mating Females

RECAP: In the middle of menstrual cycle: -> Estradiol increases,

which results in the release of an egg (from ovaries)

In Humans: “ovulation”, in Non-humans: “estrus”

Most female mammals (e.g., dogs) only accept and make advances when in estrus

Primates: Human and Non-Human (Apes and Monkeys)

Compared to lower animals, sexual behavior is less governed by sex hormones/fertility

Still, human females initiate sexual activity more often at ovulation....

.... maybe because estradiol increases the sensitivity of the

pudendal nerve and lubricates the vagina

Effects of Sex Hormones on Mating Males

Animals: Some male animals only mate when TTT is high

Human Males

• TTT is key! After castration, lose sexual drive

• Low TTT can result in impotence

• Sexual “prime” and TTT levels are maximal: 15 - 25 years

Does TTT cycle in Males?

• Annually? Yes, for birds

• Daily? Yes, all male mammals, including humans, cycle TTT as part of the circadian rhythm (peak TTT is in the early morning around the time they wake up)

Brains of Homosexual vs. Heterosexual Males

Sexually Dimorphic Nuclei (SDN) in the Hypothalamus

• Interstitial Nucleus of Anterior Hypothalamus-3 (INAH-3)

  Heterosexual MALE > Heterosexual FEMALE (by ~2x)

Levay study (1993): measured the size of nucleus in:

• 16 hetero MALE: size = 0.12 mm3

• 6 hetero FEMALE: size = 0.056 mm3

• 19 homosexual MALE: size = 0.051 mm3

** Shows how homosexual males have similar brain structure to heterosexual females.

Fear and Anger

Are negative emotions, which are short-lived and lead to a “short-term” stress response

How does your body respond to fear/anger?

Fight or flight which is adaptive! Increase heart rate, blood pressure and breathing to bring fuel to brain and muscles!

Anxiety

a condition of “long-term" stress, which is not adaptive!

How is the body affected by anxiety?

Illness

Encoding

proessing new information into a form that can be stored

Storage

retaining a memory. Library files

Retrieval

getting information out of storage into conscious awareness

• recall

• recognition

recall

to bring back to mind (search one’s emeory bank)

Recognition

to percieve so ething as previously known it is familiar

Short term memory

for things that just happened (or currently occupy your attention) which has limited storage capacity

Long term memory

memory for things that do not currently occupy you attention that must be retrieved which has a large storage capacity

Permanent memories

those that are stored and can later be retrieved require:

STM → consolidtion → LTM

What do we need to retain information

1. you need glucose (brains energy source)

   a. get. it from food

   b. get it from cortisol and adrenaline

In response to stress

Cortisol is released from the adrenal cortex

Adrenaline is released from the adrenal medulla

• both hormones result in glycogen → glucose

Glycogen

stored glucose that is ready to be broken down when we need it because it is a usable form of energy

Consolidation

processs that converts STM to LTM

When not to study

• when feeling low energy

• when you are feeling anxious

Study from different angles

• make links with other known things (It’s easier to recall a story as a whole rather than a bunch of unrelated facts)

• Don’t just “commit to memory”, you must also “commit to understanding”

Test yourself

Doing better on exams because studying method is testing yourself to see if you undrstand material instead of just reading information notes/slides

Slow down after learning

• Sleep:

• Drugs that are depressants (like alcohol and midazolam)

Stops new memories from being formed, which would otherwise

interfere with the memory consolidation of items just studied/learned

Explicit memory

Two types

• Semantic

• Episodic

Semantic

facts that can be stated, things that you “know

Episodic

memory for events that you’ve experienced, things that you “remember”

Procedural memory

procedures, motor skills, habits

• don’t require thinking

  • starts as semantic, but after some time you get used to the motion and it becomes automatic

Implicit memory

Memories that you have that do not require thinking

• procedural

• priming

• conditioned reponses

Priming

when exposure to a stimulus influences behavior (but you are not consciously aware)

• Word priming: word or non-word?

  Test = “doctor” vs. “pwnig”

  Prime = “nurse” vs. “car” (... the prime is implicitly put in memory)

• Subliminal” Advertising: ALL OVER THE PLACE!

Operant conditioning

A) Operant Conditioning:

1) Reward -> increases the likelihood of behavior X

• positive: “if you do X, I’ll give you candy (I Give something you desire)”

• negative: “if you do X, I’ll stop nagging you ( I Remove something you would like to avoid)

2) Punishment -> decreases the likelihood of behavior Y

• positive: “if you do Y, I’ll nag you (I Give something you would like to avoid)”

• negative: “if you do Y, I’ll stop giving you candy (I Remove something you desire)

Note: “Positive” and “Negative” do NOT refer to how you feel about what I do to you!

Instead, POSITIVE refers to me GIVING you something and NEGATIVE refers to me REMOVING something from you. (Both candy and nagging can be GIVEN or REMOVED)

Classical conditioning

uses natural automatic responses when i do this, you’ll do that

Donald Hebb (1950s):

Learning/Training is an increase in connectivity between neurons as a

result of simultaneous activity in those neurons (“Hebbian” Mechanisms)

hippocampus impacts

Human Hippocampal Damage → Memory Loss (“Amnesia”)

First, let’s define different types of Amnesia

• Retrograde Amnesia: loss of events prior to the injury

• Anterograde Amnesia: inability to create new memories after the injury

The story of patient H.M. (1926 – 2008) (seizure sufferer):

Hippocampus (and Amygdala) Removed

Symptoms after Hippocampus Damage (H.M. and others)

• Severe Anterograde amnesia, but only mild Retrograde amnesia

• Anterograde Amnesia for LTM, not STM, memories

• Anterograde Amnesia for explicit, but not implicit, LTM (e.g., can still learn mirror drawing

Role of the Hippocampus

Not where memories are stored (since only mild retrograde amnesia)

• Consolidates STM -> LTM

• Consolidates Explicit, but not Implicit, LTM

Emotions

10 emotions:

distress, anger, disgust, contempt, fear, shame, guilt, interest, happiness, surprise

Emotional Behaviors

• Avoidance (resulting from fear)

• • Aggression (resulting from anger)

• (Positively) Reinforced Behavior (in order to achieve happiness

Happiness” is what usually results from a positively reinforced behavior

INCREASES the likelihood of a behavior

ex. A hungry rat desires (will be made happy by) eating food. In a Skinner box, the rat presses a lever to get food. Thus, food is a reinforcement for pressing the lever

RESULT → The rat continues to press the lever

Fear & Anger

not anxiety

• fear and Anger = short-term, immediate (emotions)

• Anxiety (”Chronic Stress") = long-term (not an emotion)

The Amygdala

Emotions: Fear / Anger (in animals, must be inferred from behavior)

Behaviors: Avoidance / Aggression

Input to Amygdala

1) Visual and Auditory Cortex

2) Thalamus

What kind of stimuli does the amygdala respond to?

• Facial Expressions of Emotion

• Vocal Emotions

• Responds to subliminal stimuli (because of direct input from the thalamus doesn’t reach consciousness

Output of amygdala

1) Hypothalamus

• Sympathetic Autonomic Response → increased heart rate, blood pressure, breathing.

2) Midbrain → Pons (Hindbrain) → Muscles: flinching, freezing (”startle reflex”

**(Flinching/freezing is also NOT good for posture/breathing/health!)

The Amygdala and Fear/Avoidance (Animals

Emotion = FEAR, Behavior = AVOIDANCE

• The Amygdala involved in LEARNING (i.e., making memories) NEW fears

  • e.g., a robot that, when touched, shocks you....so you learn to AVOID it

What happens if LESION the Amygdala (animals)?

• Cannot learn new fear associations (animal doesn’t learn to avoid)

• Also, lose old learned fear associations (animal forgets to avoid

So, this means that the amygdala must store memories

Is it possible that they simply cannot learn anything new?

NO, the learning is restricted to fears

Can the animal show any fear at all?

YES, still show a startle response to a loud noise, which is an innate (fear?) reflex

The Amygdala and Anger/Aggression (Animals)

Emotion = ANGER, Behavior = AGGRESSION

What happens if LESION the Amygdala (cats and monkeys)?

• Excessively tame, lack of aggression

What happens if STIMULATE the Amygdala (cats)?

• “affective” attack (shrieks, hiss, hunch back)

Aggressive Behaviors vs. Amygdala activity

• Defensive/aggressive behavior in cats presented with threatening stimuli (dog

Hormonal Control of Aggression: Testosterone (TTT)

Correlational Evidence from Humans

1. Males (with higher TTT) are more physically aggressive than female

   Coincidental correlation? Maybe some other factor in males

2. Body Builders using Anabolic Steroids (which mimics the effects of TTT on muscle) are more aggressive than Body Builders who don’t use steroids

3. Inmate Violence vs. TTT Levels (Men & Women) higher in men than women

Hormonal Control of Aggression: Testosterone (TTT)

Necessary and Causal Evidence from Animals:

1) Castrated male rats:

• Become less aggressive

• Become more aggressive when given TTT

2) Female rats:

• Become more aggressive when given TTT

• Also.... Become less aggressive when given Estradiol!

How does this relate to the menstrual cycle in human females?

Short-Term Stress Response "Fight or Flight"

3 neural systems for responding

• involving → pons (through the midbrain)

• hypothalamus

System 1: DIRECT BEHAVIORAL

Via Pons (Subconscious, no “thinking” required!)

e.g., freeze and flinch (i.e., startle reflex)

System 2: SYMPATHETIC SYSTEM (global effects)

Neural projections from the hypothaamus to

• Heart

• Lungs

• Adrenal medulla

SYMPATHETIC

fight or flight” system, energy spending

Originates in the hypothalamus which receives from the Amygdala

PARASYMPATHETIC:

rest and digest” system, energy conserving

Neural projections from the Hypothalamus to heart (System 2)

Increases heart rate and blood pressure→ gets FUEL (glucose/oxygen) via blood to brain and muscles to make energy (ATP)

Neural projections from the Hypothalamus Lungs (system 2)

Increases breathing rate, dilate air passages→ gets FUEL (oxygen) into blood

Neural projections from the Hypothalamus Adrenal medulla (system 2)

releases hormones into blood: Adrenaline and Noradrenaline

Effects of Adrenaline/Noradrenaline (System 2 )

1) Increases heart rate, blood pressure, breathing rate

• as does direct neural input from hypothalamus to heart and lungs

2) Stimulates liver to breakdown GLYCOGEN → Glucose

System 3: HORMONAL (global effects)

via the hormone-releasing part of the Hypothalamus

Hypothalamus-Pituitary-Adrenal Cortex Axis

1) Hypothalamus secretes the hormone “CRF”into the Pituitary

2) Pituitary releases Adrenocorticotropic hormone (ACTH) into blood

3) ACTH activates Adrenal Cortex

4) Adrenal Cortex releases Cortisol (called the “stress” hormone) into blood

EFFECTS of Cortisol System 3

1) stimulates liver to breakdown GLYCOGEN → Glucose

• (as does Adrenaline and Noradrenaline)

2) increases heart rate, blood pressure

• (as does Adrenaline and Noradrenaline)

• And as does direct neural input from hypothalamus to heart and lungs

3) increases metabolic rate: glucose + oxygen → (ATP) (increases how quickly glucose and oxygen are turned into energy)

** shows redundancy as other hormones do the same thing

Summary systems

• Sympathetic System (System #2), which also has a hormonal component because the Hypothalamus

  sends neural projections to the Adrenal Medulla, which releases its hormones

• Hormonal system, through adrenal cortex (system 3)

How the systems work together

1) Amount of “fuel” in blood, i.e., glucose (through glycogen breakdown)

and oxygen (through increased breathing rate)

2) Heart rate and blood pressure (which speeds up how quickly fuel gets

to brain and muscles)

3) Metabolic rate (which makes energy (ATP) more quickly) all for the purpose of getting energy (ATP) to the brain and muscles

**there is no way to counteract the release of hormones from the Adrenal Glands! Because the parasympathetic system does not innervate the Adrenal Gland

Short-Term Stress Response (from Fear/Anger) is Adaptive

Needed for high levels of activity associated with “fight or flight

Long-Term Stress (Anxiety) Response is Not Adaptive

Can lead to long-term physical health problems and impair well-being

The Influence of (Short- and Long-Term) Psychological States

on Physical Health

1) The Placebo Effect

2) Psychosomatic Illness

The Placebo Effect

Real improvement in symptoms brought on by a belief in treatment

Psychosomatic Illness:

Real illness brought on by a negative psychological state (i.e., short-term stress, anxiety, anger, depression)

short(er)-lasting illnesses of Psychosomatic Illnesses

a. In)digestion: bloating, cramps, gas

b. Stress” migraine

Sympathetic system (stress)

vasoconstricts blood vessels -> Ischemia -> Visual Auras

Vasoconstricts blood vessels → the blood vessels narrow.

Ischemia → reduced blood flow (less oxygen and nutrients reaching tissues).

Visual Auras → changes in vision (like flashing lights, zigzags, blind spots) that can happen before a migraine or other conditions.