Physiological Psychology Final Exam

behavioral endocrinology

the study of how hormones influence behavior

Rooster study

1849, castration of chicks to study how testes impact male characteristics in roosters, concluded that the testicles were transplantable organs

Brinkley's use of testicles

almost 20 years of transplanting goat testicles into men, cure for impotence/other male ailments, very dangerous, placebo effect, made him rich

Hormones and Behavior (1948)

first behavioral endocrinology textbook, discipline takes off/becomes more scientific

the endocrine system

glands throughout the body that release hormones (chemical messengers) into the bloodstream

hormones

regulate activity of organs/cells

neurohormones

released by a neuron, not an endocrine gland

steroids

easily travel across the cellular membrane, made from cholesterol (are fat soluble), reproductive and stress hormones

ex: aldosterone, cortisol, progesterone

peptides/proteins

chains of amino acids

ex: releasing hormones, oxytocin, vasopressin, insulin, prolactin

amines

made from tyrosine (an amino acid)

ex: norepinephrine, melatonin, thyroid hormones

the role of the hypothalamus

creates vasopressin and oxytocin, creates releasing hormones

the role of the anterior pituitary

creates hormones such as growth hormone, releasing hormones travel through portal system, trigger hormone release

the role of the posterior pituitary

stores vasopressin and oxytocin, hypothalamus signals release of these hormones

portal system

a specialized blood system connecting the hypothalamus to the pituitary gland

critical period

a time in development when exposure to an experience or substance has a larger developmental effect

androgens

male reproductive hormones

estrogens

female reproductive hormones

aromatization

conversion of androgens to estrogens, occurs in females

role of Wolffian ducts in sexual development in utero

androgens transform into male genitalia

role of Mullerian ducts in sexual development in utero

without androgens, develop into female genitalia (default)

the Guinea Pig study

injecting pregnant guinea pigs with testosterone, males largely unaffected, females develop ambiguous genitalia, reorganization of brain regions involved in sexual behavior, females later given androgen injections as adults, display male-typical behavior, activation of brain regions changed

congenital adrenal hyperplasia (CAH)

genetic (both for males and females), higher levels of androgens in womb, larger impact on female, at birth: ambiguous genitalia that is treated with hormone therapy, engage in more masculine play, more interest in masculine professions (engineer, pilot...), better spatial abilities

5-alpha reductase deficiency

genetic males; genetic condition, inhibits production of 5-alpha reductase, needed for development of male external genitalia in gestation, at puberty no longer needed, female develops male external genitalia, secondary sex characteristics

androgen insensitivity syndrome (AIS)

insensitive to androgens in fetal development, genetically male, appear as female, unable to have children, brain response to sexual images more typical of females, treated with surgery (testicle removal), hormone replacement

role of vasopressin in bonding

correlated to the quality of pair bonding/romantic commitment

role of oxytocin in bonding

promotes prosocial behaviors such as trust, empathy, and altruism

monogamous prairie voles

differences in processing vasopressin/oxytocin, more vasopressin receptor density in reward systems (prairie), changes present just after birth

role of dopamine in partner preference

more receptors in medial PFC, administration of agonist increases partner preference

the Trust Game study

control: money form unknown source, oxytocin increased, correlations with: amount received and amount sent back, higher oxytocin levels were correlated with more generous behavior- and profit- on the part of both subjects

oxytocin and pets (the pet dog study)

method: 30 minute dog interaction

IV: gaze at dog or no gaze

DV: urinary oxytocin levels (before and after), result: time gazing correlated with oxytocin levels

sex differences with rats

glucocorticoid receptor sensitivity (higher in females), stress (tail shock) enhances conditioned learning in males/impaired female learning

sex differences with humans

serotonin synthesis 52% higher in men

amygdala larger in men: left more active for women; right for men

serotonin

synthesis is 52% higher in men

amygdala

left: heterosexual women and homosexual men, no volume bias

right: homosexual women and heterosexual men, volume was biased to the right

hypothalamus

suprachiasmatic nucleus (2x larger in homosexual men), anterior hypothalamus (smaller in women, homosexual men)

serotonin knockout mice

prevents serotonin synthesis, male knockouts had no sex preference, injection of serotonin: preferred females

brain structure of transsexuals

high variability, white matter structures in female-to-male transsexuals are more similar to those in heterosexual male brains than those in female brains in several brain areas including superior longitudinal fasciculus, forceps minor, and corticospinal tract

the role of hormones in expectant and new fathers

prolactin/cortisol increase in fathers just before birth, testosterone decreases in fathers after birth

hypothalamus in parental behavior

medial preoptic area (MPOA): damage leads to lack of parental responses (rat)

oxytocin/vasopressin levels in parental behavior

correlated with paternal responsiveness

rat mother memory

babies are rewarding: rats will press a level for a pup (up to 16 days old) and prefer a pup to cocaine

pregnancy: neural downsizing (shrinking) is restored after birth

motherhood: improves "foraging memory"

alloparenting

relative or unrelated others care for offspring, more alloparents = better chance of survival, seen in many species (paper wasp, wolf, scrub jays)

alloparenting benefits

offspring grows faster, more available, safety, shorter intervals between pregnancies

classical conditioning (Pavlov's Dogs study)

learn to associate a stimulus with another stimulus, appear together, participant is a passive observer

Pavlov's Dogs: buzzer -> food in mouth -> saliva leads to buzzer -> saliva

Thorndike's law of effect

positive consequences encourage behavior, negative consequences discourage behavior

Skinner and operant conditioning

reinforcement encourages behavior, punishment discourages behavior

reinforcement and punishment

reinforcers are stimuli that encourage behavior, punishers are stimuli that decrease behavior

contingency

probability that an outcome will follow a response, time (e.g., only 1 reinforcer per minute), response ratios (e.g., 1 reinforcer per 5 behaviors)

Hebbian learning: synapse theory

precursor to neuroplasticity/long-term potentiation, when Neuron A repeatedly excites Neuron B, synaptic changes occur to the synapse making their connection more efficient

Hebbian learning: cellular assembly study

several neurons fire together during memory formation, start of neural networks

Hebb's famous phrase

the neurons that fire together, wire together

Aplysia: habituation and sensitization

habituation: after exposure, a smaller response to a continued stimulus, less retraction over time

sensitization: after exposure, a larger response to a repeated stimulus, touch paired with shock (classical conditioning), retraction gets larger

Aplysia: neural pathways

serotonin: facilitating interneuron releases it, binds to receptors on sensory neuron, leads to protein kinase (PKA) release

PKA: influences sensory neuron, enzyme which facilitates sensitization, blocks K+ flow during action potential which leads to longer AP and more Ca2+ flow at the presynaptic terminal, results in increased neurotransmitter release

long term potentiation in the hippocampus

experience changes the physical structures in the synapse within the hippocampus, when LTP is blocked learning/memory abilities are reduced

glutamate example of LTP

glutamate: primary excitatory neurotransmitter, two receptors: 1. AMPA and NMDA

without LTP: Mg2+ blocks NMDA receptors, small influence on post-synaptic neuron

with LTP: post-synaptic neuron is depolarized, Mg2+ unblocks NMDA receptor, glutamate has a bigger effect

synaptic restructuring

changing the synapse: shape of dendritic spines and new spines, occurs quickly

activity-mediated spine enlargement due to long-term potentiation

neurogenesis

formation of new neurons within the hippocampus, occurs slowly, relationship with learning is complex

H. M. 's role in understanding memory

1953: surgery to remove bilateral hippocampi

led to implicating hippocampus in memory formation

declarative memory vs. procedural memory

declarative memory

memory of knowledge that can be called forth consciously as needed

procedural memory

a type of implicit memory that involves motor skills and behavioral habits

anterograde amnesia

inability to form new long-term declarative memories

theory of equipotentiality

all regions of the cortex contribute equally to memory formation

the Delayed-Match-To-Sample task (and nonmatch)

Matching

1\. present a single stimulus

2\. delay

3\. present 2 stimuli; monkey chooses familiar item

NonMatching

same process but monkey chooses unfamiliar item

monkeys with hippocampal lesions

hippocampal lesions do not affect classical conditioning, focus on spatial learning

morris water maze

goal: find a platform in a pool

train: water is transparent

test: water is murky

radial arm maze

8 runways

food reward at each arm: collect efficiently

damage to hippocampus increases errors

human imaging study

1. present participants with pairs of words

\-condition 1: try to associate the words

\-condition 2: determine how familiar the words are

\-condition 3: consider the meanings of the words

reconsolidation

re-strengthening connections of a memory after re-activating the memory

opportunity to make adjustments

role of the orbitofrontal cortex

damage leads to spontaneous confabulation

filling in gaps in memory

honest lying

rats and cats study

during a stressful event: memory can be impaired

rats stressed by a cat outside cage

\-more errors on morris water maze task

\-less evidence of LTP

\-memory recovers later

role of the amygdala in emotional/stressful memory enhancement

stress-enhanced memories

PTSD

\-smaller hippocampus, hyperactive amygdala, and no clear link to stress hormone cortisol

moderate arousal may increase memory

highly superior autobiographical memory (HSAM)

enhanced memory for episodic life events

linked with compulsive behaviors, larger caudate and putamen

larger insula/parahippocampal cortex

the history of society's approach to mental illness

witchcraft?

demonic possession?

psychoanalysis: unconscious desires

“treatments”: bloodletting, burning at stake, drowning, trepanning

today: evidence-based therapies

electroconvulsive therapy (ECT)

a biomedical therapy for severely depressed patients in which a brief electric current is sent through the brain of an anesthetized patient (developed in the 1930s)

transorbital lobotomy

Inserting and ice-pick-like device under the eyelid, driving it through the orbit and pushing it into the frontal lobes, waved back and forth to sever connections between the prefrontal lobe and the rest of the brain (inspired by Becky and Lucy, destroyed the id with no clear evidence of effectiveness)

DSM and classification of mental illness

about 400 disorders in the DSM-5

difficulties of mental illness diagnosis

diagnosis is more subjective than in other medical fields

single nucleotide polymorphisms (SNPs)

change to a gene involving only one nucleotide pair

SNPs associated with multiple disorders, not just one

influence voltage-gated Ca2+ channels

positive symptoms of schizophrenia

delusions (false beliefs), hallucinations, repetitive behaviors

negative symptoms of schizophrenia

reduced speech, reduced affect

cognitive symptoms of schizophrenia

disorganized thoughts, interrupted thoughts

chlorpromazine

first antipsychotic

discovered by mistake

calmed patients and reduced positive symptoms

the dopamine theory of schizophrenia

excessive dopamine leads to schizophrenia

dopamine agonists lead to symptoms

drug effectiveness related to how well they block dopamine

role of acetylcholine

80% of schizophrenics are smokers

**inhale more deeply: activation of alpha 7-nicotinic receptors**

role of glutamate in schizophrenia

involved in negative and cognitive symptoms

antagonists produce symptoms

NMDA receptor modification improves symptoms

anti-NMDA receptor autoimmune encephalitis

disorder; body attacks NMDA receptors

leads to schizophrenia symptoms

structural brain changes in schizophrenia

larger lateral ventricles

smaller temporal lobes

smaller frontal lobes

loss of gray matter

declines occur in adolescence and then stabilize

dorsolateral prefrontal cortex (DLPFC)

integrates cognitive/emotional information

pyramid cells are not as highly connected: weak synapses

chandelier cells have reduced proteins in synapses

role of genetics in risk of schizophrenia

1% prevalence in general population

risk increases regardless of adoption status

role of urban living in risk of schizophrenia

living in cities: risk factor

\-toxicity, decreased social contacts

\-increased time=increased risk

first-generation antipsychotics

chlorpromazine, haloperidol (more potent)

dopamine antagonists

uncontrollable facial tics, impairment of gait

20% responded well

second-generation antipsychotics

influenced more neurotransmitters

30% responded well

increased risk of diabetes, weight loss

therapy for schizophrenia

cognitive remediation and compensatory therapy:

\-restoring function through cognitive exercises

\-enhances neuroplasticity

\-creates strategies to compensate for impairment

\-video game training

emotional symptoms of major depression

profound sadness, diminished pleasure, anhedonia, decreased motivation

cognitive symptoms of major depression

cognitive slowing, lethargy, decreased memory, suicidal ideation

monoamine hypothesis of depression

caused by low levels of serotonin, norepinephrine

supporting evidence of monoamine hypothesis of depression

monoamine drugs reduce symptoms (SSRIs), CSF of patients contains lower levels of breakdown products. eating less tryptophan can exacerbate symptoms

problems with monoamine hypothesis of depression

little evidence of reduced serotonin activity in depression, eating less tryptophan not problematic for healthy individuals, drugs do not have immediate impact on symptoms

molecular hypothesis of depression

caused by long-term molecular changes in the brain

focus on stress, neuroplasticity

role of corticosteroids in major depression

associated with stress, higher levels in patients, patients less sensitive to cortisol, fewer binding sites for CRH, antidepressants affect these symptoms