Exam 1 Flashcards
brain stem
controls heart rate and breathing
begins where spinal cord swells after entering skull
brain’s oldest region, contains medulla, reticular formation, and pons
medulla
controls heart rate and breathing
damage usually results in death
pons
helps coordinate movements
reticular formation
nerve network running through thalamus and brain stem
filters and directs incoming sensory input
important in controlling arousal
contains cells producing most serotonin
thalamus
directs sensory messages (except smell) to cortex, processes input
cerebellum
“little brain”, enables nonverbal and skill learning
coordinates and smoothens voluntary movement
helps process and store info outside of awareness
limbic system
contains amygdala, hippocampus, hypothalamus
neural center bordering older parts of brain and cerebral hemispheres
amygdala
linked to fear and aggression emotions
hippocampus
consolidates short term into long term memory
loss results in anterograde and retrograde amnesia
hypothalamus
maintains homeostasis
controls endocrine system using pituitary gland
emotion and reward
cerebrum
2 hemispheres containing cerebral cortex and underlying sub-cortical structures
has 4 lobes
cerebral cortex
thin layer of interconnected neural cells covering cerebral hemispheres
same structure in all humans (grooves/valleys)
larger = increased learning, thinking, adaptation capacity
frontal lobe
contains motor cortex
speaking, muscle movements, planning, judgment, decision making
last part of brain to fully develop
Phineas Gage
RR tie destroyed most of frontal lobe of cortex
“wasn’t gage”, went from kind to profane and dishonest
parietal lobe
contains somatosensory cortex
integrates sensory info, manipulation of objects, numbers and their relationships, spatial vision
occipital lobe
receives input from eyes
smallest lobe
in the back
temporal lobe
auditory processing, language comprehension, memory, emotion
directly above hippocampus
motor cortex
rear of frontal lobes
controls voluntary movements
contralaterally oriented: right controls left
body parts with larger portion of motor cortex have more control
somatosensory cortex
parietal lobe
processes info from skin senses and movement of body parts
each part’s sensitivity determined by size in cortex
association areas
integrate, interpret, and act on sensory information while linking it with stored memories
found in all lobes of cortex, not involved in primary sensory or motor functions
brain plasticity
ability of brain to remap and make new connections to allow regions to perform atypical functions in case of damage to regular region
diminishes later in life
corpus callosum
large band of neural fibers connecting two hemispheres of cortex
split brain
cut corpus callosum to treat epilepsy
brain’s hemispheres cannot communicate
heart: says they saw art, points to he w/left hand
Henry Molaison
case study after most of temporal lobe and hippocampus removed to treat epilepsy
could not recall old memories or form new ones
could learn/improve at skills
EEG
electroencephalogram
readout of brain’s electrical activity, shows function
only superficial of cortex
small time range (ms)
PET
positron emission tomography, shows brain’s consumption of glucose (hot spots)
some structure and function, seconds long
MRI
details soft tissues, gives structural information
fMRI
functional MRI, shows function and structure by adding blood flow
central nervous system
contains brain and spinal cord, make decisions
peripheral nervous system
contains autonomic and peripheral nervous systems, everything but brain and spinal cord
autonomic nervous system
contains sympathetic and parasympathetic parts
controls self-regulated action of internal organs and glands
sympathetic vs. parasympathetic nervous systems
sympathetic: arousing, fight or flight, stress
parasympathetic: calming
somatic nervous system
controls voluntary movements of skeletal muscles
spinal reflex
signal travels up sensory neuron to interneuron, then immediately to motor neuron (bypassing brain)
movement before pain is registered in brain
can be bypasses consciously by brain
endocrine system
releases hormones in bloodstream that bind to receptors on cells
longer-lasting and slower-acting than nervous system
first psychology lab
Wilhelm Wundt, 1879
structuralism
pioneered by Titchener
uses introspection to search for mind’s structural elements
introspection
making observations on self while doing something, i.e. why or thoughts during
abandoned as unreliable
used to look for mind’s structural elements
functionalism
James
studied higher-order thoughts, feelings, and behaviors
looked for evolutionary functions
ex. fight or flight response
behaviorism
Watson and Skinner
scientific study of observable behavior, rejected introspection
stimuli > brain > response
if it cannot be measured, cannot be studied
conditioning
Freudian psychology
emphasis on unconscious thoughts and emotional responses to childhood events that affect our behavior
iceberg theory of conciousness
cognitive revolution
return to interest in mental processes
how info is perceived, stored, and remembered
more scientific
nature vs. nurture
behavior determined by genes vs. environment
usually answer is both
3 factors influencing behavior
biological: genes and their expression, naturally selected traits, mutations
psychological: learned fears and expectations, emotional responses
sociocultural: presence of others, cultural, familial, peer expectations
types of exploratory/descriptive research
case studies and naturalistic observation
case studies
using individual cases of interest to look for universal principles
can be misleading if individual is atypical
naturalistic observation
unobtrusively observing behavior in a natural setting without affecting it
describes, but does not explain, behavior
correlation
how much two continuous factors vary together
NOT distinct groups
ex. age, weight, income
not gender, race, or boss
correlation coefficient
tells how related two variables are, from -1 to 1
positive: both increase, >0
negative: one increases while other decreases, <0
none: not correlated, about 0
independent variable
what is being studied, altering it produces measurable effect on another variable
manipulated variable
independent variable in true experimental design, manipulated by experimenters
subject variable
independent variable in quasi design, subjects enter with this variable already determined
When can causation be inferred?
True experiments, not quasi
quasi experimentation
IV not manipulated, subject variables instead
subject groups determined before study i.e. gender, race, weight
can conclude differences exist between groups but not the cause
true experimentation
“true” IV manipulated by experimenters
employs random assignment, experimental and control groups
CAN infer causation as groups are random
how to control a true experiment
double-blind assignment: both participants and experimenter unaware of participant’s group
placebo: any effect caused by an inert substance that participant believes is active
measures of central tendency
single score that represents a set of scores
mean, median, mode, range, st. deviation
When is an observed difference reliable?
When it is representative of population (i.e. not biased)
less variable observations are more reliable than more variable ones (smaller range)
large sample size, n
uses random sampling
random sampling
group of people that represent your population of interest
everyone in the population has equal chance of participating in study
phrenology
Gall, bumps on head revealed mental abilities or character traits
beginning of idea of brain function localization
resting potential
negative charge inside neuron at rest
selectively permeable membrane
dynamic equilibrium allows ions to continuously flow in and out while overall charge of cell remains the same
action potential
firing of neuron when sufficiently excited/depolarized
EPSPs make cell more positive/closer to AP
IPSPs make cell more negative/further from AP
excitatory threshold
charge required for neuron to send signal
all or nothing response
rate law
APs are all same strength
stronger stimulus causes higher firing rate, not stronger AP
reuptake
excess neurotransmitters reabsorbed by sending neuron
SSRIS inhibit serotonin uptake, make it more active
enzyme breakdown
excess neurotransmitters broken down by enzymes in synapse
acetylcholine esterase
antagonists
block or inhibit postsynaptic effects, curare (poison darts)
agonists
facilitate postsynaptic effects, morphine
ligands
anything that can bind to cell receptors
pharmacodynamic tolerance
brains overcompensate for exogenous ligands by reducing their effectiveness, even to endogenous ligands
alcohol, GABA deficiency
conciousness
our awareness of ourselves and our environment
dual processing
info is often processed simultaneously on separate conscious and unconscious tracks
high road
conscious, deliberate actions, problem solving, naming an object
more accurate but slower, less efficient
low road
unconscious, auto actions, walking, making memories
more efficient but less accurate
visual perception track
thinking consciously about the world, reorganize and plan future actions
visual action track
guides moment-to-moment movements
selective attention
focusing conscious awareness on a particular stimulus
spotlight analogy
can only listen to one convo at a time
cocktail party effect
hearing your name will shift your attention from one convo to another
selective inattention
we are “blind” to anything we are not looking at/paying attention to
inattentional blindness
failing to see visible objects because our attention is directed elsewhere
change blindness
occurs when we fail to notice a change in the environment while focusing on something else
watch for cyclist, card trick
multi-tasking
humans are bad at it
our attention has limits, if 2 actions require same part of brain/similar activities can only do one at once
walking and talking but texting and driving
sleep
characterized by an absence of conscious behavior
higher threshold for arousal by external stimuli
1/3 of lifespan but not sure how much we need, 8 hours is estimate
theories of sleep
adaptation theory: sleep is a result of our internal “clock”, evolved to protect us from dangers of nighttime
recuperation theory: wakefulness causes deviation from homeostasis, sleep returns us to it
EEG during sleep
shows neural oscillations, records excitation of neurons in cerebral cortex
amplitude = # of neurons firing
sinusoidal waves
reflect flow of current thru cell membranes
close relationship to neuronal firing
different wave types based on frequency
alpha oscillations
awake, 8-12 hz and smooth, relaxation
beta oscillations
awake, 13-30 hz and irregular, arousal
stage 1 sleep
characterized by theta oscillations (3.5-7.5 Hz), transition between wakefulness and sleep
stage 2 sleep
irregular neural activity
theta oscillations, K complexes, sleep spindles
K complexes
sharp sudden EEG waves, thought to be involved in memory consolidation
stage 2 sleep
sleep spindles
short 12-14 Hz bursts of rapid activity
stage 3 sleep
delta oscillations of less than 3.5 Hz
about 20-50% of all
stage 4 sleep
more than half of oscillations are delta
slow-wave sleep
less than 1 Hz, can collectively be classified as stage 3
up state: high firing of neocortex neurons
down state: lack of firing, cell rest period
sleep cycle
roughly 90 minutes after the start of sleep
1 > 4 back to 1, includes REM
REM sleep
rapid eye movement
characterized by irregular activity, rapid lateral eye movement, lack of muscle tone
theta and beta oscillations
most spinal/cranial motor neurons inhibited
increased blood flow, oxygen consumption in brain
genital arousal (not necessarily sexual)
Circadian Rhythm
roughly 24-hour cycle of biological rhythms
controlled by light
natural rise and fall of body temp (higher in morning), alertness, strength
lark
people who physically and mentally peak in the morning, tend to do better in school, eat healthier
owl
physical and mental peak at night, more creative
SCN
suprachiasmatic nucleus of hypothalamus
signaled by light activated retinal proteins
controls melatonin secretion via pineal gland
inhibited during morning, increased at night
insomnia
recurring problems in falling or staying asleep
self-report sleep for diagnosis but we usually underestimate
aggravated by sleeping pills or alcohol
narcolepsy
cause sleep attacks, cataplexy, sleep paralysis, hynagogic hallucination
lapse directly into REM sleep
hereditary autoimmune disorder, orexinergic neurons disturbed or destroyed
treated with stimulants or antidepressants
sleep attacks
irresistible urge of narcoleptics to sleep during day, 2-5 mins, awaken feeling rested
cataplexy
complete paralysis while awake, caused by strong emotional reactions or sudden physical effort
dog
sleep paralysis
paralysis just before falling asleep
hypnagogic hallucinations
vivid dreams occurring just before sleep
sleep apnea
temporary cessation of breathing that causes repeated awakenings
CO2 builds up in blood, wake up gasping for air
treatable with CPAP or surgery
orexin
hypothalamus peptide that prevents sleep
CPAP
continuous positive airway pressure
mask that prevents airway from collapsing while sleeping
REM rebound
when we have sleep debt/deprived of REM
reach REM faster and stay in it longer
sleep deprivation
causes sleep debt: increased sleeping till repaid
suppresses immune system activity
can predict depression/life dissatisfaction
increased cognitive errors i.e. auto accidents
tolerance
taking more of a drug to achieve same effect over time
alcohol metabolism increases over time
sensitization
opposite of tolerance, taking same amount creates larger effect
addiction
dependency on drug to function and/or feel normal
psychoactive drug
chemical substance that alters perceptions and moods
GABA
inhibitory neurotransmitter
glutamate
excitatory neurotransmitter
alcohol
low dose: mild euphoria, reduce anxiety
high dose: incoordination, sedation
releases us from responses to averse stimuli
+ (euphoria) and - (anxiety) reinforcer
increases dopamine production, release in nucleus accumbens (+)
depressant
2 major sites of action of alcohol
antagonist: indirectly at NMDA receptors for glutamate
agonist: indirectly at GABA receptor, - reinforcement and sedative effect
heroine
releases dopamine in nucleus accumbens at 150-300% higher levels
produces analgesia, hypothermia, sedation, reinforcement
passes thru placental barrier, newborns addicted
high tolerance buildup means high addiction
different opiate receptors in different locations produce different effects
narcan
competitive antagonist to opiates by binding to opiate receptors
cocaine
binds and deactivates dopamine transporters, preventing their reuptake
also blocks voltage-gated sodium channels
amphetamines
cause dopamine and norepinephrine channels to run in reverse, sending neurotransmitters into synapse and blocking reuptake
meth is more potent
mesolimbic dopamine system
essential for all forms of reinforcement
drugs alter it
blocking receptors causes loss of cocaine reinforcement effect
cannabis
THC stimulates dopamine release
acts on cannabinoid 1 receptors in brain
nicotine
more deaths than hard drugs
releases many neurotransmitters
diminishes appetite and anxiety, boosts alertness, reduces pain sensitivity
stimulates nicotinic acetylcholine receptors
increases activity of mesolimbic DA neurons, causing release of DA in nucleus accumbens
caffeine
displaces adenosine in brain, which causes tiredness
hallucinogens
drugs that distort perceptions and evoke sensory images without input
LSD and marijuana
addiction risk factors
high comorbidity with high stress, anxiety, personality/mood disorders
self-medication
etiological: high stress and addiction caused by same thing
personality
familial factors: copying parents
