PSYCH 230 exam 3

memory

two basic categories: short-term + long-term

not always beneficial (e.g. PTSD)

short-term memory

capacity for storage of small amount of information in an accessible state for a short period of time (usually seconds) (e.g. remembering a phone number until jotting it down)

george a. miller (1956): “the magical number seven, plus or minus two”, claim: number of objects a human can hold in short-term memory is 7 ± 2, later research shows this varies for digits, letters, words, etc.

working memory

involves temporary storage of information in order to manipulate it, i.e. not just temporary storage (short-term memory) but temporary storage and processing

long-term memory

lasting storage of information

general stages: encoding, storage (consolidation), retrieval (reconsolidation, extinction)

declarative memory

explicit; a memory you can consciously recall or ‘declare’

episodic: memories of events, autobiographical

semantic: memories of facts

non-declarative memory

implicit; a memory that is expressed through actions, not recollection

procedural: the knowledge of how to do something (ex. riding a bike)

conditioning (associative learning)

classical conditioning

also known as pavlovian conditioning; ivan pavlov found that dogs salivate in response to the sight of food, conditioned to salivate to the sound of a person approaching bringing the food and the sound of a bell associated with being brought food, involuntary behavior

unconditioned stimulus - sight of food

unconditioned response - salivation (naturally evoked)

conditioned stimulus - bell, associated with unconditioned stimulus so that the conditioned stimulus also evokes the conditioned response

operant conditioning

instrumental conditioning: learning through reward and punishment, reinforcement after behavior, voluntary behavior

behaviorism

john watson, “little albert” study conditioning phobias

argued that human behavior can be fully accounted for by classical and operant conditioning, discounts independent thought, feelings, imagination, creativity…

patient ep

unable to form new memories, but old ones before his hippocampus was damaged by a virus is fully intact, also short term memory is functional

was able to feel positive rapport with researchers who frequented his home, but unable to recall their names or ever meeting them before

engram

the neural representation of memories

karl lashley (1890-1958)

first research of brain mechanisms of learning and memory

examined learning in rats following lesions of different cortical regions; cortical transections failed to block learning but cortical lesions impaired learning

equipotentiality: all areas of the cortex equally involved in memory

mass action: ability to form memories depends only on mass (amount) of brain

patient h.m.

suffered from epilepsy as a child, epileptic center in hippocampus; doctors removed the hippocampus and adjacent structures on both hemispheres, epilepsy largely relieved; lost the ability to form new episodic memories ; could still learn skilled movements and intact procedural memory

anterograde amnesia

lost ability to form new episodic memories, but can still recall past memories (ex. patient h.m.)

retrograde amnesia

lost ability to retrieve older episodic memories, but can still form new ones

clive wearing

“worst case of amnesia ever known”; could not remember more than 30 seconds at a time, only able to remember the emotions he feels towards his wife, memory of how to play the piano

morris water maze

rats are placed in a small pool of water, they want to stop having to swim as soon as possible; they find a platform in this bath so they can rest, eventually after multiple trials, rats will swim immediately to this platform rather than swim around at random; rats with lesioned hippocampus were not able to perform this task

synaptic plasticity hypothesis

experience can leave a memory trace by causing long-lasting changes in synaptic connections

hebbian plasticity/learning

if a cell A persistently and repeatedly excites cell B, the efficacy of the synapse between them will increase

also, if cell A is consistently active when cell B is not active, weakening of synaptic connection (long-term depression)

long-term potentiation (LTP)

a potential mechanism for experience-dependent synaptic plasticity, changes caused by the NMDA receptor

measuring LTP: (before LTP) briefly stimulating the presynaptic axon causes a mild depolarization in the postsynaptic cell (EPSP); (inducing LTP) high-frequency stimulation of the axon produces repetitive EPSPs on the postsynaptic cells; (after LTP) briefly stimulating the presynaptic axon causes a bigger EPSP in the postsynaptic cell

steps of LTP

AMPA receptor: binding of glutamate to an AMPA receptor causes a sodium channel to open, results in depolarization/EPSP in the postsynaptic cell

NMDA receptor: opens a calcium channel, however at resting membrane potential the NMDA calcium channel is blocked by a magnesium ion; therefore, even when glutamate binds to the NMDA receptor, the channel does not allow calcium to enter

AMPA + NMDA receptor: glutamate binding to the AMPA receptor causes depolarization, strong and persistent depolarization repels the magnesium ion in the NMDA receptor so now calcium can enter the cell

second messenger cascades

calcium-activated to induce long-lasting changes, more than sodium: (1) transport of intracellular AMPA receptors to the membrane, (2) changes in gene expression that results in production of more AMPA receptors

trisynaptic circuit of the hippocampus

information about experience arrives into the hippocampus from the entorhinal cortex into the dentate gyrus through the perforant pathway (LPP/MPP)

from dentate gyrus, information goes to CA3 pyramidal cells through mossy fibers (MF)

then, to CA1 pyramidal cells through schaeffer collaterals (SF)

pattern completion

reinstatement of a memory from partial cue because of strengthened neuron synapses from LTP

two stage model of memory formation

stage 1: experience → cortex → hippocampus

stage 2: stays in hippocampus for a short-term, but not cortex (post-experience)

stage 3: information propagates from the hippocampus to the cortex during sleep

stage 4: stays in cortex, but not in hippocampus (long-term memory); hippocampus “teaches” cortex about experiences, “slow learner”

place cells and place field

spatial receptive field of hippocampal cells

hippocampal replay

a time-compressed re-occurrence of the same sequence of place-cell firing as during recent behavior

reflects recent experience, generated in the hippocampus, prominent during sleep, coordinated with cortical regions, supports learning

plasticity of hippocampus vs. cortex

the cortex (“slow learner”) is said to be less plastic than the hippocampus (“fast learner”)

electrophysiological as a technique for recording memory

trajectories in space are encoded by sequences of hippocampal place cell spiking, trackable by electrophysiological equipment

episodic memory as “mental travel”

episodic memory is 'mental travel' in time and space referenced to self

episodic memory may share evolutionary origin with navigation

feeling vs. emotion

emotions are mental reactions typically accompanied by physiological and behavioral changes in the body (six primary emotions: anger, disgust, fear, happiness, sadness, and surprise)

feelings are conscious awareness and reactions to emotions (worry, homesick, content, jealous, etc.)

charles darwin, “the expression of emotions in man and animals”

13 years after “on the origin of species”, emotional expression as involuntary indicators of internal state, argued that animal’s emotional expressions are homologues of human emotions, and that common facial expressions appear in humans of all ages, genders, cultures

james-lange theory of emotion

physiological reactions in the body cause the emotion, “bottom-up”

emotion of fear is a response, stimulus cause physiological reactions (ex. hair raising, increased heart rate, respiration, etc.) which causes brain to perceive this as fear

cannon-bard theory of emotion

emotional states arise in the brain, which then sends signals to the body to produce physiological reactions, “top-down”

challenged james-lange theory: (1) cats with disconnected visceral innervations still hissed and growled towards dogs; (2) similar visceral changes like increased heart rate occur in different emotions like fear, rage, excitement; (3) bodily response is too slow to generate an emotion

conducted experiment demonstrating the role of the thalamus and hypothalamus in emotional behavior

two-factor theories (schacter & singer’s experiment)

subjects injected with either saline or epinephrine (increasing heartbeat, trembling, and rapid breathing); of those injected with epinephrine, half were told of expected effects; subjects interacted with an actor, both physiology and cognition affected the subject’s emotional state

hypothalamus and emotions

internal states, homeostatic drives

highly conserved structure; contains nuclei that influence reproductive, appetitive, and agonistic behaviors; fundamental to animals; receptors monitor the composition of blood

3 main hypothalamus pathways

autonomic output pathway stimulates sympathetic + parasympathetic nervous systems

motivational pathway stimulates the forebrain to generate complex plans

neuroendocrine pathway regulates hormone levels throughout the body

HPA (hypothalamic-pituitary-adrenal) axis connections and hormones

hypothalamus: releases corticotropin releasing factor (CRF), master stress trigger

pituitary gland: secretes adrenocorticotropic hormone (ACTH)

adrenal glands (kidneys): secretes glucocorticoid hormones (cortisol in humans, corticosterone in rats); cortisol triggers flight-or-fight reactions: elevate blood sugar, increase metabolic rate, suppress immune system

negative feedback on the hypothalamus and pituitary

HPA axis is involved in anxiety disorders, bipolar, insomnia, PTSD, depression…

optogenetics

a method for inducing or suppressing neural activity (action potentials) with light

some algae produce light-sensitive ion channels (e.g. channelrhodopsin), the gene for these channels is inserted into neurons, now neurons express light-sensitive channels in membrane, shining light causes neurons to spike

medial hypothalamus stimulation

in cats: induced defensive rage behavior

in humans: inadvertent stimulation caused rage attack and attempt to forcibly remove stereotactic frame

basolateral (BLA) + central (CeA) amygdala

lesions of BLA block conditioned fear, prevent new fear learning

kluver-busy syndrome

in 1930s, kluver and busy removed temporal lobes of monkeys (including amygdala); displayed hyperorality, hypersexuality, lack of fear

became known as kluver-busy syndrome: deficiency in predicting negative outcome, fear prediction

amygdala and fear

in 1950s, weiskrantz tested role of amygdala in fear learning; monkeys underwent avoidance conditioning (e.g. press lever to avoid shock); control monkeys learn rapidly, monkeys with amygdala lesions do not

types of motivation

“high-level”: strategic, long-term (e.g. “i want to be a tennis player”)

“low-level”: immediate, innate (e.g. “i’m hungry and want to eat”)

motivation as homeostasis

the drive to stay at homeostasis: ex. blood sugar levels, body fluid levels, body temperature, social + sexual drives

1. sense the current state

2. compare to wanted state

3. correct the difference

lateral hypothalamus (LH) and ventromedial hypothalamus (VMH)

early studies lesioned the LH in cats → results in aphasia (loss of motivation to eat); “hunger center”, also involved in arousal, narcolepsy is associated with LHA neuronal loss

VMH lesions cause hyperphagia: loss of knowing when full, satiated → abnormally increased eating; “satiety center”

leptin

a satiety hormone; hormone produced by fat-storing cells, a long-term signal of stored energy

its level in the blood is correlated with amounts of fat, can cross blood-brain barrier

in normal-weighted individuals, leptin reduces fat intake, increases energy expenditure and thermogenesis

obesity and leptin

a mutation in the Ob gene impairs leptin production → results in overweight mice

people who lack leptin due to a mutation are morbidly obese + hypothermic; can be partially reversed by leptin injections

ghrelin

a hunger hormone; stomach hormone secreted before meal, promotes eating

injection of ghrelin into the hypothalamus induces eating

arcuate nucleus of the hypothalamus

involved in control of hunger and feeding; projects to LHA, VMN, and the paraventricular nucleus (PVN)

POMC (pro-opiomelanocortin)/CART (cocaine- & amphetamine- related-transcript) neurons: stimulated by leptin, increases satiety

NPY (neuropeptide Y)/AgRP (agouti related protein) neurons: inhibited by leptin, stimulated by ghrelin, increases feeding, overrides long-term satiety signal

hypovolemic thirst

reduction in blood volume; result of dehydration, blood loss, vomiting, diarrhea

blood pressure drop detected by baroreceptors in heart and veins, sends information to the brain via two pathways (neural + endocrine)

neural pathway of hypovolemic thirst

baroreceptors send information to the nucleus of the solitary tract in the brainstem

brainstem circuits increase heart rate, constrict blood vessels

information sent to hypothalamus, which sends signals to increase reabsorption of water in kidney and triggering thirst

endocrine pathway of hypovolemic thirst

low blood pressure causes kidneys to release renin

angiotensin ii produced in blood: renin cleaves angiotensinogen to angiotensin i; angiotensin i cleaved to angiotensin ii

angiotensin ii enters brain to cause thirst

osmotic thirst

increase in extracellular solute concentration; result of high intake of sodium in diet

hypertonic extracellular fluid pulls water from neurons, detected by osmoreceptor neurons in the hypothalamus, sends signal to decrease urinary output and increase thirst

sexual dimorphism

males and females typically exhibit differences in sexual behavior

males: mounting, penile erection, ejaculation

females: lordosis

ventromedial hypothalamus (VMH) and lordosis

lesions in females disrupt lordosis, stimulation in females elicits proceptive behavior + lordosis, does not elicit sexual behavior in males

preoptic area and male behavior

lesions eliminate male sexual behavior (mounting, pelvic thrust), stimulation triggers sexual partners in males, lesions or stimulation do not influence lordosis in females

hypothalamus and consummatory effect

male rat trained to press bar for receptive female, copulates when accessible

after preoptic hypothalamic lesion: still presses bar to gain access, but fails to copulate

preoptic lesion block consummatory phase, leaves appetitive sexual motivation intact

amygdala and appetitive effect

after amygdala lesion, male rat no longer works to gain access to female, but if given a receptive female is still able to copulate

amygdala lesion blocks appetitive phase of sexual motivation

olds & milner self-stimulation

rats press lever for electrical brain stimulation, rats trade eating to self-stimulate, stimulation appears “rewarding”, rats will work for it

dopamine mesolimbic pathway

self-stimulation sites concentrated along the dopamine mesolimbic pathway, midbrain ventral tegmental area (VTA) contains dopamine neurons, projects to nucleus accumbens

pleasure/liking vs. motivation/wanting

many addictive substances are pleasant at first but that decreases with exposure; yet, the amount of effort to obtain the drug increases

different neural circuits for “liking” and “wanting”

hedonic “liking” vs. aversive “disgust”

facial expressions in liking

facial expressions as a window into core processes of emotions (re: darwin, “emotions in man and animals”)

prediction error

the discrepancy between expectation and what actually occurs, may also reflect reward anticipation

before learning: rat has increase of dopamine once it receives reward

after learning: rat has increase of dopamine once light turns on, anticipating and predicting reward is to come

absent reward: rat has increase of dopamine once light turns on, but big decrease when there is no reward

monetary incentive delay (MID) task

in each trial, one of three colored squares is shown (cue); then, fixate on a crosshair as they wait a variable interval (delay); finally, respond with a button press to a white target square which appears for a short time (target)

cues signal potentially rewarded trial (yellow), unrewarded trial (blue), or no response requirement (red)

nucleus accumbens vs. ventromedial prefrontal cortex

in MID task, greater nucleus accumbens activity during anticipation of rewarded vs. non-rewarded trials

greater ventromedial prefrontal cortex activity during rewarded vs. non-rewarded outcomes

reward prediction/anticipation

dopamine mesolimbic pathway involved in reward anticipation/motivation

the frontal cortex involved in reward outcome, distinct brain regions for reward anticipation and outcome

medial prefrontal cortex and decision-making

anatomical link between motivation and decision-making in the medial prefrontal cortex

prefrontal cortex damage

subjects often have normal perception, motor behavior, intelligence

yet, show impairment in “executive functions”: higher-level cognitive skills used to control other cognitive abilities and behaviors (decision-making, planning, behavioral inhibition, social behavior)

ex. phineas gage

ventromedial prefrontal cortex (vmPFC) and orbitofrontal cortex (OFC)

• connected to VTA, amygdala, temporal lobe, olfactory system, lateral hypothalamus, and other regions of the prefrontal cortex

• connectivity allows it to make calculations that include external and internal signal

• activity in vmPFC correlates with the subjective reward value of a chosen option (ex. when hungry individual is given more and more chocolate)

• activity in medial OFC show decreased activity with each additional piece of chocolate, different desirability of options

• injury impairs anticipation of the consequences of actions

rational choice theory

homo economicus: a theoretical person who always make the same rational decisions and maximizes utility

maximize gains, minimize losses

prospect theory

kahneman & tversky: how people decide under uncertainty and risk

risk aversion

when given a choice between 50% chance of $100 or $45 right now, most people choose $45 (not a “rational economic choice”

when confronted with a gamble with a moderate chance of success, people tend to be risk averse; we don’t treat gains and losses symmetrically

a utility curve describes how people assign value to options with the prospect of a gain or loss

endowment effect (loss aversion)

a classroom of students offered to choose between a mug (59%) and a chocolate bar (41%)

a second classroom was given a chocolate bar and asked to trade for a mug (10% said yes)

a third classroom was given a mug and asked to trade for a chocolate bar (11% said yes)

owning something endows it with greater value

why do we make irrational decisions?

one idea is that our poor decision occur because we are simply limited in our cognitive abilities or that we have an “obsolete brain” (we are still transitioning from a more intuitive/primal/emotional system to a more rational/conscious system)

other animals are also “irrational”: bonobos prefer a bowl with 100% chance of 4 grapes instead of a bowl with 50/50 chance of containing either 1 or 7 grapes

neural mechanisms of decisions under risk

damage to the prefrontal cortex is associated with increased risk-taking

strong activity in the amygdala is associated with risk aversion, damage associated with risk-taking

disruption of nucleus accumbens activity reduces preference for larger, uncertain rewards