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PSY 410 Final Exam
last exam of undergrad wish me luck
| Question | Answer |
|---|---|
| what is habituation | decreased responsiveness to a stimulus, declines with repeated exposure |
| what is sensitization | i-ncreased reactivity to environmental events, more generalized than habituation -ex. PTSD victims, drug addicts can become sensitized to drug-related stimuli -involves modulatory interneurons |
| what is dishabituation | -recovery of a habituated response following presentation of sensitizing stimulus (when conditions change) -new learning caused by sensitization, not unlearning |
| what is the neuron doctrine | Cajal's theory that the brain is composed of independent, discrete nerve cells |
| what is reticular theory | Golgi's theory that all neurons are an interconnected network |
| describe synaptic vs volume transmission | -synaptic: fast, high-energy, quick temporal dynamics -volume: slow, low-energy, diffuse chemical signaling |
| describe the molecular conditions of normal conditions and LTP conditions | -normal: glutamate binds AMPA and Mg2+ blocks NMDA -LTP: depolarization dislodges Mg2+ from NMDA, CaMKII activates, more AMPA -NMDA antagonists (AP5) disrupt hippocampal-dependent LTP and learning |
| what is cREB involved in | LTP, sleep, long-term memory consolidation |
| describe delayed conditioning | -CS onset precedes and overlaps with US -most effective, (~450ms optimal) |
| describe trace conditioning | -CS ends before US begins (gap=trace interval) -fairly effective, but harder for participant than delayed conditioning |
| describe simultaneous conditioning | -CS and US presented at the same time -poor effectiveness |
| describe backward conditioning | -US precedes CS -very poor effectiveness |
| describe temporal conditioning | -US presented at regular intervals, no CS -moderate effectiveness |
| describe the 3 influential variables in classical conditioning | -contiguity, intensity, and predictiveness -intensity: higher US intensity = stronger/faster conditioning. Higher CS intensity = faster learning -predictiveness: CS must reliably predict the US, otherwise no strong CR develops |
| what is extinction | CS is presented repeatedly without US, leading to a decrease in CR. Extinction is NEW learning (CS -->no US), not unlearning of old CS-US |
| what is the renewal effect | return of extinguishing CR when CS is tested in a different contest (ABA, ABC, AAB patterns), original CS-US memory survives extinction |
| what is spontaneous recovery | passage of time leads to return of extinguished CR w/o additional training |
| what is reinstatement | exposure to the US alone (after extinction) restores CR to the CS |
| what is latent inhibition | pre-exposure to CS alone (before conditioning) makes conditioning harder. disrupted in schizophrenia |
| what is external inhibition | temporary suppression of CR when a novel stimulus is presented |
| amygdala (BLA) involvement in conditioning | -critical for fear conditioning, people with amygdala damage show no fear -involved in cue-potentiated feeding |
| hippocampus involvement in conditioning | -contextual fear conditioning -spatial memory -interacts with amygdala |
| medial prefrontal cortex involvement in conditioning | -critical for extinction |
| lateral hypothalamus involvement in conditioning | mediated cue-potentiated feeding with amygdala and prefrontal cortex projections |
| describe the aversive conditioning circuit | -CS and US activate BLA -BLA and central nucleus activate fear response -context -> hippocampus -> BLA -> contextual fear -extinction = infralimbic cortex -> inhibits BLA -> reduces fear expression |
| describe the appetitive conditioning circuit | CS+ activates amygdala and prefrontal cortex neurons projecting to lateral hypothalamus -BLA activation associated with cue-potentiated feeding in humans -PFC is critical for extinction of appetitive responses |
| what do different areas of the hippocampus do | -dorsal hippocampus = external spatial world -ventral hippocampus = internal/emotional state -spatial tasks are hippocampal-dependent, cued tasks are striatum-dependent |
| what did patient H.M. teach us about hippocampal involvement in memory | -had bilateral medial temporal lobe removal to treat epilepsy -severe anterograde amnesia for declarative memories -intact procedural/skill learning -supports theory of multiple types of memory |
| how does each schedule of reinforcement affect response patterns? | -Fixed ratio = high & steady rate of responding, post-reinforcement pause -variable ratio = highest & most consistent rate of responding, no pause -fixed interval = scalloped pattern variable interval = moderate, steady rate, good for habits |
| describe habitual S-R learning | -stimulus -> response automatically -requires minimal cognitive effort -develops with extensive training -insensitive to outcome devaluation or contingency degradation |
| describe goal directed R-O behavior | -flexible -requires greater cognitive effort -sensitive to devaluation and contingency degradation |
| what brain systems are homologous in rodents and humans and what are processes are they involved in | -dorsolateral striatum (rodent) -> putamen (human). habit formation -infralimbic cortex -> anterior cingulate. habit expression -dorsomedial striatum -> caudate. goal-directed -prelimbic cortex -> PFC/dorsal cingulate. goal expression |
| how does NMDA affect behavior | NMDA preserves goal-directed behavior even after extensive training |
| what does infralimbic (IL) musicmol inactivation do | prevent habit expression even after extensive training |
| enhanced error-related activity in what brain region is associated with which disorder | anterior cingulate cortex; OCD |
| brain structure evidence for maladaptive habit responding in addiction | -cocaine users show increased putamen (dorsolateral striatum) activity to drug cues and reduced D2 receptor binding in dorsal striatum |
| what is consolidation | newly acquired, liable memories become stabilized into long-term storage |
| how is epinephrine involved in consolidation | -released during stress/arousal -projects to amygdala -enhances memory consolidation for emotionally arousing events |
| how do glucocorticoids (cortisol, etc.) | -act on neural circuitry like amygdala, hippocampus -enhances memory retention in inhibitory avoidance tasks |
| describe the central mechanisms in consolidation | -BLA is the central hub for modulating consolidation -hippocampus = spatial/declarative memories -dorsal striatum = procedural/habit memories -CaMKII antagonist infused into hippocampus or amygdala blocks consolidation |
| which memory type is associated with each brian region | -episodic = hippocampus -semantic = medial temporal lobe -procedural/skill = striatum -priming = neocortex -iconic memory = visual cortex |
| which kinds of cells are involved in cognitive maps | -place cells, grid cells, direction cells, and time cells -place = hippocampus -grid = entorhinal cortex -direction = thalamus -time = hippocampus |
| what is Hull's drive reduction theory | behavior maintains homeostatic balance, primary drives (hunger, thirst) create internal arousal. behavior reduces drive |
| break down the elements of Hull's formula for behavior | SER (reaction potentiality) = D x K x H - I -D = drive -K = incentive motivation (value of goal) -H = habit strength -I = reactive inhibition (fatigue from repeated responding) |
| provide examples for evidence of drive theory | -reactive inhibition in rats, spontaneous alteration in T-maze -when multiple habits compete, the dominant habit wins -older adults show lane variability in driving |
| what is Tolman's purposive behaviorist theory | behavior is goal-directed, not automatic. organisms form internal representations |
| what is latent learning | learning that occurs in an environment without immediate reinforcement, but remains hidden until motivation reveals its importance |
| what is cathexis in purposive behaviorism | a learned association between an object/reward and a drive state (ex. liking a specific food when hungry) |
| what is deprivation in purposive behaviorism | biological need states, similar to Hull's drive states |
| what is model-free learning | trial and error learning based on whether experience matches current expectations, computed by prediction errors |
| what is prediction error | -discrepancy between the observed and anticipated reward -high prediction error = lots of learning low prediction error = little learning |
| what is blocking | if A already predicts the US, then adding B (AB -> US) results in little learning about B. No prediction error, so no learningq |
| how does dopamine relate to prediction error | -DA neurons in VTA and substantia nigra encode prediction error -unexpected reward = DA fires (pos pred error) -expected reward = DA shows no change -unexpected omission = DA supresses (neg pred error) -w/ learning, DA firing shifts from US to CS |
| why can model-free learning NOT account for devaluation effects | model-free learning does not consider the specific identity of the reward or transitions between states, it's just value-based |
| what is model-based learning | organisms form an internal model of the environment, encoding reward (R) and transitions between states (T) |
| what is a state transition (T) | knowledge of what happens if action x is taken in state Y |
| what is a reward model (R) | detailed representation of the reward itself |
| compare model-free and model-based learning | model-free: -rigid -fast -low cognitive cost -habitual -striatum and dopamine pred error involved model-based: -flexible -slow -high cognitive cost -goal directed -PFC, dorsomedial striatum, dopamine for reward encoding |
| what is the maladaptive habit hypothesis | Drug-taking becomes a habitual S-R behavior, insensitive to consequences. Cocaine enhances habit-like learning. Dorsal striatum (DLS/putamen) critical. |
| what is incentive sensitization | Drug-associated stimuli gain incentive value through learning. drug cues trigger sensitized DA response |
| what is the prediction error hypothesis | drugs evoke larger pred errors than natural rewards, causing excessive learning about drug cues |
| what is the opponent process theory | -every drug high (A-process) triggers an opponent state like withdrawal (B-process) -w/repeated exposure, A-process weakens and B-process strengthens -drug is then taken not for the high but to avoid withdrawal |
| what is the allostatic stress model | -maintaining stability through change -addict's natural state becomes worse, so they take drug to avoid the negative effects -stress hormones (cortisol) interactw/reward system (DA) to create negative state which promotes drug taking |
| what is some neurobiological evidence for addiction | -Cocaine users: Reduced D2 receptor binding in dorsal striatum (putamen) — consistent with maladaptive habit formation. -D2 binding correlates with craving when viewing cocaine cues |
| what is the retrieval-extinction procedure | Brief drug cue reminder → opens reconsolidation window → extinction training disrupts reconsolidation → reduced cravings. |
| what is impaired reality testing | -in schizophrenia -Failure to distinguish internal representations from external reality — a form of impaired learning/memory. |
| how does schizophrenia affect latent inhibition | latent inhibition is reduced, inability to filter irrelevant stimuli |
| what is delay discounting | -Tendency to prefer smaller immediate rewards over larger delayed rewards. ADHD children show steeper delay discounting (impulsive choice) -ADHD kids less sensitive to changing reward contingencies |
Created by:
jwesmsu