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PSY 410 Exam 4
Modules 9-11
| Question | Answer |
|---|---|
| Who is Clark Hull and what did he propose | -behavioral psychologist who proposed drive reduction theory -said that affective states (hunger, thirst) elicit internal arousal (drive) -individuals perform a behavior to reduce drive state and return to homeostasis |
| Drive theory reflects what type of learning process | -reflects S-R habitual learning -behavior is automatically reinforced when reducing drives |
| What does: D x K x H – I refer to | -Hull's equation for Reaction Potentiality (sEr) -drive (D) x incentive motivation(K) x habit strength (H) - reactive inhibition (I) = reaction potentiality (likelihood of behavior) |
| How does reactive inhibition manifest, how does it dissipate | -Reactive inhibition (I) develops when a response is emitted -each performance of a behavior increases inhibition of that same response, suppressing it as time goes on -dissipates when an organism rests, accounting for spontaneous recovery |
| What evidence is there in support of drive reduction theory | -Hull's drive theory says more powerful habits will manifest over weaker ones & multiple habits can compete with each other -spontaneous alternation in the T-maze from rats -driving simulator in adults, older adults show higher lane variability |
| Who is Edward Tolman and what did he propose | -proposed cognitive view of learning, initially poorly received -disagreed with Hull, thought behavior was NOT an automatic response to env. event -proposed purposive behaviorism (goal-directed) |
| What is purposive behaviorism | -behavioral theory that says: - behavior is goal-directed -we can expect specific outcomes to follow sp behaviors -env can be represented cognitively, and there are 2 kinds of motivation (Deprivation & Cathexis) -experience -> "black box" -> behavior |
| What is latent learning | - learning w/o imm reinf., learning remains hidden until motivation is revealed later -ex navigating a familiar city even if you've never been to your exact destination before -ex rats learning a maze without a reward as well as rats that were rewarded |
| What type of learning did Tolman suggest controls behavior | -goal-directed, specifically R-O -thought learning comes from cognitive experiences that can be recalled and applied flexibly, not automatic -cognitive maps -"what leads to what" |
| What evidence is there in support purposive behaviorism | -reward devaluation to reveal motivation (R-O) -contingency degradation -latent learning in mazes -place vs response learning (rats still navigate maze even when starting position changes) |
| What is blocking and what does it tell us about learning | -if an animal is trained that stimulus A predicts a reward and AB also predicts a reward, the animal will learn nothing about B -learning only occurs when stimulus provides new predictive information aka learning depends on PE not just pairing |
| What is prediction error, what does it encode and what does it not encode | -difference between the received reward and the predicted reward -prediction error (PE) of 0 = no learning occurred -positive PE = dopamine spike -negative PE = dopamine dip -PE does not encode |
| What neurons have been shown to display a prediction error, how was this tested | -dopamine neurons in pars compacts of substantia nigra and the VTA -primate study involving dopamine monitoring : monkeys got a surprise juice reward, then a cue presented before juice (learned cue predicts reward), then cue but no juice (negative PE) |
| What evidence is there that neurons in humans show prediction error | -electrode monitoring in patient with epilepsy, individual neurons in striatum show responding to PE -fMRIs showing increase in BOLD signaling in cingulate cortex -people w/Parkinson's (low dopamine) show disrupted PE |
| What is the Iowa gambling task | -studies role of emotion in decision-making -choose either risky deck w/high reward or safer deck w/lower reward -patients with vmPFC damage dont shift to safer decks like healthy people |
| What is the functional evidence that dopamine plays a role in model-free learning | -drugs that increase dopamine enhance reward learning and drugs that block dopamine inhibit reward learning -lesion studies show dopamine depletion in striatum inhibit S-R learning -Parkinson's patients -optogenetics |
| What happens to dopamine signaling as training goes on | -as training goes on, dopamine neuron starts responding to the reward predictor (cue) instead of reward -response to reward itself disappears -when reward becomes expected (no PE), dopamine dips |
| What do fMRI studies in humans suggest about the brain mechanisms implicated in prediction error | -ventral striatum (nucleus accumbens) shows BOLD activation & positive PE -VTA and substantia nigra show PE-related signals -orbitofrontal cortex & vmPFC encode reward value & expected outcomes -Neg pE = dec striatal activity |
| What are the implications of prediction error | -enables learning, only surprising events update predictions -explains blocking -neural mechanism for model-free habit formation -clinical implications (disrupted PE in addicts, schizo = dysregulated dopamine, depression = blunted pos PE responses) |
| What is model-based learning | -building cognitive map to simulate action sequences, plan ahead to get rewards -flexible and goal-directed -model-FREE learning is faster but not flexible |
| What evidence is there that dopamine plays a role in model based learning | -food aversion training in rats, they needed to encode the reward itself AND understand transition between states -devaluation tasks, must recall reward and simulate consequences w/o experience -dopamine encodes stimulus-outcome relationships |
| What are the implications of model-based learning | -flexible, goal-directed behavior that adapts immediately to changes in reward value -planning and prospective cognition -model-based = goal-directed, model-free = habitual |
| What is the DSM-5 and how does the discussion on substance use disorders relate to concepts discussed over the semester | -psych disorder classification system -substance abuse is habitual (model-free) behavior -tolerance reflects changes in PE signaling |
| What is intravenous drug self-administration and how can it be used to study addiction | -lever press to receive intravenous drug infusion -animals will work hard to get drugs -escalation of intake w/extended qccess models compulsive use |
| What is a dose-response curve | -plots magnitude of response against drug dose -at low doses, responding increases and at very high doses, responding decreases (takes less drugs to get big effect) |
| How do rats that have had a history of cocaine exposure behave | -cocaine enhances habitual behavior -sensitization, compulsive behavior, changes in areas like dorsal striatum and PFC towards inflexible behavior |
| What evidence is there that habit areas of the brain become altered in addicts | -neuroimaging shows reduced PFC grey matter and activity -dorsal striatum shows increased activation -reduced D2 receptor availability -lesions in dorsal striatum disrupt compulsive behavior |
| Describe the incentive sensitization model of addiction | -incentive salience becomes sensitized with repeated drug use -pleasure of drug does NO sensitize and can even decrease (tolerance) -addicts can want drugs they don't like anymore |
| How does prediction error relate to addiction | -dopaminergic drugs generate massive positive PEs by stimulating DA release -drug-associated cues acquire extreme incentive salience -tolerance develops w/use (expected drug effect increases so PE decreases |
| What is 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 |
| How can extinction and consolidation be used to treat addiction | -extinction-based therapy: presenting drug-assoc cues w/o drug -memory reconsolidation: trigger drug memory then apply new info causing PE so drug memory becomes weaker -class ex: drug memory retrieval, brief delay, watching drug taking video, reassess |
| What is deprivation in purposive behaviorism | biological need states, similar to Hull's drive states |
| 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 the "black box" in Tolman's theory | the internal mental activity that connects stimulus to response (ex. cognitive maps, expectations, goals, etc) |
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jwesmsu