PSYC 340 1st Edition Lecture 22 Extinction and Forgetting What you missed last class (04.16)I. Drugs and Reward Learning A. Modes of drug actionB. Sites of Action1. Nucleus accumbens (NA)2. Glutamate input (cortex)3. Dopamine input (ventrial tegmental area [VTA])C. Dopamine activity within the VTA (Schultz)1. Reward prediction error2. Dopamine response = Reward occurred - Reward predictedD. Drugs of abuse artificially drive dopamine activityII. Problem of relapse A. Opponent process theory and drug addiction1. Evidence (Stewart)B. Role of conditioning1. Behavioral sensitizationC. What fuels drug taking1. Hedonic experience (liking)a. Opioid-induced liking in the VTAi. Hedonic hot spotsb. Ventral pallidum hot spot and induced liking of salt2. Dopamine activity and addictiona. Dopamine appears to have little effect on likingi. But drug taking depends on dopamine activityExtinctionI. Two commonly held views:A. The greater the number of reinforced trials – the greater the learning 1. Thorndike, Hull, Rescorla-Wagner B. A way to measure to associative strength is through resistance to extinction II. Partial reinforcement extinction effect (PREE) A. Implications 1. Partially reinforced animals take longer to extinguish than animals reinforced 100% of the time 2. But one of these theories have a problem – extinction ends up to be a bit backwards These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.a. The theory (A) is correct… but there has to be something wrong with the extinction test B. Accounts 1. Discrimination hypothesis a. Partially reinforced animals don’t know that they are on extinctioni. An animal who gets reinforced 30% of the time is used to non-reinforced trials; does not realize right away that they are on extinction ii. But an animal who gets reinforced 100% of the time will realize it’s on extinction right away iii. Should be able to eliminate the effect by making it easy to discriminate between the reinforced contingency - Interposing a long period of 100% reinforcement, it should make it easy to discriminate 1. But has virtually no effect b. Thus, not due solely to discrimination hypothesis i. Not just difficulty in discrimination; something else?2. Frustration theory (Amsel) a. Partial reinforcement leads to frustrationi. Maybe the absence of food acts like an unconditioned stimulus to produce frustrationb. Assumes it: i. Induces drive – increases motivationii. Can be conditioned – an environment you get frustrated incan elicit a conditioned response iii. Has stimulus properties – you know that you’re frustrated iv. Means that if you are partially reinforced, you become frustrated; will become frustrated in that particular context; you will be reinforced for producing the response in the face of frustrationc. Learning to respond in the face of frustrationi. This new association is learned then preserved ii. As a result, you keep persevering Role of Protein Synthesis I. Forms of learning A. Short-term: alterations in synaptic function B. Long-term: structural modifications 1. Depends on protein synthesis 2. Ex: LTP, fear conditioning II. Extinction A. Requires protein synthesis B. Consolidation 1. Using drugs like anisomycin and cycloheximidea. Blocks the induction of long-term sensitization in aplysia (blocks new connections) i. Because no protein synthesis2. Drug is only effective when administered soon after traininga. Short-term effects of training do not require protein synthesis – short-term effects can still be observed even if you give anisomycin b. Anisomycin blocks long-term (protein synthesis) c. There is a period of consolidation after the training in which the memory is being laid down i. Disrupt this = disrupt the memory ii. Process involves protein synthesis 3. If you delay the anisomycin for 6 hours – no effecta. Amnesia is not due to a lingering affect; due to effect from time after testing b. Must have effect in window right after training (3-4hrs) i. Implies how long the consolidation period lasts 2. Inject locally into basolateral amygdala – same effects C. ALL DAT? ^^^ Applies to extinction.1. Instead of administering anisomycin after training, administer after extinction a. Shows that extinction relies on protein synthesis D. Reconsolidation (Nader and LeDoux) 1. Re-exposure to a CS places memory in a labile state |CS – US|24hrs|CS-|24hr|Test CS a. Give them CS- just once b. Places the memory in a labile state2. Amnesia occurs when you remind them of the CS and then shock them/give them anisomycin a. Presenting the CS gives them a period of reconsolidation, during which memory is in a labile state 3. Disrupted by inhibiting protein synthesis 4. Only effective if given soon after CS exposure 5. Electrophysiological evidence a. Correlates in the amygdala show reconsolidation 6. All of that stuff with consolidation also applies to reconsolidation E. Random question – why does exposure to the CS- sometimes lead to extinction and other times help memory (reconsolidation) 1. Weak memory – reconsolidation from the reminder cue 2. Strong memory – reconsolidation cue doesn’t do anything 3. Extinction – get CS- many times, but you only get it once in reconsolidation
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