1. Current Theoretical Approaches and Issues in Classical Conditioning Psychology 3306

2. Everything you know is wrong So, the number of pairings is an important, maybe all important, variable in determining the amount of conditioning, right? Fine, then explain Kamin Blocking to me…

3. Kamin (1968) Group Group Phase 1 Phase 1 Phase 2 Phase 2 Test Test Result Result ControlNothing LT+ LT+ T CR CR Blocking L+ L+ LT+ LT+ T No CR No CR L = Light T = Tone + = CS (shock)

4. Blocking is rocking Same number of tone shock pairings in both groups It is NOT just number of pairings The tone predicts nothing in the blocking group (nothing extra anyway) These results, and some others, lead to the Rescorla Wagner Model

5. You said there ’ d be no math! Yes, it is a math model Trial by trial Assumes you can get excitatory conditioning, inhibitory conditioning or nothing All based on what the CS predicts Let ’ s look at the rules

6. The Rules If the strength of the US is greater than expected then excitatory conditioning to the CS is the result If the strength of the US is LESS than expected, then you will get inhibitory conditioning The larger the discrepancy between what is observed and what is expected, the greater the conditioning

7. More rules The more salient the CS, the more conditioning you will get Two or more CSs together, their strength is additive This is, in essence, a model of surprise! The more surprised the animal, the more it learns

8. The model makes some groovy predictions Slope of the acquisition curve Blocking Conditioned inhibition Overshadowing Overexpectation

9. Group Phase I Phase II TestResult Exp L+ T+ LT+ L, T Weak CR Control L+ T+ nothing L, T Strong CR

10. The Model: Δv i = S i (A j -V sum ) i = CS j = US S = Salience A = Value of the US V = amount of conditioning These quantities are, of course, hypothetical

11. An example OK, say a food pellet = 100 Say salience of a light CS =.2 V sum = 0 (at the start of the experiment, there is no conditioning yet

12. OK, now for the numbers Trial 1 Δv i = S i (A j -V sum ) – =.2(100 – 0) – =20 Trial 2 – ΔV i =.2(100-20) – =16

13. Continued…. Trial 3 – Δv i = S i (A j -V sum ) – ΔV i =.2(100-36) – =12.8 And so on…. Less and less conditioning as time goes by Cool eh

14. Overshadowing CS1 -> Light, S =.2 CS2 -> Noise, S=.5 2 CSs, so two calculations per trial Trial 1 – ΔV Light =.2(100-0) = 20 – ΔV Noise =.5(100-0) = 50

15. Overshadowing Trial – ΔV Light =.2(100-70) = 6 – ΔV Noise =.5(100-70) = 15 OK, how does blocking work? Well there is no strength left Conditioned inhibition? Negative for old CS Additive model

16. Stuff it cannot deal with CS preexposure Change S? Mackintosh ’ s attentional theory does this, S becomes an attention parameter Pearce Hall model Gallistel ’ s model

17. Types of associations First order conditioning is S-S Second order is S-S and S-R CS - context associations too US context associations Context Blocking CS CS associations in compound stimulus experiments Occasion setting (Holland)

18. Constraints on Pavlovian Conditioning Taste aversions Not just sickness Not the aftertaste Only to certain elements of the food, which depends on the species Special? Could just be a quantitative difference (Andrews and Braverman, 1975)

19. Form of the CR CR is often like the UR but not always – Weaker – Opposite direction Drug tolerance Compensatory CRs with opiates Context as CS – Shooting gallery effect Could depend on drug action being in PNS or CNS (Stewart et al)

20. Physiological Basis New synapses formed in Aplysia Increase in transmitter release in neurons sensitive to CS (very cool) – Just like habituation! What about more complex creatures

21. Five points about Physiology and conditioning 1)CR and UR pathways are often different 2)CR production is distributed 3)Conditioning is distributed 4)Different CRs, different brain regions 5)Sometimes it is individual neurons My conclusion then is that we have a very basic mechanism at work here