1. Theories of Classical Conditioning

2. Critical CS-US relationship
Important (critical) things to note about classical conditioning:
the CS MUST precede the US
the CS MUST predict the US
if the CS does not predict the US, no conditioning occurs
the CR does not have to be identical to the UR
E.g., subtle differences even Pavlov noticed)
may even be opposite: Morphine studies
Any response is a classically conditioned response if it
occurs to a CS
after that CS has been paired with a US
but does NOT occur to a randomly presented CS-US pairing

3. Theories of Classical Conditioning: WHY do organisms respond to predictability?
Pavlov: Stimulus substitutability theory
Kamin: Surprise theory
Rescorla and Wagner: Computational Model
Current Attentional Models

4. Pavlov: Stimulus Substitution Theory
Basic premise of theory: CS substitutes for US
w/repeated pairings between CS and US, CS becomes substitute for the US
thus, the response initially elicited only by US is now also elicited by CS
sounds pretty good:
salivary conditioning: US and CS both elicit salivation
eyeblink conditioning: both elicit eyeblinks
Theory was doing well until we found compensatory CRs

5. Pavlov: Stimulus Substitution Theory
Criticisms and Flaws:
CR is almost never an exact replica of the UR
An eyeblink to UR of air puff = large, rapid closure
Eyeblink to CS of tone = smaller, more gradual closure
Defense of theory: Hilgard (1936): Why differences in CR and UR:
Intensity and stimulus modality of the CS and US are different
Thus: differences in Response magnitude and timing are to be expected
But still doesn’t explain OPPOSITE CR

6. Pavlov: Stimulus Substitution Theory
BIGGER PROBLEM:
Whereas many US's elicit several different R's, as a general rule not all of these R's are later elicited by the CS
CS seems to select for certain CRs
E.g. Zener (1937)
Dog presented w/food as US:
found that the dog elicited a number of UR responses to the food
E.g., salivation, chewing, swallowing, etc.
CS not elicit all of those responses
NO CRs of chewing and swallowing
Just the CR of just salivation
On other hand: CR may contain some of responses that are not part of CR:
Zener found that dogs turned head to bell
But no head turns to presentation of food

7. Modifications of SST MODIFICATIONS OF SST: (Hilgard)
Only some components of UR transferred to CR
CS such as a bell often elicits unconditioned responses of its own, and these may become part of CR
Remember SIGN TRACKING: Brown and Jenkins 1974
Emphasized this change in form of CR vs. UR
Also Jenkins, Barrara, Ireland and Woodside (1976)
Sign Tracking : animals tend to
Orient themselves toward the CS (not the US)
Approach
Explore any stimuli that are good predictors of important events such as the delivery of food

8. 1
Set up:
Initial training: Light turns on above feederfeeder releases pieces of hot dog
Test:
Light turns on above feeder, then above each of the other walls
Forms a sequence of 1234
3. What is optimal response?
4. But: Dog “tracked the sign” 4 2 3
Jenkins, Barrara, Ireland and Woodside (1976)

9. Modifications of SST
Strongest data against SST theory: Paradoxical conditioning
CR in opposite direction of UR
Black (1965):
heart rate decreases to CS paired w/shock
US of shock elicits UR of heart rate INCREASE
But CS of light or tone elicits CR of heart rate DECREASE
Seigel (1979): conditioned compensatory responses
Morphine studies
evidence of down regulation in addiction
Actual cellular process in neurons (and other cells, too!)
thus SST theory appears incorrect

10. Perceptual Gating Theory
Idea that only if CS is biologically relevant will it get processed
If a CS doesn’t get processed it can be predictive/informative
Animals attend to biologically relevant stimuli
Problem:
Data show that under certain circumstances a stimulus is “attended to” or “processed”, but still does not serve as a CS with an accompanying CR
Issue remains: is the stimulus the most predictive?
Second issue: Defining “biologically relevant”

11. Kamin’s work: 1967-1974 Blocking and overshadowing
use one "weak" and one "strong" CS
CS1+CS2US
reaction to weaker stimulus is blotted out by stronger CS
Demonstrated by Pavlov
Blocking:
Train 1 CS, then add a second CS to it:
CS1 US
test each individually after training
Find that only one supports a CR
One stimulus “blocks” learning to second CS
Demonstrated by Kamin

12. Kamin’s blocking experiment
Used multiple CS's and 4 groups of rats
The blocking group receives
series of L+ trials which produce strong CR
series of L+T+ trials
then tested to just the T
The Control groups receives
SAME TOTAL NUMBER OF TRIALS AS BLOCKING GROUP
no first phase
L+ only; Test T
T+ only; Test T
LT+ only: Test T

13. Kamin’s blocking experiment
Prediction: since both received same # of trials to the tone- should get equal conditioning to the tone
Results quite different: Blocking group shows no CR to the tone- the prior conditioning to the light "blocked" any more conditioning to the tone
Directly contradicts frequency principle (remember associationism!)
Group Phase I Phase II Test Phase Result
Control L T T elicits no CR
Control T T T elicits CR
Control LT T T elicits a CR
Blocking L LT T T elicits no CR

14. Things we know about blocking:
The animal does "detect" the stimulus:
can’t be perceptual gating issue
EXT of CR with either T alone or with LT
EXT occurred faster with compound LT
Appears to be independent of:
length of presentation of the CS
number of trials of conditioning to compound CS
Constancy of US from phase 1 to 2 important!!!!
US must remain identical between the two phases or no blocking
Influenced by:
Type of CR measure (used CER, not as stable as non fear CR)
nature of CS may be important- e.g. modality
intensity of CS or US stimuli important
Depends on amount of conditioning to blocking stimulus which already occurred

15. Change in either US or CS can prevent/ overcome blocking
Change the intensity of the CS from phase 1 to phase 2
Overshadowing could be playing a role
strong vs weak stimulus
e.g. experiments when changed from 1 ma to 4 ma shock
quickly condition to compound stimulus
little or no overshadowing or blocking
Change in intensity of either CS stimulus-
Change in context from Phase 1 to Phase 2
lT then T
Lt then T
presents a different learning situation and no blocking
Any ideas about what is happening?

16. Explanations of Blocking:
Poor Explanation: Perceptual gating theory:
tone never gets processed
tone not informative
data not really support this (evidence that do “hear” tone)
Good Explanation: Kamin's Surprise theory:
to condition requires some mental work on part of animal
animal only does mental work when surprised
bio genetic advantage: prevents having to carry around excess mental baggage
thus only learn with "surprise"
situation must be different from original learning situation
Better Explanation: Rescorla Wagner model:
particular US only supports a certain amount of conditioning
if one CS “hogs” all that conditioning- none is left over for another CS to be added
question- how do we show this?

17. A Brief Aside Must determine how CS-US relationship works
Rescorla (1966) spent a lot of time on control groups
What exactly IS a control group in classical conditioning?
Why is this important?
Question of contiguity vs. predictability at play here.

18. Recorla: Which is more important? CS-US correlation vs. contiguity
CS-US contiguity:
CS and US are next to one another in time/space
In most cases, CS and US are continguous
CS-US correlation: CS followed by the US in a predictive correlation:
If perfect correlation (most predictive)- most conditioning
p(US/CS) = 1.0
p(US/no CS) = 0.0
But: life not always a perfect correlation

19. CS-US correlation is more critical
Rescorla (1966, 1968): Showed how 2 probabilities interact to determine size of the CS
CS = 2 min tone; presented at random intervals (M = 8 min)
Group 1: p(shock/CS) = 0.4 during 2 min presentation
Group 2: p(shock/no CS) = 0.2
Which group should show more conditioning?
WHY?

20. Robert Rescorla (1966) Examined predictability 6 types of Groups
CS-alone
present CS alone with no US pairing
problem: not have same number of US trials as experimental animals do, may actually be extinction effect
Novel CS group:
looks at whether stimulus is truly "neutral"
may produce habituation- animal doesn't respond because it "gets used to it"
US-alone
present US alone with no CS pairing
problem: not have same number of CS trials

21. Rescorla: 6 types of control groups
Explicitly unpaired control
CS NEVER predicts US
that is- presence of CS is really CS-, predicts NO US
animal learns new rule: if CS, then no US
Backward conditioning:
US precedes CS
assumes temporal order is important (but not able to explain why)
again, animal learns that CS predicts no US
Discrimination conditioning (CS+ vs CS-)
use one CS as a plus; one CS as a minus
same problem as explicitly unpaired and backward- works, but can work in certain circumstances (taste avoidance)

22. Rescorla: Results with 6 Groups
CS-alone: No conditioning, but habituation to CS
Novel CS group: novel worked better than CS with previous experience.
US-alone: habituation to CS
Explicitly unpaired control:
Got GREAT conditioning
Learned that the CS NEVER predicts the US!
Backward conditioning:
US preceded CS
assumed temporal order is important
It was: Animal learned that CS predicts NO US, but US predicted CS
Discrimination conditioning (CS+ vs CS-)
use one CS as a plus; one CS as a minus
Got discrimination
Animals paid attention to whatever stimulus was MOST PREDICTIVE!

23. CS-US correlation: Summary of Results
Whenever p(US|CS) > p(US|NO cs):
CS = EXCITATORY CS
that is, CS predicts US
Amount of learning depended on size difference between p(US/CS) and p(US/no CS)
Whenever p(US|CS) <p(US|NO CS):
CS = INHIBITORY CS
CS predicts ABSENCE of US
Whenever p(US|CS) = p(US|NO CS):
CS = NEUTRAL CS
CS doesn’t predict or not predict CS
No learning will occur because there is no predictability.

24. CS-US correlation vs. contiguity
Thus: appears to be the CORRELATION between the CS and US, not the contiguity (closeness in time) that is important
Can write this more succinctly:
correlation carries more information than contiguity
if r = + then excitatory CS
if r = - then inhibitory CS
if r = 0 then neutral CS (not really even a CS)

25. Classical condition is “cognitive” (oh the horror of that statement, I am in pain)
PREDICTABILITY is critical
Learning occurs slowly, trial by trial
Each time the CS predicts the US, the strength of the correlation is increased
The resulting learning curve is monotonically increasing:
Initial steep curve
Levels off as reaches asymptote
There is an asymptote to conditioning to the CS:
Maximum amount of learning that can occur
Maximum amount of responding that can occur to CS in anticipation of the upcoming US
We can explain this through an equation!

26. The Rescorla Wagner Equation!:
Yields an equation: THE Rescorla Wagner (1974) model!!!!!
Vi =αißj(Λj-Vsum)
Vi = amount learned (conditioned) on a given trial
Αi = the salience of the CS
ßj = the salience of the US
(Λj-Vsum) = total amount of conditioning that can occur to a particular CS-US pairing

27. The Rescorla Wagner Equation!:
Yields an equation: THE Rescorla Wagner (1974) model!!!!!
Vi =αißj(Λj-Vsum)
What does this equation say?
The amount of conditioning that will occur on a given trial is a function of:
The size of the salience of the CS multiplied by
The size of the salience of the US multiplied by
(The maximum amount of learning) - (the amount of learning that has already occurred).

28. Can say this easier!
How much you will learn on a given trial (Vi) is a function of:
αi or how good a stimulus the CS is (how well it grabs your attention)
ßj or how good a stimulus the US is (how well it grabs your attention
Λj or how much can learning can be learned about the CS-US relationship
AND Vsum or how much you have learned ALREADY!

29. Assumptions of Rescorla-Wagner (1974) model
Model developed to accurately predict and map learning as it occurs trial by trial
Assumes a bunch of givens:
Assume animal can perceive CS and US, and can exhibit UR and CR
Helpful for the animal to know 2 things about conditioning:
what TYPE of event is coming
the SIZE of the upcoming event
Thus, classical conditioning is really learning about:
signals (CS's) which are PREDICTORS for
important events (US's)

30. Assumptions of R-W model
Assumes that with each CS-US pairing 1 of 3 things can happen:
The CS might become more INHIBITORY
The CS might become more EXCITATORY
There is no change in the CS
How do these 3 rules work?
If US is larger than expected: CS = excitatory
If US is smaller than expected: CS= inhibitory
If US = expectations: No change in CS
The effect of reinforcers or nonreinforcers on the change of associative strength depends upon:
The existing associative strength of THAT CS
AND on the associative strength of other stimuli concurrently present

31. More assumptions
Explanation of how an animal anticipates what type of CS is coming:
Direct link is assumed between "CS center" and "US center":
E.g. between a tone center and food center
In 1970’s: other researchers thought R and W were crazy with this idea
Now: neuroscience shows formation of neural circuits!
Assumes that STRENGTH of an event is given
The conditioning situation is predicted by the strength of the learned connection
THUS: when learning is complete:
The strength of the association relates directly to the size or intensity of the CS
Asymptote of learning = max learning that can occur to that size or intensity of a CS
Maximum amount of learning that a given CS can support

32. More assumptions
The change in associative strength of a CS as the result of any given trial can be predicted from the composite strength resulting from all stimuli presented on that trial:
Composite strength = summation of conditioning that occurs to all stimuli present during a conditioning trial
If composite strength is LOW:
the ability of reinforcer to produce increments in the strength of component stimuli is HIGH
More can be learned for this trial
If the composite strength is HIGH:
reinforcement is relatively less effective (LOW)
Less can be learned for this trial- approaching max of learning

33. More assumptions: Can expand to extinction, or nonreinforced trials:
if composite associative strength of a stimulus compound is high, then the degree to which a nonreinforced presentation will produce a decrease in associative strength of the components is LARGE
if composite associative strength is low- nonreinforcement effects reduced

34. WHY is this equation important?
We can use the three rules to make predictions about amount and direction of classical conditioning
λ j > Vsum = excitatory conditioning
The degree to which the CS predicted the size of the US was GREATER than expected, so you react MORE to the CS next trial
λ j < Vsum = inhibitory conditioning
The degree to which the CS predicted the size of the US was LESS than expected, so you react LESS to the CS next trial
λ j = Vsum = no change:
The CS predicted the size of the US exactly as you expected

35. The Equation: Let’s USE it to Explain Learning, Overshadowing and Blocking!:
Vi =αißj(Λj-Vsum)
Vi = amount learned (conditioned) on a given trial
Αi = the salience of the CS
ßj = the salience of the US
(Λj-Vsum) = total amount of conditioning that can occur to a particular CS-US pairing

36. Let’s put this baby to work…….. …….we will try a few examples
Okay, you got all that?
Let’s put this baby to work……..
…….we will try a few examples

37. The equation: Vi =αißj(λ j-Vsum)
Vi = change in associative strength that occurs for any CS, i, on a single trial
αi = stimulus salience (assumes that different stimuli may acquire associative strength at different rates, despite equal reinforcement)
ßj = learning rate parameters associated with the US (assumes that different beta values may depend upon the particular US employed)
Vsum = associative strength of the sum of the CS's (strength of CS-US pairing)
λ j= associative strength that some CS, i, can support at asymptote
In English: How much you learn on a given trial is a function of the value of the stimulus x value of the reinforcer x (the absolute amount you can learn minus the amount you have already learned).

38. Acquisition Vsum = Vl; no trials so Vl = 0
first conditioning trial: Assume (our givens)
CS = light; US= 1 ma Shock
Vsum = Vl; no trials so Vl = 0
thus: λ j-Vsum = = 100
-first trial must be EXCITATORY
BUT: must consider the salience of the light:
αi = 1.0
ßj = 0.5

39. Acquisition first conditioning trial: CS = light; US= 1 ma Shock
Vsum = Vl; no trials so Vl = 0
thus: λ j-Vsum = = 100
-first trial must be EXCITATORY
BUT: must consider the salience of the light: αi = 1.0 and learning rate: ßj = 0.5
Plug into the equation: for TRIAL 1
VL = (1.0)(0.)(100-0) = 0.5(100) = 50
thus: V only equals 50% of the discrepancy between Aj an Vsum for the first trial

40. Acquisition Plug into the equation:
for TRIAL 1
VL = (1.0)(0.)(100-0) = 0.5(100) = 50
thus: VL only approaches 50% of the discrepancy between Aj and Vsum is learned for the first trial

41. Acquisition TRIAL 2: VL = (1.0)(0.5)(100-50) = 0.5(50) = 25
Same assumptions!
VL = (1.0)(0.5)(100-50) = 0.5(50) = 25
Vsum = (50+25) = 75

42. Acquisition TRIAL 3: VL = (1.0)(0.5)(100-75) = 0.5(25) = 12.5
Vsum = ( ) = 87.5

43. Acquisition TRIAL 4: VL = (1.0)(0.5)(100-87.5) = 0.5(12.5) = 6.25
Vsum = ( ) = 93.75
TRIAL 10: Vsum = 99.81, etc., until reach ~100 on approx. trial 14
When will you reach asymptote?

45. Now: Back to Explaining Blocking and Overshadowing
use one "weak" and one "strong" CS
reaction to weaker stimulus: less CR
Reaction to stronger stimulus: more CR
Blocking: 1st CS blocks learning to 2nd CS
At issue: What is predicting what?
Does LT give any more information/predictability than L alone?
If not, then L “blocks” learning to LT

46. How to explain overshadowing?
Yep, it is good old Rescorla-Wagner to the rescue!

47. Remember Overshadowing
Pavlov: compound CS with 1 intense CS, 1 weak
after a number of trials found: strong CS elicits strong CR
Weak CS elicits weak or no CR
Note: BOTH CSs are presented at same time
Why would one over shadow or overpower the other?
Why did animal not attend equally to both?

48. Overshadowing Rescorla-Wagner model helps to explain why: Assume
αL = light = 0.2; αT = tone = 0.5
ßL = light = 1.0 ; ßt = tone = 1.0
Plug into equation:
Vsum = Vl + Vt = 0 on trial 1
VL = 0.2(1)(100-0) = 20
Vt = 0.5(1)(100-0) = 50
after trial 1: Vsum = 70

49. Overshadowing
TRIAL 2:
VL = 0.2(1)(100-(50+20)) = 6
Vt = 0.5(1)(100-(50+20)) = 15
Vsum = (70+(6+15)) = 91
TRIAL 3:
VL = 0.2(1)(100-(91)) = 1.8
Vt = 0.5(1)(100-(91)) = 4.5
Vsum = (91+( )) = 97.3 and so on
thus: reaches asymptote (by trial 6) MUCH faster w/2 CS's
NOTE: CSt takes up over 70 units of assoc. strength CSl takes up only 30 units of assoc. strength

50. Overshadowing

51. Blocking Why? Similar explanation to overshadowing:
Does not matter whether VL has more or less saliency than Vt,
CS has basically absorbed all the associative strength that the CS can support
Why?

52. Blocking give trials of A-alone to asymptote:
reach asymptote: VL = λ j =100 =Vsum
NOW add trials to compound stimuli:
CS of the light has salience: αL =.5465
CS of tone has salience of: ßt =0.464
Note that CStone has higher salience!
Eh, oh, the math is going to be TOO HARD to do!!!!!

53. Blocking Or IS the math to hard to do? First compound V1 Trial:
Vt= αß(Λj-Vsum)
What is Vsum after the training to the CS light?
That’s right Vsum = ___________
Vt=0.*1.0*( )= _____________
No learning!

54. How could one eliminate blocking effect?
increase the intensity of the US to 2 mA with λ j now equals = 160
Learning so far: Vsum still equals 100 (learned to 1 mA shock)
But now: TOTAL learning is increased to 160!

55. How could one eliminate blocking effect?
plug into the equation:
(assume Vl and Vt equally salient)
Vt = 0.2(1)( ) = 0.2(60) = 12
Vl = 0.2(1)( ) = 0.2(60) = 12
Vsum = =124

56. How could one eliminate blocking effect?
on trial 2:
Vsum = 124
Vt = 0.2(1)( ) = 0.2(36) = 7.2
Vl = 0.2(1)( ) = 0.2(36) = 7.2
Vsum now = ( ) = 138.
Again, monotonically increasing curve.
Thus, altering the salience of the US alters the learning
Does altering the CS make the same change?

57. π = probability of US given the CS or No US given No CS
Can also explain why probability of reward given CS vs no CS makes a difference:
π = probability of US given the CS or No US given No CS
can make up three rules:
if πax > πa then Vx should be POSITIVE
if πax < πa then Vx should be NEGATIVE
if πax = πa then Vx should be ZERO
modified formula: (assume λ1 =1.0; λ 2 =0; ß1 =.10; ß2=.05; α1=.10; α2=.5)
Πa = probability of reward.

58. Explaining loss of Associate Value despite pairings with the US:
Is an unusual prediction: Associative value of a CS can decrease despite continued pairings with the US
Show this with three-phase experiment:
Phase 1: A and B stimuli  US (1 food pellet) on separate trials (equal #)
Phase 2: A and B paired together 1 food pellet
Same US, so same amount of conditioning, right??
RW model predicts that conditional properties of A and B individually will DECREASE in phase 2.
Why: VA= λ ; VB= λ for phase 1; so VA+B = VA+B=2 λ
This is an over-expectation
Not get 2 pellets, so Phase 2 = decremental conditioning
When test A and B alone: do indeed get decremental responding or Conditioned Inhibition

59. Conditioned Inhibition
RW model also predicts Conditioned inhibition
Can test for Conditioned inhibition
2 kinds of trials
CS+US trials
CS-  no US trials
Consider 2 kinds of trials separately
Reinforced trials: CS+ gains excitatory properties
Unreinforced trials: CS- gains inhibitory properties
When presented together: cancel one another out (assuming equal conditioning)
Is a SUMMATIVE effect

60. Extinction of excitation and inhibition
During extinction: EXT: CS+ no US
Initially: animal expects CS-US and is excitatory
This excitatory expectation is quickly diminished with repeated trials of no US
Decreases the excitatory conditioning incrementally, just like the excitatory conditioning was increased incrementally during learning

61. Dopamine and Rescorla Wagner Model
Turns out that changes in dopamine (DA) levels in dorsal striatal limbic cortical pathway vary as we learn
And guess what: these levels can be predicted by the RW model!
But, once a CS-US pairing (or an operant R-SR pairing) become well learned, the circuit begins to involve lower parts of the brain
Circuit begins to involve basal striatal areas
Becomes an “automated” or mastered behavior
No longer involves being “surprised”
Only returns to this pathway if the CS-US relation change!!!!!

62. Critique of the Rescorla-Wagner Model:
R-W model really a theory about the US effectiveness:
Says little about CS effectiveness
How WELL a CS predicts as a combo of salience and probability but doesn’t really evaluate this
States that an unpredicted US is effective in promoting learning, whereas a well-predicted US is ineffective because nothing is left to learn.

63. Critique of the Rescorla-Wagner Model:
Fails to predict the CS-pre-exposure effect:
Two groups of subjects
Grp I CS-US pairings Control
Grp II CS alone CS-US pairings PRE-Expos
Bob and Tom effect
Bob always hangs with Tom
You are dating Tom
You have a BAAAAAD breakup with Tom
Now you hate Bob….why?
Original model didn’t address how exposure could change salience/learning to CS

64. Critique of the Rescorla-Wagner Model:
In pre-exposure effect, simply being around a neutral stimulus alters its ability to become conditioned
Original R-W model doesn't predict any difference,
Assumes no conditioning trials occur when CSs presented in absence of US so Vsum = 0
This appears to be wrong
Conditioning likely occurring any time 2 stimuli are together
Form an incidental association
Need to modify the equation to account for this
They have, but we won’t!

65. Critique of the Rescorla-Wagner Model:
Original R-W model implies that salience is fixed for any given CS
R-W assume CS salience doesn't change w/experience
More recent data strongly suggest CS salience DOES change w/experience
Why changes in CS salience?
Data suggest that Salience to a CS DECREASES when CS is repeatedly presented without consequence
CS that is accidentally paired with another CS INCREASES in salience
Thus: ppears that CS and US effectiveness are both highly important
Model has stood test of time, now widely used in neuroscience
Given birth to attentional models of CC

66. Extensions and Alternatives to RW theory
Attentional models
Timing and Information models
Comparator hypothesis

67. Attentional Models of CC
How well does the CS command attention
Assumes that increased attention facilitates learning about a stimulus
Procedures that disrupt attention to CS disrupt learning
Different attentional models differ in assumptions about what determines how much attention a CS commands on any given trial
Single attentional mechanisms: Kamin’s surprise
Multiple attentional mechanisms:

68. Multiple attentional mechanisms:
Three attentions:
Looking for action: attention a CS commands after it has become a good predictor of the CS
Looking for learning: how well the organism processes cues that are not yet good predictors of the US, and thus have to be “learned about”
Looking for liking: the emotional/affective properties of the CS
Assume that the outcome of a given trial alters the degree of attention commanded by the CS on future trials
Surprise? Then an increase in looking for learning on next trial
Pleasant outcome? Increases emotional value of CS on next trial

69. Timing/Information Theory Models
Recognized that time is important factor in CC
Focal search responses become conditioned when CS-US interval is short
General search responses become conditioned when CS-US interval is long
Suggests that organisms learn both
WHAT is predicted
WHEN what is predicted will occur

70. Temporal coding hypothesis
Organisms learn when the US occurs in relation to the CS
Use this information in blocking, second-order conditioning, etc.
What is learned in one phase of training influences what is learned in subsequent phase
Large literature supports this

71. Importance of Inter-trial interval
More conditioned responding observed with a longer inter-trial interval
Intertrial interval and CS duration (CS-US interval) act in combination to determine responding
Critical factor: Relative duration of these two temporal intervals rather than absolute value of either one by itself
Holland (2000)
Conditioned rats to an auditory cue that was presented just before delivery to food
CR to CS: nosing of food cup (goal tracking)
Each group conditioned with
1 of 2 CS durations: 10 or 20 sec
1 of 6 intertrial intervals: 15 to 960 sec
Characterized responses in terms of theratio of the intertrial interval (I) and the CS duration (T).
Time spent nosing the food cup during CS plotted as function of relative value of I/T
Results: as IT ratio increases, the percentage of time the rats spend with the nose in the food cup increases

72. Importance of Inter-trial interval
Relative Waiting Time Hypothesis
Organism making comparison between events during the Intertrial interval (I) and Trial interval (T)
How long one has to wait for the US during the CS vs. how long one has to wait for the US during the intertrial interval
When US waiting time during CS is shorter than intertrial interval:
I/T ratio is high
CS is highly informative about the next occurrence of the US
Lots of responding
When US waiting time during CS is same/longer than intertrial interval wait:
I/T ratio is low
CS is not highly informative
Less responding

73. Comparitor Hypothesis
Ralph Miller, et al.: organism compares across learning situations
Assumes: Conditional responding depends on
What happens during CS
ALSO what happens in other aspects of experimental situation (when CS is not presented)
That is, animal compares presence of CS to absence of CS
Revaluation effects: Can better explain blocking
What is blocked is RESPONDING to CSAB, not learning of CSAB
Can unmask blocking to CSAB by presented CSA alone without US (EXT CSA).
Changes conditional value of CSA
Now CSAB has different, predictive value
Animal “revalues” CSAB and now responds as it is predictive, whereas CSA is not.

74. Comparator Hypothesis
Note: this is a theory of PERFORMANCE, not learning!
Assumes conditioned responding depends on BOTH associations between CS-US and between US and other stimuli when CS not there
These other stimuli form the “comparator” cues
Also assumes formation of excitatory associations with US ONLY
Instead of forming inhibitory associations with CS, form stronger excitatory associations with “not CS”
Animal compares the relative associative value of “CS vs. “not CS”
Whatever is stronger is what you respond to

75. Why are these theories important?
Helps explain the PROCESS of classical conditioning
Describes conditions and allows predictions of
Who is likely to form associations between stimuli
To What kinds of stimuli it will occur
When classical conditioning will occur
Where associations form: what settings/conditions are important
How well: how fast/slow, what quality of associations are formed.
Important for predicting/controlling in applied settings
Understanding and treatment of pedophilia, sexual fetishes, etc.
Phobia treatment
Commercials and advertising
Social behaviors