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Current Theoretical
Approaches and Issues in
Classical Conditioning
Psychology 3306
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…

Kamin (1968)
Group
Control
Blocking
Phase 1 Phase 2
Nothing
L+
Test
Result
LT+
T
CR
LT+
T
No CR
L = Light T = Tone + = CS (shock)
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
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

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

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

The model makes some groovy
predictions
Slope of the acquisition curve
 Blocking
 Conditioned inhibition
 Overshadowing
 Overexpectation

Overexpectation
Group
Phase I
Phase II Test
Result
Exp
L+ T+
LT+
L, T
Weak
CR
Control
L+ T+
nothing
L, T
Strong
CR
The Model:
ΔVi – Si(Aj-Vsum)
 i = CS
 j = US
 S = Salience
 A = Value of the US
 V = amount of conditioning
 These quantities are, of course,
hypothetical

An example
OK, say a food pellet = 100
 Say salience of a light CS = .2
 Vsum = 0 (at the start of the experiment,
there is no conditioning yet

OK, now for the numbers
Trial 1
 ΔVi – Si(Aj-Vsum)

=.2(100 – 0)
 =20


Trial 2
ΔVi = .2(100-20)
 =16

Continued….

Trial 3
ΔVi – Si(Aj-Vsum)
 ΔVi = .2(100-36)
 -12.8

And so on….
 Less and less conditioning as time goes
by
 Coo eh

Overshadowing
CS1 -> Light, S = .2
 CS2 -> Noise, S= .5
 2 CSs, so two calculations per trial
 Trial 1

ΔVLight = .2(100-0) = 20
 ΔVNoise = .5(100-0) = 50

Overshadowing

Trial







ΔVLight = .2(100-70) = 6
ΔVNoise = .5(100-70) = 15
OK, how does blocking work?
Well there is no strength left
Conditioned inhibition?
Negative for old CS
Additive model
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

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)

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)

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)
Physiological Basis
New synapses formed in Aplysia
 Increase in transmitter release in neurons
sensitive to CS (very cool)

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Just like habituation!
What about more complex creatures
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
