Current Theoretical Approaches and Issues in Classical
Download
Report
Transcript Current Theoretical Approaches and Issues in Classical
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)
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