chapter 5 theories of pavlovian conditioningnalvarado/psy402 ppts/new klein/pdfs...chapter 5...

PSY402

Theories of Learning

Chapter 5

Theories of Pavlovian Conditioning

Contemporary Theories

Nature of the CR – stimulus substitution theory, SOP and AESOP theory

Nature of the conditioning process:

Predictiveness of the CS – the Rescorla-Wagner associative model

Comparator theory

Mackintosh’s attentional theory

Retrospective processing approach

Stimulus-Substitution Theory

What is the nature of the CR – is it just the

UCR or is it different?

Pavlov – stimulus-substitution theory:

The CS stimulates the same areas of the brain as

the UCS, producing the same response.

Activation of CS with UCS establishes a neural

connection between brain areas.

Connections are formed between

brain regions

Conditioned Opponent Response

The CR and UCR are often different:

CR of fear is different than UCR of pain.

Siegel – best evidence of difference: Morphine (UCS) produced analgesia, reduced pain (UCR)

Light or tone (CS) produced hyperalgesia, increased pain (CR).

Rats remove paws from heat quickly with CS, slowly with UCS.

Insulin (glycemia) works the same way

Conditioning of the Opponent

Response (Tolerance)

The M-P-M condition

presents the CS without the

UCS so the tolerance is

extinguished.

Drug Tolerance Overdoses

Elimination of a CS results in a stronger

response to the UCS, drug.

Extinction of responding to environ-mental cues

strengthens drug response

Changing the context in which a drug is

administered increases response to the drug.

Novel environment does not elicit an opponent

CR.

SOP Theory

Sometimes Opponent-Process theory (SOP) – explains why CR varies.

UCS elicits primary A1 (fast) and secondary A2 (longer) responses.

A1 & A2 can be same or different.

Conditioning only occurs to A2 – the CR is always an A2 response.

When A1 & A2 differ, UCR & CR differ.

SOP Explains Timing Effects

None of the previous models explain why the

timing of CS-US matters.

SOP model requires that both CS and UCS be

in the A1 stage for learning to occur.

With delay more elements of CS decay from A1,

becoming A2.

Activation of a memory node in SOP theory

Two-Phase Reactions

Shock – results in:

A1 -- Initial agitated hyperactivity

A2 -- Long-lasting hypoactivity (freezing)

CER (fear) elicited by CS is A2

Morphine – results in:

A1 – sedation, analgesia & hypoactivity

A2 – hyperactivity two hours later & hyperalgesia (greater pain sensitivity)

CR elicited by CS is A2 (hyper)

A2 Morphine Hyperactivity

When A1 & A2 Are the Same

Grau showed that unconditioned responding

to radiant heat produced:

Instant, short-duration hypoalgesia (decreased

sensitivity to pain)

Followed by persistent hypoalgesia

The existence of distinct A1 & A2 responses

demonstrated using naloxone, which blocks

A2 (opioid) but not A1 (non-opioid).

Two Circuits in Rabbit Eyeblinks

Fast-acting direct

circuit (A1) to

sensory trigeminal

nucleus to motor

nuclei

Slow-acting A2

circuit through

inferior olive

Affective Extension of SOP Theory

Why do different A2 responses have different optimal CS-UCS intervals?

Two distinct UCR sequences activate distinct A1 & A2 sequences:

Sensory

Emotive

These distinct sequences can have different strengths, time scales (latencies), or eliciting CS’s.

Faster

Slower

Rescorla-Wagner Theory

There is a maximum associative strength between CS and UCS.

UCS determines the limit

Strength gained on each training trial depends on prior training.

More learning early, less later on

Rate of conditioning varies.

Conditioning of a CS depends on prior conditioning to other stimuli.

Rates of Conditioning Vary

UCS Preexposure Effect

If the UCS is encountered without the CS prior to pairing of the two, less learning occurs.

UCS becomes associated with other environmental stimuli (without CS).

Since there is a limit to association strength, some is drained off by such prior associations.

CS-UCS association is weakened.

Problems with Rescorla-Wagner

Overshadowing – salient cues have more

associative strength.

Sometimes a salient cue potentiates another cue

instead of overshadowing.

Garcia says cues are indexed.

R-W says cues are seen as unitary stimulus.

Unclear which explanation is correct.

UCS Preexposure Effect

More Problems

CS preexposure effect – appearance of CS without UCS prior to learning weakens learning.

Shouldn’t have any effect according to Rescorla-Wagner theory, but it does.

Cue-deflation effect – extinction of a more salient cue enhances learning for the less salient cue.

Should be no change according to R-W.

Comparator Theory

If two CS’s are associated, extinction of one should reduce responding to the other.

Sometimes true, other times not.

CS-UCS associations exist for many stimuli but are exhibited only for the strongest.

Comparator theory says the CS’s are judged in relation to each other.

Organisms might learn about elemental or configural

CS nodes

Pearce

Wagner & Brandon

Attentional View

Mackintosh – learned irrelevance occurs during preexposure of CS.

Animals exposed to a novel stimulus exhibit an orienting response.

No orienting with preexposure.

Habituation results in failure of conditioning – no attention is paid to a habituated stimulus.

Pairing of CS/UCS in novel context results in learning.

Learned Irrelevance

Retrospective Processing

Most theories assume the level of responding will be constant after learning.

Baker & Mercier suggest association can change after learning.

Retrospective processing – CS-UCS contingency reevaluated after learning.

Backward blocking – support for theory

Suggests animals have mental representations, memory for events.

Comparison of Theories