Time and Causality

What should associative learning be sensitive to?

• Directionality of cause→effect

• Delay between cause and effect (Trace interval)

• Correlation

Why wouldn’t a pure contingency model such as Hebb’s what fires together wires together work to explain associative learning?

It cannot be sensitive to direction, correlation, or predictable outcomes

Why wouldn’t Rescorla-Wagner’s model work to explain associative learning?

It can’t explain why backward conditioning does not work, and cannot easily explain the effect of trace intervals.

What is Wagner’s (1981) theory called?

Sometimes Opponent Process (SOP)

What is the basic idea of Wagner’s SOP?

It incorporates time by exploiting the idea that the processing of a stimulus can vary as a function of both time and recent events.

When is stimulus processing reduced?

Self-generated priming

Retrieval-generated priming

What is self-generated priming?

When the same stimulus has just been presented

What is retrieval-generated priming?

When a predictor (CS) for the stimulus has just been presented

How is the stimulus represented in SOP?

As a set of elements, some of which may be activated by stimulus presentation.

What are the 3 states elements can be in?

• Inactive

• A1

• A2

What is A1?

A primary state of limited capacity, corresponding to rehearsal / STM

What is A2?

A secondary state of activation, which elicits a less intense response than that of A1, and may even oppose A1 activity

Explain the process that takes place when food is presented

1. Lots of elements enter A1, food is the centre of attention

2. Food elements decay rapidly from A1 into A2 - food is in the periphery of attention

3. Food elements have completely decayed from A1, but are still slowly decaying from A2 back to the inactive state - food is still in the periphery but getting weake

4. Decay from A2 back to inactive state is comple, all food elements are now in the inacive state, and food is no longer being thought about at all

How does SOP produce self-generated priming?

• The first time the stimulus is presented its elements go into A1

• Then when food gets taken away they quickly decay into A2

• Then slowly decay into inactive again

• Elements cannot go from A2 directly to A1, they must decay to I first, and that takes time - and there is only a finite number of elements

• So, if the next US occurs before this decay is complete, this time the US is presented, there are fewer inactive elements available to go into A1 so the response is weaker

How does SOP produce retrieval-generated priming?

• If an associate of the stimulus is presented, then its elements are activated directly to the A2 state - misses out A1 state all together

• If you pair can opener and food, strong association forms

• If you then present the can opener, food elements go directly into A2

• Presenting a predictor of food makes you think of food, but less intensely than if food were actually presented

• So if food is actually presented after a CS that predicts in, only they few inactive elements are available to enter A1, so the overall response to food is weaker is predicted

• This leads to conditioned diminution of the UR

What must happen to form an excitatory association?

• CS must be in A1

• US must be in A1

What must happen to form an inhibitory association?

• CS must be in A1

• US must be in A2

How does conditioning happen?

A1/A1 overlap of CS and US causes excitatory conditioning.

How does conditioning stop?

Presenting CS puts US elements into A2 before US is presented, so when US actually occurs there is less A1 activity. There is therefore less A1/A1 overlap and less conditioning. This leads to less excitatory conditioning and some A1/A2 overlap and inhibitory conditioning - eventually they cancel each other out, and there is no net learning.

How does extinction happen?

CS is presented but nothing comes after. CS in A1 but US all in A2 leads to inhibitory learning.

How does SOP produce inhibitory conditioning?

CS→US

Then CS+NS→no US

NS becomes signal for absence of US, a condiioned inhibitor

WHen established CS→US association, presentation of CS puts US elements into A2. Then introduce inhibition trials - CS in A1, US all in A2 leads to inhibitory learning.

How does inhibitory conditioning happen?

Inhibitor prevents inactive elements of US from entering A2 - will therefore interfere with the action of a conditioned excitor, which is trying to put inactive US elements into A2. So, SOP predicts the properties of conditioned inhibitors

How does blocking work?

• In Phase 1, the pretrained cue A is already a strong predictor of the US, so on later trials it quickly moves to A2 (a less active state).

• When the compound A + B is presented in Phase 2, A occupies A2, leaving little associative discrepancy for the US to explain.

• Cue B, although physically present, enters A1 but cannot gain associative strength because the US is already fully predicted by A; thus no prediction error remains, and B is blocked.

What happens when there s excitatory conditioning with a longer ISI?

1. There are fewer CS elements in A1 by the time US is presented, leading to a weaker excitatory association

2. When there is a very long ISI, there are no CS elements in A1 by the time US is presented, so there is no excitatory association

What is backward conditioning and how does it occur?

1. CS is in A1, US is in A1 and A2

2. Leads to a mixture of excitatory and inhibitory learning

What is drug tolerance?

when addicts experience less effect for the same quantity of drug, so will increase intake to achieve same high

Why is this a misnomer?

about 75% of people who died from heroin overdose had no more morphine in their systems post-mortem than control group of heroin addicts who died from homicide (Monforte, 1977)

What does Siegel (2001) suggest is the reason for this?

Conditioning

Drug = US, Environment = CS

Body’s compensatory response = CR

Repeated drug experience repeatedly pairs environment CS and drug US, so environment will come to predict and offset the effects of the drug - so more and more is needed to obtain the same effect

How can this explain overdose?

If you take away the environmental cues that predict the drug, the compensatory effect of CR is removed and UR increases even if the dose is the same

What is the first way Wagner’s SOP model can explain this and who said it?

• Baker and Tiffany (1985) - CSs predicting a drug could reduce its subsequent effects, through the mechanism of conditioned diminution of the UR

  • Retrieval-generated priming allows CS to send drug US elements directly into A2 - thus fewer available to enter A1 when drug is presented, resulting in reduced CR

What is the second way Wagner’s SOP model can explain this and who said it?

• Paletta and Wagner (1986) - extended analysis, allowed that CR might not just reduce but also oppose the effect of the UR

  • If CR is in opposite direction to UR, this could actively counteract the effect of the drug - conditioned compensatory response

  • Response to A1 activity may be opposite to response to A2 activity, not just weaker

  • The two possibilities make different predictions as to what happens when CS is presented in the absence of the US

  • Conditioned diminution of UR - CS will have no effect in drug absence

  • Conditioned compensatory response - CS will produce the opposite effect to the drug in the drug's absence

What phenomenon did Paletta & Wagner (1986) study?

They investigated context-specific tolerance to morphine in rats, showing that repeated morphine use in a specific context leads to reduced drug effects in that same context.

Experiment 1

Tested activity and analgesia, morphine, and saline

Tests at series of intervals after injection

All groups get morphine and saline in a balanced order, and half morphine conditions test activity, and the rest analgesia

Activity - A2 opposite to A1

Algesia - A2 is just reduced A1

Experiment 2

Group M-E given morphine in a distinctive context

Group M-HC give morphine in a home cage

Group S - no morphine

Tested activity in the distinctive context, then analgesia, under morphine and saline

Activity - Test at series of intervals after injectionIn context group, group that had experienced morphine in that context in training showed less hypoactivity (more active, less UR), both in the presence and absence of morphine

Algesia - In morphine test group, M-E showed less analgesia (lower RT, more pain-sensitive, less UR), in the presence of morphine but not its absence