L3 Time and Causality Flashcards
Associative learning is a useful tool for animals. It helps make inferences of ______________, and learn about _______________ of what goes with what.
AL helps us make causal inferences
and learn about what goes with what
What 4 things enhance or better associative learning?
Explain them
Directionality - cause before effect
Time - trace interval between cause and effect, better if shorter
Perfect correlations (contingency) - For A to be a high predictor of B then they should co occur together more than they occur alone
Predictable outcomes
When CS and US are paired the _________ in ______________ strength is proportional to the intensity of the ____ and _____, as well as how ___________ the US is. This is known as the __________-____________ model of associative learning.
CS US pairing, change in associative strength proportional to i tensity of US and CS, as well as how surprising the Us is. This is the Rescorla wagner model.
How does the Rescorla Wagner model explain how correlations enhance associative strength?
If you want to pair CS (tin opener sound) with US (food), need to pair them together. If always paired together, then presenting them both will increase their associative strength - hence more correlations, larger inc in associative strength between the two.
However, if you sometimes pair food alone, without tin opener, food may pair with the context - the kitchen. Therefor kitchen context will take over as a cue, and will see bigger inc in associatve strength.
The RWM may explain how ___________ _____________, and ________________ enhance associative strength, but it fails to explain things like _____________ and ______________. This is where Wagner’s _____ model improves upon the RWM.
Can explain predictable outcomes and correlations enhance associative strength, but fails to explain time interval and backwards conditioning.
This is where SOP model improves.
The Rescorla wagner model never refers to ______, which is essential for causal relationships.
time
According to SOP, what 2 things will reduce the processing of a stimulus (reduce learning or make less salient)?
If the stimulus itself has only recenlty been presented
If a predictor for the stimulus has recently been presented.
A general assumption of the SOP is that a stimulus is made up of what?
A Aspects
B Parts
C Elements
D Concepts
C Elements
The elements of a stimulus can be either ___________, or in two active states _____ or ____.
Either inactive or in A1 or in A2 states of activity.
A1 is a ____________ state of activity, with limited ____________. A2 is a ___________ state of activity, with a larger _________. Stimuli are only _________ in A1 state, before they ___________ pass on to A2 state. They must fully _________ in A2 state before they can become __________ again.
A1 is a primary activity state, with limited capacity, whereas A2 is secondary state with larger capacity. Only spend short time in A1 before quickly decaying into A2 on to A2. Must fully decay in A2 before becoming inactive.
Explain the 3 step process in SOP, of self generated priming, when a stimulus is presented?
Stimulus presented, elements enter A1 state from inactive. Now in focal centre of attention.
Stimulus removed (i.e food eaten), elements decay rapidly into A2. Now in periphery of attention.
Elements in A2 then slowly decay into inactive again. Now no longer in attention.
True or false, elements can go directly from A2 to A1.
False, they must fully decay first and be inactive before they go into A1 again.
The response elicited by A2 is less ________ than the response elicited by A1, and it may even ________ the A1 response.
A2 response less intense than A1, and may even oppose A1
How does retrieval generated priming work in the SOP?
If a stimulus is presented (CS), that is an associate of the US, (due to pairing), the elements of the US will be activated in A2 state, but not A1 state. This is strong enough to produce a response, but will never be as strong as the US presentation itself.
For excitatory lesrning to occur, the US needs to be in _______ state, and the CS needs to be in _____ state.
The US and CS both need to be in A1 activity state.
Inhibitory associative learning will occur if the CS is in ________ state, and the US is in ______ state. An example of this would be ______________ conditioning.
CS in A1 state, and US in A2 state, leads to inhibitory learning.
For example backwards condiitoning.
What happens if the US is presented again, whilst its elements are still decaying from A2 to I?
If this occurs, there are fewer elements of the US to go into A1, as they are not fully inactive yet, and still decaying from A2. Therefore repeatedly presenting the US can lead to a weaker response.
How does SOP explain when conditioning stops (weakened response, asymptote of learning)?
If the CS activates the US elements to go into A2, then there are fewer US elements to go into A1, when the US is actually presented. There is some associative learning (A1 A1 match), but also some inhibitory learning (A1 A2)., which cancel each other out. This leads to weakened response.
How does SOP explain how conditioning begins (neutral stimulus pairing with US)?
Present NS, elements go into A1, then decay slightly into A2. Then present US, elements enter A1.
Both neutral stimulus elements and US elements are now in A1, leading to excitatory associative learning.
How does SOP explain how extinction occurs?
Repeated presentations of CS without US, means that CS will activate US elements in A2, and CS elements will be activated in A1. This leads to inhibitory learning - so exctinction
How does SOP explain blocking?
CS1 + US pairing means CS1 now predicts US, and CS1 presentation in future will cause US elements to be activated in A2 state.
If you then present CS1 +CS2, and then present US, CS1 will activate some of US elements into A2, therefore not enough elements of US in A1, meaning despite CS2 being in A1, US is not, so no excitiatory learning. Previously learnt stimulus blocks learning about another stimulus.
How does SOP solve both time intervals, and directionality, something which RWM could not explain?
Time - present CS then large delay between US, means CS elements allowed to decay into A2. Therefore, not enough A1 A1 overlap of CS and US as less CS elements in A1 due to decay over time. Therefore less excitatory learning.
Directionality and backwards conditioning - present US first, and then CS, US elements will decay into A2, but some still in A1. This means that some A1 A1 overlap, so excitatory learning, but also some A1 A2, so therefore some inhibitory learning. Therefore CS US pairing not learnt about due to US element decay into A2.
Explain tolerance in drug use?
Take x amount of drug to achieve x amount of high. Over time, x amount of drug will no longer produce x amount of high, but somewhat less, as drug is no longer novel, body has been accustomed to the drug, so drug has a weaker effect. Therefore must take X +1 amount of drug to achieve X why. Now drug user can tolerate more of the substance than they initally could.
Explain drug taking tolerance in terms of conditioning (CS and US)
Drug is US, high is UR, and environment, surroundings, certain object predictors are all CS. After repeated pairings CS (bedroom) comes to predict US, drug, and presence of CS will produce a CR - a compensatory response, reducing the effects of the US.
Explain overdose from drug taking in terms of conditioning.
If the CS such as context produces a counteractive compensatory response to the drug, before it is taken, then removing the CS, such as doing the drug in a novel context, will remove this compensatory effect. Meaning when taking the drug, the body no longer produces counteractive effect prior to drug, and the drug effect (UR) is stronger on the body.
What is true about the conditioning account of overdose.
A Overdose only occurs when the user takes more drug than usual.
B Overdose can occur when the drug user takes their usual dose, but in a novel context.
C The context that the drug user is typically in can produce a compensatory effect to the drug.
D Both B and C
D
How does Wagner’s SOP model explain conditioned diminution effect of drugs (Baker and Tiffany)?
Context CS sends drug elements into A2.
Therefore fewer drug elements to enter A1 when drug actually presented, therefore weaker effect.
What 2 main effects can a context or CS have on the drug?
Opposing effect/conditioned compensatory effect
Conditioned diminution (reduced effect)
What is the A1 response to morphine in rats (initial high)?
Hypoactivity and analgesia
What is the A2 response to morphine in rats (aftereffect)?
Hyperactivity and hyperalgesia
What were the main 2 findings of ‘Experiment 1’ by Paletta and Wagner?
In terms of activity the A2 state of hyperactivity was an opposite effect to the A1 state of hypoactivity (conditioned compensation for activity)
In terms of algesia the A2 state of hyperalgesia was not an opposite to A1, but a reduced A1 (conditioned diminution for algesia)
What was the premise of experiment 2 of Wagner and Paletta’s study? How many groups were there?
To test effect of context when drug is present vs absent, on algesia and activity effects of morphine in rats.
Essentially one group given morphine in same context as test.
One group given morphine in different context compared to test.
Control group.
Then measure algesia and activity, when given saline and when given morphine
In experiment 2 by Paletta ansd Wagner, what was the effect of context (same vs different) on activity, when given morphine vs saline?
In different context, morphine produced hypoactivity, as the context was novel. Therefore morphine had regular effect. Saline had no effect.
However when the context was the same, morphine produced heperactivity - counter effect. Saline test also led to hyperactivity, produced by the context. Therefore when in same context, group showed hyperactivity when given morpphine, and in context alone.
In experiment 2 by Paletta and Wagner, what was the effect of context (same vs different) on algesia, when given morphine vs saline?
In different context, morphine produced anelgesia/hypoalgesia as normal, as context was novel. No effect of context alone when given saline.
In same context, morphine lead to less hypoalgesia (hyperalgesia), as context produced reduced effect of drug. However, when just in context (saline inj not morphine), context did not produced hyperalgesia compensatory effect.
What does the study on context and morphine effects in rats tell us about conditioning effects of drugs?
Context can have a large effect on experience of the drug itself, and some effects are more affected than others, such as activity effects of morphine being stronger than algesia effects. Context can also lead to a compensatory/complete opposite response, or just have a reduced effect.
