What is the difference between an omnivorous species & a specialist species?
- Omnivorous species eat both plants & animals.
- A specialist species however is restricted to the niche in which they have evolved their particular adaption & may only be able to eat a few types of foods
What is the main advantage of being an omnivorous (as opposed to specialist) species?
Humans are less vunerable to reductions in the availability of a particular food source
What are the disadvantages of being an omnivorous (as opposed to specialist) species? (3 things)
- Less adaption in enzymes & other mechanisms to deal with problems specific to a particular food
- Risk of ingesting toxins that are spread across a wide range of potential foods
- Risk of nutritional imbalances bcos there are many potential foods with nutritive value but not complete nutrients
What did Davis find in his 1920's study of 2-3yr old children in an institutional context?
That young children can select an adequate diet with minimal social tuition
How do people select an adequate diet? (3things)
- Necessity (what is available & affordable)
- Instrumental reasons (dietary or religious requirements)
- Hedonics - Major factor (ingest what we like & reject what we dislike)
What are our few innate biases when it comes to food selection & rejection? (3things)
- We like sweet & salty tastes (correlated with calories in nature)
- We dislike bitter & sour tastes (correlated with toxins in nature)
- We ingest small amounts of novel foods (neophilia) & prefer familiar foods (neophobia)
What is the role of experience in food selection? (4things)
- We rapidly come to like foods rich in energy or protein
- We learn to select foods that correct a nutritional imbalance or aid recovery from sickness
- We come to dislike foods prohibted by our culture
- We come to dislike foods whose ingestion was followed by malaise
What did Myers & Sclafani show in 2003? (food selection)
That conditioned preferences can be established by pairing flavour with nutrtive infusions (rats drank more when flavour was paired with glucose than with water IG infusions)
What did Garcia & Koelling show in 1966? (food selection)
- That Learned Aversion has selectivity - sickness related to flavour & environment to physical events
- (That later sickness will cause the rats to avoid water with a certain flavour & that later electric shock will cause the rats to avoid water associated with certain light & noise)
What are the biological adaptions we have developed to ensure adequate energy & nutrients? (2things)
- Excess food in times of plenty stored as fat (to be used in times of famine)
- Developing satiety to the food just ingested to allow us to ingest different foods (with different range of nutrients)
What did Martire, Parkes, & Westbrook (in press) show?
That after drinking a solution to satiety (sucrose or ensure), when offered the same or different solution 1hr later, rats drink more of the different than the same solution (also show more clusters & licks per cluster [measures of liking or hedonics] to the different solution)
How do we know that the increase in obesity cannot be due to changes in the human genome?
Because the increase (over the last 30yrs) has been too rapid
What percent of Australians are overweight & obese?
40% are overweight (25% of whom are obese)
What percent of Americans & young Americans are overweight & obese?
65% overweight (30% of whom are obese) & of young Americans 30% are overweight (16% of whom are obese)
Why is it so hard to lose weight & maintain the loss?
The neuronal systems evolved to seek & ingest energy-rich foods (& other natural rewards) are the same that underlie seeking & taking of drugs of abuse (so energy-rich food is a substance of abuse which forms natural addiction)
What is the link between the HPA-axis & energy rich food?
Stress activates the HPA-axis, triggering release of endogenous opiods which presumedly enhances the hedonic attractiveness of certain kinds of foods (physiological mechanism linking stress & hedonically pleasant "comfort" foods)
What did the Berridge (2009) study show? (regarding location & response of hedonic hotspots)
That hedonic hotspots in the nucleus accumbens, ventral pallidum & brainstem parabrachial nucleus, respond to opioid or other signals (cannabinoids) with amplification of core 'liking' reactions to sweetness
What are the 4 areas of the brain through which flavour information is transmitted to the cortex? (which then discriminates tastes/textures & assigns hedonic value)
- VTA (ventral tegmental area)
- VP (ventral pallidum)
- NAc (nucleus accumbens)
What are dopamine projections from the VTA to the NAc strongly implicated in?
The control of behaviour by food related cues (incentive salience or "wanting") [so if u inject dopamine antagonists the rat will still show liking reaction to a food, but will no longer behave in a way to precure the food, ie no longer wants it]
What is opioid & cannabinoid (CB) signalling in the NAc & adjacent forebrain structures critical for?
The hedonic reactions to food (liking)
What is an agonist?
A drug that bind to a receptor of a cell & triggers a response by the cell (produces an action)
What is an antagonist?
A drug that binds to a cell receptor without eliciting a biological response, blocking binding of substances that could elicit such reponses (blocks action)
What does the observed decrease of CB1 & Dopamine D2 receptors in the late stages of diet-induced obesity imply?
That chronic overfeeding may decrease both the incentive salience (wanting) & liking of hedonically pleasant food [similiar to the adaptation to the effects of drug-taking in which more drug is required to get the same effect]
Why are all treatments for obesity (bar bariatric surgery), marginally effective in the short-term (1yr) & largely ineffective in the long-term (5yrs)?
Because whatever the treatment is, their common ingredient is the placebo effect
In her study regarding the social transmission of fears, what did Susan Mineka provide evidence of?
That we may be biased towards selecting some stimuli as fear elicitors when we have observed important others exhibiting fear reactions (we have a bias towards fear of only some stimuli after observing the fear in others)
What are the effects produced by dieting that are alleviated by relapse to energy-rich food (& are also characteristics of withdrawal from drugs which are alleviated by taking the drug again)?
stress, anxiety & depression
What is the HPA-axis (Hypothalamic–pituitary–adrenal axis) central to?
The stress response
What is Berridge's argument in regards to "liking" & "wanting"?
That 'liking' & 'wanting' are served by very different substrates in the brain & that we can want without liking, & like without wanting (& that wanting without liking is 1 of the prime characteristics of seriously addicted behaviours)
What is the definition of "endogenous"?
Originating or produced within an organism, tissue, or cell (So an 'endogenous opioid' example is an endorphin produced by the body)
What is the hypothalamus very important in?
Regulating homeostatic feeding (feeding that is in response to energy deficits)
What does the brain picture taken from Koob & Kestler (1999) show?
Illustrates the neural substrates underlying precurement & administration of drugs of abuse
What is the final stage in addictions?
Now it is not just a habit, it becomes a compulsion (the argument is that changes in cortical regions importantly related to executive functions [abilities to plan & monitor activities] & these changes are in some way responsible for the compulsions for drug-taking behaviour)
What is the difference between drug addiction & food addiction? (regarding compulsion)
There is no evidence to suggest that food addiction causes changes in pre-frontal regions that could lead to compulsive eating
What did Mineka & Cook (1993) show (in regards to social transmission of fear)?
That lab-reared monkeys (with no previous fear of snakes) will acquire fear reactions to snakes after observing wild monkeys exhibiting fear reactions to snakes
What did Mineka & Cook (1989) show (in regards to social transmission of fear)?
Stimulus selection bias - we may be innately predisposed to select certain stimuli over other as fear elicitors (lab-reared monkeys shown a video of a monkey displaying fear reactions to either a snake or flowers, will only acquire a fear reaction to the snake)
What happens if you show lab-reared monkeys (who have been pre-familiarised with snakes), videos of other monkeys displaying fear reactions to snakes?
They do not acquire a fear reaction to snakes (once you have acquired a strong familiarity with potential objects of fear, you do not seem to acquire this fear through imitation)
How is fear socially transmitted between mother & child?
Young children use mother's gaze direction to identify object of gaze, if the mother shows an emotional reaction then the child learns about the association between object & reaction
How does a child experience the reaction they observe their mother having to an object?
Mimicking the expression causes the child to experience the associated emotion (there is a bi-conditional link between emotional experience & its associated expression)
What is the function of imitation in animals?
To allow communication of certain types of information
What did the study by Marler (1970) show?
That young sparrows after leaving the nest at 10 days old, will then 1yr later, sing a song remarkably like its father's (dialects characterise a particular region) & that production of the full song is dependent on the sparrow hearing the full song during a critical period (10-50 days old). When exposure is before 10 days or after 50 days of age, the production of the song is impaired.
What are the parallels between sparrow song & human acquisition of dialects, that was shown by Marler's studies?
Studies of young children who were not exposed to speech at certain periods of their development, showed that when they were exposed, the acquisition of speech was remarkably impaire (critical periods for language development in both humans & sparrows)
What did Cheney & Seyfarth show with alarm calls in Vervet monkeys?
That young monkeys are unable to discriminate between alarm calls, but young monkeys orient towards mother during alarm calls & eventually learn to copy the mother's response
Why is it interesting that older Vervet monkeys will not make an alarm call when they see Baboons approaching (given that Baboons are dangerous to young monkeys but not older monkeys)?
It implies that perhaps the alarm calls are not intentional (because one would assume if intentional, they would try to protrct their young)
Why is it interesting that a subdominant vervet male monkey will make an alarm call alerting the dominant monkey to a danger?
It implies that perhaps the alarm calls are not intentional (because it is not in the genetic interest of the subdominant monkey to make the call)
What does it mean to have theory of other minds?
To understand that other people do not necessarily know what you know, & understanding that lying can trick other people
What did Woodruff & Premack (1979) show about theory of mind in chimps?
That chimps have theory of mind - bcos they can distinguish between the advice of a trainer who they have observed to be aware of the location of food versus a trainer who they have observed to not be aware of the location of food (& then only trust the advice of the trainer observed to be aware of location of food)
What did Gallup (1970) show?
That some animals can learn that the image seen in a mirror themselves (suggests self-awareness), he did this by drawing dots on their face
What do Suddendorf & Corballis argue about mental time travel?
That it is unique to humans (& its emergence was crucial to hominid evolution)
What do the studies by Clayton & Dickinson, show about episodic memory in birds?
- That the birds remember the relative time of caching, as well as the location & content of their caches (so they can mentally travel back in time).
- Also that they will cache based on if they know they will have food in the future (they can mentally travel forward in time too - planning)
What does the re-caching behaviour of birds (whose initial cache was observed by another bird) imply?
That they are able to project states of mind onto other birds (by assuming that the observing bird may try to steal their food if they are aware of where it was cached)
What are examples of 'excitatory conditioning'? (4things) (pavlovian conditioning)
- Eye-blink conditioning (typically used in rabbits, with a brief CS [tone] followed by a US [mild cheek shock])
- Autoshaping (typically used in pigeons, acrylic panel illuminated [CS] then food is delivered [US] & pigeon learns to peck the panel during CS)
- Conditioned supression (typically used in rats, trained to press lever for food, then CS [tone] is paired with US [shock] & rat learns to supress lever pressing during CS)
- Taste-aversion learning (normally used in rats bcos they don't vomit, animal consumes food [CS] followed by injection of lithium chloride [US] then shows aversion to the CS after getting sick)
What is 'excitatory conditioning'? (pavlovian conditioning)
The production of positive links between 2 events in the world (typically a CS which is neutral & a US which has motivational significance)
What is stimulus generalisation & generalisation decrement? (Pavlovian conditioning)
- Stimulus Generalisation - the extent to which the learning about a particular CS generalises to other similar cues,
- Generalisation Decrement - the extent to which performance falls off as you get more dissimilar to that cue
How is the 'supression ratio' (measure of learning in 'conditioned supression') calculated? (pavlovian conditioning)
a/(a+b), where a= lever pressing during the CS, & b= lever pressing during the inter-trial interval
Many other types of CR's may be present other than what is being measured. What are some examples that may be present in Pavlovian fear conditioning using rats? (5things)
- Changes in heart rate
- Changes in blood pressure
- Freezing behaviours
- Ultrasonic vocalisations
- Supression of activity
What is the clinical relevance that causes people like Davis to be interested in conditioned fear in animals? (pavlovian conditioning)
Because all of the measures of fear in animals are equivilant to generalised anxiety in humans (neural underpinnings of fear in animals has a lot of relevance for the treatment of anxiety in humans)
How is 'truly random control' (Rescorla, 1967) performed in 'excitatory conditioning' experiments? (pavlovian conditioning)
The CS & US are presented in a completely uncorrelated fashion (so the animals get equal numbers of exposure to the CS as to the US but in a completely random manner)
What is 'inhibitory conditioning'? (in terms of conditioning techniques) (pavlovian conditioning)
Forming an inhibitory relationship between the CS & US, predicting an absence rather than presence of something based on the presence of a certain cue (so presenting the cue inhibits activation of some representation of the US)
What is a retardation test? (pavlovian conditioning)
When you take the inhibitory CS, & pair it with the US, then compare reactions from both experimental & control groups (the control group has not receieved the inhibitory training for the CS). Learning about the shock association for previously inhibited CS should be retarded in the experimental group.
What is a summation test? (pavlovian conditioning)
Where an inhibitory & an excitatory CS are paired together & then reactions from both the experimental & the control group are compared (The control group has not been trained for the inhibitory CS). The experimental group should show a weaker responding to the combined CS's than to the solitary excitatory CS.
What is the benefit of using the Aplysia as a neural model of excitatory learning? (Pavlovian Conditioning)
The structure of the Aplysia's nervous system contains a small number (20,000) of relatively large (1mm in diameter) neurons, making it easy to identify individual neurons & neural pathways
What did Carey, Hawkins & Kandel (1983) find? (Pavlovian conditioning)
That when you take 2 CS's that already elicit a UR & pair 1 CS with a shock (CS+) & the other not paired with a shock (CS-), the association between CS+ & the US strengthens the UR for the CS+ (Alpha conditioning)
What are the 2 explanations for Alpha conditioning? (Pavlovian conditioning)
- CS-US account of learning
- S-R account of learning
What is the CS-US account of learning? (Pavlovian conditioning)
With pairing of the CS & US, the CS makes me think of the US (ie, creates a memory representation) & the thinking about the US causes me to produce a CR (Colwill & Motzkin, 1994)
What is the S-R account of learning? (Pavlovian conditioning)
The CS occurs as the same time as the US, the US elicits a response, therefore I strengthen a connection (an S-R connection) between the stimulus & response & that is what the animal learns (apylsia example suggestive of this)
What did the study by Colwill & Motzkin (1994) using rats show? (Pavlovian conditioning)
That if you associate food with a tone & then food with illness, the rats will become aversive to the tone (suggests CS-US learning bcos if the learning was S-R then the rat should only be turned off food & not the tone)
What did the study using rats by Holland (1990) show? (Pavlovian conditioning)
Evidence of CS-US account of learning - [That rats will show appetitive responses (paw licking) to a CS that was not associated with an aversive US, & show aversive responses (head shaking) to a CS that has been associated with an aversive US (poison)]
What is serial conditioning? (Pavlovian conditioning)
Training in which 2 or more CS (eg, tone, light) are presented in sequence & then followed by a US (eg, food) [& the 1st CS will often elicit a CR although weaker than the CR elicited by the 2nd CS]
What did Holland & Ross (1981) show with serial conditioning? (Pavlovian conditioning)
That an association can be formed between 2 CS (after training the sequence CS1 ([ight], CS2 [tone], US [food], the response normally evoked by CS1 [rearing] is replaced by the response normally evoked by CS2 [head jerking])
What did Rizley & Rescorla (1972) show with serial conditioning? (Pavlovian conditioning)
That a 2nd CS can form an association with a 1st CS & cause the 2nd CS to elicit a fear CR that is associated with the US associated with the 1st CS (pair light & tone, pair tone & shock, light now elicits fear CR)
What did Rescorla (1980) propose as an explanation for the contradictory results in 2nd order conditioning (where some studies suggest CS-US learning & some studies suggest S-R learning? (Pavlovian conditioning)
That when CS1 & CS2 are similar (such as different coloured lights) then CS-US learning occurs & that when CS1 & CS2 are dissimilar (light & tone) S-R (CS1-CR) learning occurs
What are the 2 characteristics of US representations outlined by Konorski (1967)? (Pavlovian conditioning)
- Specific (characteristics that make the US unique, such as its duration or flavour)
- Affective (characteristics that the US has in common with other stimuli & reflect its motivational properties)
What did Hearst & Franklin (1977) show about conditioned inhibitors that was surprising? (Pavlovian conditioning)
That a conditioned inhibitor can elicit withdrawal responses (ie, not just block a response)
When is a consummatory CR (Konorski, 1967) evoked? (Influence of the US on the CR - Pavlovian conditioning)
Whenever a CS retrieves specific properties of the US (mimics the response of the US) [involves the consummatory response system]
When are preparatory CR's (Konorski, 1967) evoked? (Influence of the US on the CR - Pavlovian conditioning)
Whenever a CS retrieves affective properties of the US (so may involve an appetitive or aversive CR with approach or withdrawal) [involves the motivational system]
What are compensatory CR's? (Influence of the US on the CR - Pavlovian conditioning)
A CR that opposes or compensates for the UR (eg, Siegal 1977 - reduction in the analgesic effects of morphine bcos the animal produces a opposing CR with the CS [injection/handling cues], bcos rat creates association between CS & compensatory CR)
What is the influence of the CS on the CR? (Pavlovian conditioning)
The nature of the CS changes the nature of the CR (eg, CS is another rat - CR is social behaviour, CS is block of wood - CR is not social)
How does the reflexive nature of the CR cause it to sometimes be maladaptive? (Pavlovian conditioning)
Because the CR is so automatic that even if it causes the animal to miss the appetitive US (such as in omission schedule), they still cannot stop the CR (pigeons pecking in response to CS cause them to miss US [food] but they cant stop pecking)
What are some examples of the multiple forms of association likely to determine excitatory & inhibitory learning? (5 things) (Pavlovian conditioning)
- CS-US vs S-R associations
- Aversive US's vs Appetitive US's
- Single CS vs Paired CS's in sequence
- CS-US vs CS-CS associations
- Consummatory CR's vs Preparatory CR's
What did Kamin's 1969 study on blocking show that contradicted earlier assumptions of Pavlovian Conditioning & led to the Rescorla Wagner (1972) model?
That compound conditioning (CS2-US followed by CS1-CS2-US), can block associations to be made between CS1 & US which implies that for a CS-US association to occur, the US must be unexpected (surprising)
What are the 3 conditions necessary for learning? (Pavlovian Conditioning)
- Contingency (the degree to which the CS provides a clear & informative marker for the US)
- Contiguity (the temporal relationship between the US & CS)
- Predictive value (level of surprise)
What is the main premise of the Rescorla & Wagner (1972) model?
- Strength of the CS-US association = strength of the CR
- Learning of CS-US association increases quickly at 1st (when assoc is most surprising), then slows down as with each trial the association becomes less surprising
What does the negative acceleration of Recscorla & Wagner's (1972) Idealised Learning Curve, illustrate?
- That the amount of change in conditioning strength (in arbitrary units) gets smaller & smaller with repeated trials
- (Initially - zero CS-US association & low CR.. Then - surprise at CS-US pairing causing rapid learning.. Then - learning slows as CS-US pairing becomes more expected & conditioning strength stabilises)
ΔV = αβ(λ-V) is the equation from the Rescorla Wagner (1972) model of associative learning. Explain the meaning of the equation & its symbols.
- ΔV: refers to the change in associative strength on a particular trial
- αβ: learning rate parameter determined by the properties of the CS (does not vary during conditioning, value between 0-1 [1 is strongest])
- λ: value set by the magnitude of the US (& reflects the maximum CS-US association possible)
- V: refers to the current strength of the CS-US association (initially = zero, then on each subsequent trial = Σ(ΔV) for all previous trials)
- SO, change in associative strength = value of the CS x (the magnitude of the US - the current CS-US associative strength)
- Conditioning progresses to asymptote when V = λ, bcos then ΔV = 0
What 2 effects did Annau & Kamin (1961) find that reducing the value of λ [intensity of US] had? (Pavlovian conditioning)
- 1. The rate of conditioning is slower (this is true also when αβ is smaller)
- 2. The ultimate level of conditioning is less
What effect did Kamin & Schaub (1963) find that reducing the value of αβ [intensity of CS] had? (Pavlovian conditioning)
The rate of conditioning is slower (but no difference in the ultimate level of conditioning)
What does the S-R account of learning assume in terms of the animal's knowledge of the US that has caused the UR? (Pavlovian conditioning)
Holland & Straub (1979) - That the animal does not know the identity of the US (food) that has led to the UR (sickness) & should therefore show no decreased CR (licking) to the CS (noise) associated with the US (food)
Rescorla Wagner (1972), and Mackintosh (1975), provide alternate accounts of blocking. How are the 2 accounts of blocking different? (Pavlovian conditioning)
Mackintosh rejects the idea that blocking occurs bcos stimuli training is complete & states that blocking occurs bcos animals pay attention to the stimuli that is the best predictor of US & the added cue is a worse predictor than the stimulus already conditioned
What is a conditioned suppression procedure? (Pavlovian conditioning)
Where a CS (eg, tone) is paired with an aversive US (eg, shock), & then fear is measured by the extent to which the CS now suppresses previously learned lever pressing for food [often used in studying acquisition & extinction of fear]
What changes are made to the Rescorla Wagner (1972) equation [ΔV = αβ(λ-V)] when conditioning with a compound CS?
The associative strengths of the individual stimuli are added together (VALL= VA+VX), so that now ΔV = α(λ-VALL)
What was the support Kehoe et al (1994) showed for ΔV = α(λ-VALL), in their rabbit eye-blink conditioning trials? (Pavlovian conditioning)
After training tone-shock & light-shock, the CR to the Light or the Tone < CR to the Tone+Light compound
How does the Rescorla Wagner model explain blocking in compound conditioning?
Bcos the US has already reached maximum predictive association in training with CS1, when training begins including CS2 in the compound, there is no surprise at the occurance of the US therefore no learning occurs for CS2
How does the Rescorla Wagner model explain overshadowing in compound conditioning?
Bcos for the control group the compund of CS1 & CS2 = λ, each CS gains less associative strength than if they were paired independently with the US & CS1 or CS2 alone is now < λ
How does the Rescorla Wagner model explain inhibitory conditioning in compound conditioning?
- Bcos CS2 is 1st trained with the US it has V2=100, but CS1 has not been trained therefore V1=0.
- Over training, CS1 can only become a negative value, so when VALL is summed in compound conditioning, the negative strength of CS1 eventually cancels out the positive strength of CS2
What are the pros of the Rescorla Wagner (1972) model? (4 things)
- Can explain many known phenomena in animal learning (even counter-intuitive ones)
- The mathematical equation can be used to make specific predictions
- It is an important senior relative to many contemporary theories of learning
- Can be applied beyond the study of animal learning
What are the cons of the Rescorla Wagner (1972) model? (3 things)
- No mechanism to explain attentional phenomena (eg, latent inhibition)
- Fails to explain all results in blocking studies
- Incomplete account for discrimination & configural learning
What does Wagner's (1981) SOP (standard operating procedures) state about the representation of stimuli? (Pavlovian conditioning)
- Stimuli can be in 3 states
- Inactive - memory not modifiable or able to influence behaviour
- A1 - centre of animals attention
- A2 - at the periphery of the field of attention
- Excitatory learning only occurs when CS & US in A1
- Associatively activated stimulus can be promoted from I to A2
What is latent inhibition? (Pavlovian conditioning)
Pre-exposure to the CS retards conditioned responding
What is learned irrelevance? (Pavlovian conditioning)
The slower learning of a paired CS & US if they have previously been presented randomly without each other
What does the Pearce-Hall (1980) theory state about modes of attention? (Pavlovian conditioning)
- There are 2 modes of attention
- 1. Automatic (when tasks are familiar)
- 2. Controlled deliberate (tasks where learning is required)
What implications does the Pearce-Hall (1980) theory have for the OR (orienting response)? (Pavlovian conditioning)
That rats should orient more in response to a CS with an unpredictable outcome (attention is maintained) & less to a CS with a predictable outcome (attention falls)
What implications does the Pearce-Hall (1980) theory have for conditioning? (Pavlovian conditioning)
- The R-W equation is updated as ΔV = α. S. λ (α=attention captured by the CS, S=intensity of CS, λ=magnitude of US).
- Therefore, rapid conditioning occurring with novel CS is due to high attention paid to stimulus when 1st presented. Attention to CS reduced with familiarity of CS-US association & changes in associative strength are negatively accelerated
Can the Pearce-Hall (1980) model explain blocking, latent inhibition &/or learned irrelevance? (Pavlovian conditioning)
- Can explain blocking
- Can explain latent inhibition (but not context-specific latent inhibition)
- Cannot explain learned irrelevance
What is the difference between positive & negative reinforcers (Instrumental conditioning)?
- Positive reinforcer - consists in the delivery of a stimulus
- Negative reinforcer - involves the removal of a stimulus
What is Thorndike's (1898) Law of Effect? (Instrumental conditioning)
When a response is followed by a reinforcer, then a stimulus-response (S-R) connection is strengthened (this fails to allow the animal to anticipate the goal for which it is responding however)
How did Elliot (1928) show that animals do anticipate the reward/goal for which they are responding [contradicts the Law of Effect]? (Instrumental conditioning)
Contradictory to S-R theory, reducing the attractiveness of the task reward increased errors in the response task to even higher levels than that of a control group who had been trained consistantly with the less attractive reward
How does Tolman (1932) explain Elliot's (1928) finding that contrary to Law of Effect, rats do anticipate the rewards of their responding? (Instrumental conditioning)
By arguing that Elliot's findings indicate rats form R-US associations as a result of instrumental conditioning, ie they learn that a response will be followed by a particular outcome (problem tho is that the anticipation of reward could also be based on CS-US associations where the context-specific goal box [CS] is assoc. with the reward [US])
How does Cowill & Rescorla's (1985) study using reinforcer devaluation provide evidence for R-US associations? (Instrumental conditioning)
Bcos when the positive reinforcer (US1) for R1 was devaluated, rats responded more to R2 than R1 in testing (reluctance to perform R1 seen as evidence that the rats associate R1 with the aversive US1)
How does Cowill & Rescorla's (1985) study using reinforcer devaluation provide evidence for CS-US associations? (Instrumental conditioning)
Bcos performance to R1 was lessened but maintained despite its apparent learned association with the completely rejected US1
What is the basic distinction between S-R learning & R-US learning? (Instrumental conditioning)
- S-R learning - animals can learn to perform a particular response in the presence of a given stimulus
- R-US learning - animals can learn that a certain reinforcer will follow a response
What knowledge does a S-(R-US) association convey? (Instrumental conditioning)
That in the presence of a certain stimulus a certain response will be followed by a certain outcome
What did Rescorla suggest in his hierarchical account of S-(R-US) learning? (Instrumental conditioning)
That animals 1st learn R-US, which then become associated (in its entirety) with S
What is the gradient of delay (Logan 1960)? (Instrumental conditioning)
The progressive weakening of an instrumental response as a result of increasing the delay between completion of response & delivery of reinforcer
What is the response-reinforcer contingency (Hammond, 1980)? (Instrumental conditioning)
The degree to which the occurrence of the reinforcer depends on the instrumental response (eg, positive contingency - frequency of the reinforcer is increased by making the response)
What is the molar theory of reinforcement (Baum, 1973)? (Instrumental conditioning)
Assumption that the rate of instrumental responding is determined by the response-reinforcer contingency & instrumental conditioning is effective if responding increases the rate of reinforcement (explanation for Hammond 1980 - thirsty rats & lever pressing)
What is the molecular theory of reinforcement? (Instrumental conditioning)
- The theory that instrumental conditioning depends on the formation of associations (& contiguity is important for learning)
- - therefore it assumes that the rate of instrumental responding (the effectiveness of instrumental conditioning) is determined by response-reinforcer contiguity (specific episodes of the response being paired with a reinforcer).
- (a problem for Hammond 1980 bcos response was paired with reward in all 3 groups)
What is associative competition? (Instrumental conditioning)
- Reinforcers delivered during the inter-trial interval will strengthen a Context-US association
- Context-US association will overshadow the Response-US association, lowering the rate of responding
- (assumes that overshadowing can occur not just between stimuli, but also between stimuli & responses that signal the same reinforcer)
How did Pearce & Hall's (1978) study directly support the claim that overshadowing is possible between stimuli & responses (associative competition)? (Instrumental conditioning)
- (E Group: Response--noise & food; C Group: Response--food)
- By showing that stronger responding in the control group than the experimental group, was caused by a noise-food association overshadowing the response in the experimental group
How did Dickinson & Charnock's (1985) study support the claim that overshadowing is possible between stimuli & responses (associative competition)? (Instrumental conditioning)
- That the effect of presenting inter-trial interval US's is abolished if they are signalled
- - stimulus signals the delivery of each free (unearned) reinforcer, & instrumental responding is disrupted less than when unsignalled.
- (Creates stimulus assoc. with the reinforcer [CS2-US], which overshadows the development of an assoc. between context & the reinforcer [CS1-US])
Does a good reinforcer need to be something of biological significance? (Instrumental conditioning)
No, Schwartz (1989) showed that animals will press a lever to turn on a light
What is the Premack principle? (Instrumental conditioning)
- The proposal that reinforcers are not stimuli but opportunites to engage in behaviour -ie, activity of eating not stimulus of food
- & if both activities are freely available, then activity A will reinforce activity B, if activity A is more probable than activity B
How did Allison & Timberlake's (1974) study contradict the Premack principle idea that the preferred response/activity will act as the reinforcer for the alternative response/activity? (Instrumental conditioning)
- By showing that rats will increase their consumption of preferred drink, if it increases their access to non-preferred drink
- (A & T explained their results with an equilibrium theory of behaviour - ie, animal will to its best to reach personal bliss point (time spent engaged) for all activities, even least-preferred
What is a conditioned reinforcer? (Instrumental conditioning)
- An originally neutral stimulus that serves as a reinforcer through training, usually by being paired with a positive reinforcer
- eg, Hyde (1976), tone paired with food, later rats willing to lever-press to present the tone (even though no food presented now)
What is a token reinforcer? (Instrumental conditioning)
- A conditioned reinforcer typically in the form of a plastic chip that is earned by performing some Response & can be exchanged for food (Reinforcer)
- Hyde (1976) showed that the tone became a appetitive Pavlovian CS & served as a subsitute for food (token reinforcer)
What are other ways in which Scwartz (1958) argued that conditioned reinforcers can be effective? (3 things)
- 1. Provide feedback that the correct response was made
- 2. Cue the next response
- 3. Counteract the effect of a delay between Response & primary Reinforcer
What are 2 factors/influences which determine the vigor with which an animal will perform an instrumental response?
- 1. Deprivation state (drive centre energising motivation)
- 2. The presence of Pavlovian CS's (motivational influences, or response-cueing properties of Pavlovian CR's)
Why is Hull (1943) incorrect in his suggestion that drive is nonspecific (so can be enhanced by an increase in any need of the animal)? (Instrumental conditioning)
Bcos studies have shown that pain by shock does not invigorate responding for food, nor does hunger invigorate avoidance responses
What are dual-system theories of motivation? (Instrumental conditioning)
- Idea by Rescorla & Solomon (1967), that there are 2 motivational systems
- 1. positive (activated by deprivation states, eg hunger, thirst)
- 2. negative (activated by aversive states, eg pain)
- Assumes that behaviour is motivated by activity in positive system which energises approach to object, & negative system which energises withdrawal from object)
Can Pavlovian CS's influence instrumental behaviour? If so, how? (2 things)
- 1. Motivational influences
- 2. Response-cueing properties of Pavlovian CR's
What are the motivational influences of Pavlovian CS's that are proposed to influence instrumental behaviour? (3 things)
- 1. CS can excite an affective representation of the US & arouse positive motivational system (Konorski, 1967)
- 2. Pavlovian-instrumental transfer - train R-US association [lever-food], then train CS-US [clicker-food], CS now enhances R (Lovibond, 1983)
- 3. Modified dual systems theories - inhibitory connections between appetitive & aversive systems [aversive CS reduces positive motvational support for the response] (Dickinson & Pearce, 1977)
What are the the response-cueing properties of Pavlovian CR's that are proposed to enable Pavlovian CS's to influence instrumental behaviour?
- If 1 Response is paired with a certain US, & a 2nd Response is paired with a 2nd US, but the CS has only been paired with R1, then responding in the presence of CS will be higher to R1 than R2 bcos the CS provides response cueing properties for R1 but not R2
- (cannot be explained by motvation bcos motivational influences for both R1 & R2 are the same)
How does Insight contradict the theory of Law of Effect in explaining how animals problem-solve? (Instrumental conditioning)
States that rather than strengthening an accidentally occurring response through reward, animals are able to problem-solve through an understanding of the causal properties of the objects in their environment
Can animals problem-solve through an understanding of the physical & causal properties of the objects they are using? (Instrumental conditioning)
Impossible to say as the studies by Kohler (1925) - chimps & bananas/ceiling, Premack (1976) - chimps & apples/knives, Heinrich & Bungyar (2005) - birds & string-pulling/food, Tebbich et al (2001) - woodfinches & complex tool use, can all be explained alternatively by trial & error learning &/or generalisation of responding
What are neurons?
The fundamental units, or building blocks of the brain
What is sensory transduction?
Physical stimulus leading to neuronal signal
What is the action potential?
A signal by a neuron defined by a brief & stereotype change in the neuron membrane potential
Nerve cells have a high intracellular concentration of ..... & a low intracellular concentration of ..... ?
- High - potassium (K+)
- Low - Sodium (Na+)
What are the 2 forces that act on ions?
- 1. Chemical force
- 2. Electrical force
What is the equilibrium potential for K+?
What is the equilibrium potential for Na+?
At rest, the membrane potential is about 20 times more permeable to K+ than Na+. How is this explained by the resting potential?
Bcos the resting potential is approx. -70mV which is very close to the equilibrium potential for K+ (approx. -75mV)
What is it that causes the membrane to reach a potential very close to the equilibrium potential for potassium (K+)?
The balance between the opposing electrical & chemical forces
What is selective permeability & what changes permeability?
- Cells exhibit selective permeability by having channels for some ions & not others.
- Permeability depends on number of channels & can change rapidly when gated ion channels are opened
What creates an electrical potential or voltage?
Separation of charge (net positive charge on the outside & a net negative charge on the inside)
What does the electrical potential do to K+?
It opposes diffusion of K+ out of the cell
What do the electrical & chemical forces do to K+?
- Electrical force – moving it into the cell body
- Chemical force – moving it out of the cell body
Are resting neurons more permeable to K+ or Na+?
Resting neurons are very permeable to K+ & only slightly permeable to Na+
What happens when K+ diffuses out of a cell?
A charge seperation develops (opposite charges attract & the electrical potential resulting from the charge seperation pulls Na+ into the cell)
How does the neuron compensate for K+ & Na+ leaks? (& how many Na+ ions are pumped out to every K+ ion pumped in?)
- The Na+-K+ pump maintains the resting membrane potential by actively transporting ions to compensate for the leaks
- (for every 3 Na+ ions pumped out, 2 K+ ions are pumped in)
In what way are action potentials the signature of the cell?
Bcos they are the same in any given cell (all or none events)
What are synaptic potentials?
Small, graded, short-distance signals (the incoming signals to neurons)
What are excitatory postsynaptic potentials (EPSP's), & what are their function?
- EPSP's are local, graded depolarisations of excitable cells
- (function is to generate an action potential in the post synaptic cell)
What are inhibitory postsynaptic potentials (ISPS's), & what are their function?
- ISPS's are local, graded, hyperpolarisations of excitable cells
- (functions to prevent generation of an action potential in a postsynaptic cell)
What is the job of the cell? (hint - it is the same as the job of the whole nervous system)
To select a single output from many competing inputs
What are the competing functions of action potentials & synaptic potentials?
- action potential - the output signal of the neuron
- synaptic potential - the input signal of the neuron
What is the difference between the conduction distance for an action potential & a synaptic potential?
- Action potentials are long-distance signals continuously regenerated along the entire axon
- Synaptic potentials are local electric currents with a short-distance goal
What is the stimulus for opening ion channels in an action potential vs a synaptic potential?
- Stimulus for opening ion channels in an action potential - voltage change
- Stimulus for opening ion channels in a synaptic potential - chemical
What is the mechanism of neuron repolorisation in an action potential?
Voltage-gated Na+ channels inactivate, voltage-gated K+ channels open
What is the mechanism of neuron repolorisation in a synaptic potential?
Neurotransmitter dissociates from chemically-gated ion channel
What is the comparative amplitude of an action potential?
Large, does not decrease with distance
What is the comparative amplitude of a synaptic potential?
Small, aplitude decreases with distance
What happens (during the action potential) when voltage-gate Ca2+ (calcium) channels open & Ca2+ enters the cytoplasm?
Calcium triggers the release of transmitter into the synaptic cleft & transmitter activates postsynaptic ligand-gated ion channels (LGIC's)
What is the membrane potential?
The electrical charge across a cell membrane; the difference in electrical potential inside & outside the cell
What is the definition of a resting potential?
The membrane potential of a neuron when it is not being altered by exitatory or inhibitory postsynaptic potentials (-70mV)
What is the threshold of excitation?
The value of the membrane potential that must be reached to produce an action potential
What happens when the threshold of excitation is reached (ie, action potential)? (in order of events)
1. Sodium channels in the membrane open & Na+ rushes in, the rush of positively charged sodium ions causes the membrane potential to rapidly change from -70mV to +40mV
- 2. The (less sensitive) potassium channels begin to open (they require a greater level of depolarisation than sodium channels)
- 3. (at the peak of action potential) the sodium channels become blocked until the membrane returns to resting potential
- 4. The inside of the axon is positively charged so K+ ions are driven out of the cell by diffusion & electrostatic pressure, causing the membrane potential to return to its normal value
What did Bliss & Lomo (1973) find at glutamatergic synapses in the Hippocampus?
Long Term Potentiation (LTP) - a long-term increase in the excitability of a neuron to a particular synaptic input (caused by high-frequency repetition of that input)
What have LTP & LTD been postulated to be? (in terms of what type of brain thing)
Substrates (the material upon which an enzyme acts) for various forms of learning & memory formation
What is Hebb's (1949) rule regarding synapses & classical conditioning? (the cellular basis of learning)
That a synapse that repeatedly becomes active around the same time that the postsynaptic neuron fires, will become strengthened in connection with the other (ie, neurons that fire together wire together)
What is the cellular mechanism underlying the induction of LTP?
- Glutamatergic synapse is 1st formed with mainly NMDA receptors appearing in the postsynaptic membrane
- The postsynaptic membrane is depolarised & the magnesium block disappears
- Calcium entering through the NMDA receptor activates protein Kinases (which can cause LTP)
How does Calcium (Ca2+) entering the synapse through NMDA receptor & activating protein Kinases, cause LTP? (2 things)
- 1. Changing the effectiveness of existing postsynaptic AMPA
- 2. Stimulating the insertion of new AMPA receptors
What are the 2 conditions that must be met for the NMDA receptor to be activated?
- 1. Glutamate is released (ie, the pre-synaptic neruon is active)
- 2. The magnesium block is removed due to post-synaptic depolorisation
What is the BCM theory? (relates to neurons that fire together)
An extension of Hebb's theory that accounts for bidirectional (up & down) regulation of synaptic strength
What is the receptor underlying LTP which also underlies LTD?
What are the frequencies of stimulation that yield LTP, & LTD?
- High frequency stimulation yields LTP by causing a large elevation in Ca2+
- Low frequency stimulation yields LTD by causing a smaller elevation of Ca2+
How do LTP & LTD disrupt the equilibrium of synaptic transmission? (where AMPA receptors are constantly being added & removed, normally in equal amounts)
- LTP leads to a net increase in the synaptic membrane capacity for AMPA receptors (increases the no. of slot proteins in the membrane)
- LTD leads to a net decrease in the synaptic membrane capacity for AMPA receptors (decreases the no. of slot proteins in the membrane)
What happened when an NMDA-receptor blocker was injected into the hippocampus of rats being trained in a water maze?
They failed to learn the location of the escape platform
What happened when Tonegawa deleted the gene for 1 sub-unit of CaMKII (the protein Kinase involved in LTP)?
They found deficits in both LTP & memory
What is hyperpolorisation?
The change in a cell's membrane potential that makes it more negative inside (inhibits action potential)
What is depolarisation?
- An electrical state in an excitable cell whereby the inside of the cell is made more positive (causes action potential)
- A neuron membrane is depolarised if a stimulus decreases its voltage from the resting potential of -70mV in the direction of zero voltage
What is long-term depression (LTD)?
- A long-term decrease in the excitability of a neuron to a particular synaptic input caused by stimulation of the terminal button while the postsynaptic
- membrane is hyperpolarised (or only slightly depolarised)
What happened when Tsien & Tonegawa et al (1996) restricted the deletion of NMDA receptors to CA1 hippocampal cells, starting at 3wks of age?
The animals showed a deficit in LTP & water maze performance
What do animals engineered to produce too many NMDA receptors show?
Enhanced learning ability in some tasks
In what way does the timing of LTP & timing of fear conditioning behaviour not correspond?
- LTP requires the activity of the pre- & post-synaptic neurons to conincide within a time frame of 10's of milliseconds
- Fear conditioning as a behaviour does not rely on such precise timing
What is the problem with investigating reward functions of classical conditioning at a neural level?
There are no dedicated receptors for reward
What are 2 brain areas involved in basic & higher reward processes?
Both the dorsal & ventral striatum
What is positive prediction error?
When you are not expecting a reward but get more (elicits an activation of response)
What is negative prediction error?
When you are expecting a reward but don't get it (induces a depression of response)
How are the characteristics of phasic dopamine responses compatible with the notion of teaching signal (according to reinforcement learning theories)? [Dopamine response = reward occurred - reward predicted]
- Dopamine neurons acquire responses to reward-predicting visual & auditory CS.
- The responses covary with the expected value of reward.
- Learning is viewed as a change of behaviour following a change of prediction
How do neuronal computations using prediction errors contribute to the self-organization of behaviour?
The error signal is transmitted by dopamine neurons & influences synaptic processes in dopamine target structures (such as striatum & orbitofrontalcortex)
In what way are Pavlovian learning of reward predictors, in a key role for decision-making?
Bcos choices are (crucially) based on predictions of outcomes
Reward is the outcome of the choice. How is the reward evaluation used to update the prediction used for the next decision? (2 possible reactions)
- Receive reward (reward unchanged) - Keep prediction unchanged
- Receive reward (reward changed) - Generate error signal, Update prediction, Use prediction for action & choice
What did Lashley find when he lesioned larger & larger areas of cortex (in terms of the learning effect it had on rats, & the effects tracable to each lesioned area)?
- That greater areas of cortical destruction were associated with more errors made by rats learning to run a maze
- & therefore bcos no single area caused a specific deficit, probably all cortical areas contribute equally to learning & memory
What is another word for an action potential?
What is energy homeostasis?
- The tendency to maintain the stability of normal biological states during adjustments to environmental changes
- (ie, the precise long-term coupling of energy intake [in the form of feeding], with energy expenditure [in the form of cellular metabolism & exercise] in healthy adults)
How is energy expenditure calculated? (ie, the 3 things it consists of with %)
- 1. Basal metabolic rate (60%)
- 2. Physical activity (20-30%)
- 3. Thermic effect of food (10)%
What happens when taste molecules bind with a receptor?
Alters membrane potential & induces action potentials
What is the support for arguing that taste & liking is an evolutionary adaption? (2 things)
- The typical stimulus for sweetness receptor is sugar (calories)
- The typical stimulus for bitterness receptor is alkaloid (poison)
How does Pavlovian conditioning influence food liking & disliking? (2 things)
- Conditioned taste aversion
- Conditioned taste preference
What kind of foods are stressed rats biased towards selecting?
Fat & calorically rich foods
How is information about the taste of food conveyed to the brain?
Via a specialised pathway in the mammalian peripheral & central nervous system (from the tongue to the cortex)
What is 'adaptive self-selection' of food?
Where Pavlovian conditioning processes enable the individual to learn to like & dislike any food (depending on its post ingestional consequences)
Which 2 body parts control the entry of calories into the blood (from either food or energy stores), as well as the uptake & utilisation of these calories by different parts of the body?
The brain & the liver (both detect energy available & can convert energy from 1 form to another)
In what ways does the liver detect energy available & convert it from 1 form to another? (3 things)
- Converts carbohydrates to fat (or from amino-acids to carbohydrates)
- Detects changes in fat availability & usage
- Communicates with the brain via the vagus nerve
In what ways does the brain detect energy available? (2 things)
- Detects blood glucose levels via neurons in the brainstem & hypothalamus
- Taste pathways project to hypothalamus
How does damaging or stimulating the 'start centre' of the hypothalamus (the Lateral Hypothalamus), influence eating? (2 things)
- Damage (eg, lesion) to the lateral hypothalamus is associated with disruption of feeding
- Stimulation of the lateral hypothalamus elicits feeding & drinking
How does the damaging the 'satiety' or 'stop' centre of the hypothalamus (the Ventromedial hypothalamus), influence eating? (2 things)
Damage to the ventromedial hypothalamus is associated with disruption of feeding (Eat normal amount, just more frequently & finnicky)
What is glucostatic hypothesis? (role of internal signals in short-term regulation of hunger)
The glucostatic hypothesis suggests that the availability of glucose plays a crucial role in eliciting hunger (ie, levels drop = hunger)
How does Ghrelin (a hormone produced in stomach and small intestine), influence eating? (1 cause with 3 explanations)
- Signals (hunger to) the brain (via the bloodstream or via the vagus nerve)
- Levels peak just prior to meal initiation (in humans & other animals)
- Injections into the periphery (eg, blood stream) or brain stimulate eating
What is the evidence for physiological signals as cause of eating?
Physiological changes (changes in ghrelin, blood glucose, & metabolic activity) are proven to occur prior to the initiation of meal (suggests that hypothalamic monitoring of physiological parameters determines when we start a meal)
What stops a meal? (role of satiety signals from the periphery)
- Mechanical signals (via sympathetic nervous system afferents [signal of feeling full/satiety])
- Chemical signals (binding to receptors on vagus nerve in response to what has been eaten [innervates stomach & small & large intestine])
- Brain signals - vagus nerve projects to -- nucleus of the solitary tract in brainstem, which projects to -- hypothalamus
What did Rolls et al. (1981) show with sensory specific satiety?
- causes Reductions in palatability to same food after ingestion
- causes Reduced caloric intake in second course
What did The Party Study by Wansink & Cheney (2005) find in regards to the effect of the size of serving plate, on eating? (4 things)
- 1. Amount of food taken increased (for the large serving dish)
- 2. Calories of the food taken increased (for the large serving dish)
- 3. Amount of food eaten in total increased (for the large serving dish)
- 4. Calories consumed in total increased (for the large serving dish)
What is the Externality Hypothesis of obesity (Schachter)?
Theory that individuals differ in sensitivity to bodily/internal cues & that obese people are less sensitive to bodily cues (so therefore more likely to eat in response to environmental factors)
How is Leptin related to body mass?
- Levels of leptin in bloodstream correlate positively with the number of fat cells
- It signals the current level of adposity (fatness), to the brain
What happens to Leptin in individuals who have not eaten enough to maintain their normal weight? (undereating)
They have lower levels of leptin in blood & brain - this causes cells to release more NPY which increases meal size & decreases metabolism
What happens to Leptin in individuals who have eaten too much and gained weight, & what are the consequences? (overeating)
They have higher levels of leptin in blood & brain - this causes cells to release less NPY which decreases meal size & increases metabolism
Why do drugs of abuse have motivationally significant, rewarding, properties?
Bcos they increase neurotransmission in the mesolimbic dopamine pathway (via different actions for different drugs)
What are the sequence of neural events that lead to Dopaminergic neurotransmission? (5 steps - from synthesisation to deactivation)
- 1. Dopamine is synthesised & stored in vessicles in the pre-synaptic neuron
- 2. Action potential causes vessicles to release dopamine into synaptic cleft
- 3. Dopamine binds to 2 receptors (D1 & D2)
- 4. Dopamine is removed from the synaptic cleft via a re-uptake pump
- 5. Dopamine remaining is deactivated
What is the Incentive Motivational Theory (Berridge & Robinson, 1993)? (why do people persist in taking drugs?)
- Addictive drugs enhance transmission within the mesolimbicdopamine pathway which attributes incentive salience to the perceptions & mental representations of events associated with activation of the pathway
- Repeated administrations of addictive drugs renders the pathway hypersensitive to drugs of abuse & drug associated stimuli
- This sensitisation leads to associative learning
What is the opponent process model (Solomon & Corbit, 1974)? (why do people persist in taking drugs?)
- A process - drug euphoria or rush, B process - drug withdrawal (non-associative model)
- Over time B process increases. Although drug administrations arouse the Aprocess, B process has grown significantly & thus the drugs fail to produce an A-state. They simply alleviate the B-process
What is the Dickinson-Balleine model of incentive learning?
- Studies of incentive learning under natural motivational states suggest that animals must learn about the relevance of a reward to its current motivational state in order to seek that reward
- Likewise, withdrawal from opiates functions as a motivational state that enhances the incentive value of the drug, thereby enabling it to function as a much more cue for self-administration
What are Oxytocin & Vasopressin important for in mammals?
Reproductive behaviours & Attachment behaviours
What is the opponent process model (Solomon & Corbit, 1974) (love & attachment)
- A process - reward produced by contact with loved one, B process - separation distress
- Over time B process increases. Although romantic interactions arouse the A process, B process has grown significantly and thus the interactions fail to produce an A-state. They simply alleviate the B-process, separation distress
What does damage to the medial temporal lobe, including, hippocampus, produce in humans?
If Amnesia is not just a storage deficit, what else is it due to?
An impairment of memory retrieval
Where are permanent memories most likely stored?