lrnng&physiopsych

• 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

Humans are less vunerable to reductions in the availability of a particular food source

• 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

That young children can select an adequate diet with minimal social tuition

• Necessity (what is available & affordable)
• Instrumental reasons (dietary or religious requirements)
• Hedonics - Major factor (ingest what we like & reject what we dislike)

• 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)

• 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

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)

• 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)

• 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)

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)

Because the increase (over the last 30yrs) has been too rapid

40% are overweight (25% of whom are obese)

65% overweight (30% of whom are obese) & of young Americans 30% are overweight (16% of whom are obese)

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)

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)

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

• VTA (ventral tegmental area)
• VP (ventral pallidum)
• NAc (nucleus accumbens)
• striatum

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]

The hedonic reactions to food (liking)

A drug that bind to a receptor of a cell & triggers a response by the cell (produces an action)

A drug that binds to a cell receptor without eliciting a biological response, blocking binding of substances that could elicit such reponses (blocks action)

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]

Because whatever the treatment is, their common ingredient is the placebo effect

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)

stress, anxiety & depression

The stress response

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)

Originating or produced within an organism, tissue, or cell (So an 'endogenous opioid' example is an endorphin produced by the body)

Regulating homeostatic feeding (feeding that is in response to energy deficits)

Illustrates the neural substrates underlying precurement & administration of drugs of abuse

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)

There is no evidence to suggest that food addiction causes changes in pre-frontal regions that could lead to compulsive eating

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

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)

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)

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

Mimicking the expression causes the child to experience the associated emotion (there is a bi-conditional link between emotional experience & its associated expression)

To allow communication of certain types of information

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.

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)

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

It implies that perhaps the alarm calls are not intentional (because one would assume if intentional, they would try to protrct their young)

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)

To understand that other people do not necessarily know what you know, & understanding that lying can trick other people

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)

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

That it is unique to humans (& its emergence was crucial to hominid evolution)

• 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)

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)

• 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)

The production of positive links between 2 events in the world (typically a CS which is neutral & a US which has motivational significance)

• 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

a/(a+b), where a= lever pressing during the CS, & b= lever pressing during the inter-trial interval

• Changes in heart rate
• Changes in blood pressure
• Freezing behaviours
• Ultrasonic vocalisations
• Supression of activity

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)

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)

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)

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.

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.

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

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)

• CS-US account of learning
• S-R account of learning

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)

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)

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)

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)]

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]

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])

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)

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

• 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)

That a conditioned inhibitor can elicit withdrawal responses (ie, not just block a response)

Whenever a CS retrieves specific properties of the US (mimics the response of the US) [involves the consummatory response system]

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]

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)

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)

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)

• 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

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)

• 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)

• 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

• 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: 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

• 1. The rate of conditioning is slower (this is true also when αβ is smaller)
• 2. The ultimate level of conditioning is less

The rate of conditioning is slower (but no difference in the ultimate level of 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)

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

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]

The associative strengths of the individual stimuli are added together (VALL= VA+VX), so that now ΔV = α(λ-VALL)

After training tone-shock & light-shock, the CR to the Light or the Tone < CR to the Tone+Light compound

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

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

• 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

• 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

• No mechanism to explain attentional phenomena (eg, latent inhibition)
• Fails to explain all results in blocking studies
• Incomplete account for discrimination & configural learning

• 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

Pre-exposure to the CS retards conditioned responding

The slower learning of a paired CS & US if they have previously been presented randomly without each other

• There are 2 modes of attention
• 1. Automatic (when tasks are familiar)
• 2. Controlled deliberate (tasks where learning is required)

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)

• 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 explain blocking
• Can explain latent inhibition (but not context-specific latent inhibition)
• Cannot explain learned irrelevance

• Positive reinforcer - consists in the delivery of a stimulus
• Negative reinforcer - involves the removal of a stimulus

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)

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

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])

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)

Bcos performance to R1 was lessened but maintained despite its apparent learned association with the completely rejected US1

• 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

That in the presence of a certain stimulus a certain response will be followed by a certain outcome

That animals 1st learn R-US, which then become associated (in its entirety) with S

The progressive weakening of an instrumental response as a result of increasing the delay between completion of response & delivery of reinforcer

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)

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)

• 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)

• 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)

• (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

• 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])

No, Schwartz (1989) showed that animals will press a lever to turn on a light

• 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

• 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

• 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)

• 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)

• 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

• 1. Deprivation state (drive centre energising motivation)
• 2. The presence of Pavlovian CS's (motivational influences, or response-cueing properties of Pavlovian CR's)

Bcos studies have shown that pain by shock does not invigorate responding for food, nor does hunger invigorate avoidance responses

• 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)

• Yes,
• 1. Motivational influences
• 2. Response-cueing properties of Pavlovian CR's

• 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)

• 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)

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

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

The fundamental units, or building blocks of the brain

Physical stimulus leading to neuronal signal

A signal by a neuron defined by a brief & stereotype change in the neuron membrane potential

• High - potassium (K+)
• Low - Sodium (Na+)

• 1. Chemical force
• 2. Electrical force

approx. -75mV

approx. +55mV

Bcos the resting potential is approx. -70mV which is very close to the equilibrium potential for K+ (approx. -75mV)

The balance between the opposing electrical & chemical forces

• 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

Separation of charge (net positive charge on the outside & a net negative charge on the inside)

It opposes diffusion of K+ out of the cell

• Electrical force – moving it into the cell body
• Chemical force – moving it out of the cell body

Resting neurons are very permeable to K+ & only slightly permeable to Na+

A charge seperation develops (opposite charges attract & the electrical potential resulting from the charge seperation pulls Na+ into the cell)

• 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)

Bcos they are the same in any given cell (all or none events)

Small, graded, short-distance signals (the incoming signals to neurons)

• EPSP's are local, graded depolarisations of excitable cells
• (function is to generate an action potential in the post synaptic cell)

• ISPS's are local, graded, hyperpolarisations of excitable cells
• (functions to prevent generation of an action potential in a postsynaptic cell)

To select a single output from many competing inputs

• action potential - the output signal of the neuron
• synaptic potential - the input signal of the neuron

• Action potentials are long-distance signals continuously regenerated along the entire axon
• Synaptic potentials are local electric currents with a short-distance goal

• Stimulus for opening ion channels in an action potential - voltage change
• Stimulus for opening ion channels in a synaptic potential - chemical

Voltage-gated Na+ channels inactivate, voltage-gated K+ channels open

Neurotransmitter dissociates from chemically-gated ion channel

Large, does not decrease with distance

Small, aplitude decreases with distance

Calcium triggers the release of transmitter into the synaptic cleft & transmitter activates postsynaptic ligand-gated ion channels (LGIC's)

The electrical charge across a cell membrane; the difference in electrical potential inside & outside the cell

The membrane potential of a neuron when it is not being altered by exitatory or inhibitory postsynaptic potentials (-70mV)

The value of the membrane potential that must be reached to produce an action potential

• 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

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)

Substrates (the material upon which an enzyme acts) for various forms of learning & memory formation

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)

• 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)

• 1. Changing the effectiveness of existing postsynaptic AMPA
• 2. Stimulating the insertion of new AMPA receptors

• 1. Glutamate is released (ie, the pre-synaptic neruon is active)
• 2. The magnesium block is removed due to post-synaptic depolorisation

An extension of Hebb's theory that accounts for bidirectional (up & down) regulation of synaptic strength

NMDA receptor

• High frequency stimulation yields LTP by causing a large elevation in Ca2+
• Low frequency stimulation yields LTD by causing a smaller elevation of Ca2+

• 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)

They failed to learn the location of the escape platform

They found deficits in both LTP & memory

The change in a cell's membrane potential that makes it more negative inside (inhibits action potential)

• 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

• 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)

The animals showed a deficit in LTP & water maze performance

Enhanced learning ability in some tasks

• 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

There are no dedicated receptors for reward

Both the dorsal & ventral striatum

When you are not expecting a reward but get more (elicits an activation of response)

When you are expecting a reward but don't get it (induces a depression of response)

• 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

The error signal is transmitted by dopamine neurons & influences synaptic processes in dopamine target structures (such as striatum & orbitofrontalcortex)

Bcos choices are (crucially) based on predictions of outcomes

• Receive reward (reward unchanged) - Keep prediction unchanged
• Receive reward (reward changed) - Generate error signal, Update prediction, Use prediction for action & choice

• 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

A spike

• 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)

• 1. Basal metabolic rate (60%)
• 2. Physical activity (20-30%)
• 3. Thermic effect of food (10)%

Alters membrane potential & induces action potentials

• The typical stimulus for sweetness receptor is sugar (calories)
• The typical stimulus for bitterness receptor is alkaloid (poison)

• Conditioned taste aversion
• Conditioned taste preference

Fat & calorically rich foods

Via a specialised pathway in the mammalian peripheral & central nervous system (from the tongue to the cortex)

Where Pavlovian conditioning processes enable the individual to learn to like & dislike any food (depending on its post ingestional consequences)

The brain & the liver (both detect energy available & can convert energy from 1 form to another)

• Converts carbohydrates to fat (or from amino-acids to carbohydrates)
• Detects changes in fat availability & usage
• Communicates with the brain via the vagus nerve

• Detects blood glucose levels via neurons in the brainstem & hypothalamus
• Taste pathways project to hypothalamus

• Damage (eg, lesion) to the lateral hypothalamus is associated with disruption of feeding
• Stimulation of the lateral hypothalamus elicits feeding & drinking

Damage to the ventromedial hypothalamus is associated with disruption of feeding (Eat normal amount, just more frequently & finnicky)

The glucostatic hypothesis suggests that the availability of glucose plays a crucial role in eliciting hunger (ie, levels drop = hunger)

• 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

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)

• 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

• causes Reductions in palatability to same food after ingestion
• causes Reduced caloric intake in second course

• 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)

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)

• Levels of leptin in bloodstream correlate positively with the number of fat cells
• It signals the current level of adposity (fatness), to the brain

They have lower levels of leptin in blood & brain - this causes cells to release more NPY which increases meal size & decreases metabolism

They have higher levels of leptin in blood & brain - this causes cells to release less NPY which decreases meal size & increases metabolism

Bcos they increase neurotransmission in the mesolimbic dopamine pathway (via different actions for different drugs)

• 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

• 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

• 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

• 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

Reproductive behaviours & Attachment behaviours

• 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

Profound amnesia

An impairment of memory retrieval

The cortex