Biological basis of behaviour Flashcards

1
Q

What is exposure learning?

A
  • Most basic form of learning where learning occurs from being exposed to a stimulus
  • For example imprinting in Lorenz Geese (neural synaptic change) or learning bird songs
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2
Q

What is habituation and sensitisation?

A
  • Habituation= desensitisation to a stimulus due to continuous exposure (tires out synapse, reduces amount of neurotransmitter)
  • Sensitisation= Increased response to a stimulus due to continuous exposure (connection is facilitated by inter-neurons)
  • Aplysia (sea snail) is an example for both
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3
Q

What is the difference between conditioning and sensitisation?

A

-Sensitisation occurs at the same amount regardless if a CS & US are paired or occur randomly. Therefore, sensitisation is not causing conditioning

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4
Q

What is a suppression ratio and conditioned suppression?

A
  • Suppression ratio = Response during CS/ Responses during CS + Responses during pre-CS
  • For example rat shown light presses lever gets reward, rat now shown light and gets electric shock (lever is not present) this pre-CS conditioning. Rat now shown light with lever and shocks not given if lever pulled, this during CS condition.
  • Suppression ratio of 0.5< = no conditioning
  • Suppression ratio of 0 = strong conditioning
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5
Q

What is latent inhibition (retardation in learning) as a form of exposure learning?

A
  • Familiar stimulus’s take longer to acquire meaning than a new stimulus.
  • For example birds who have been exposed to beeping will take longer to learn that it signals the presence of water compared to birds who have never heard the beeping
  • This is also context specific, if exposed birds do task in a setting where beeping was not present latent inhibition no longer occurs
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6
Q

What is perceptual learning?

A
  • Process of learning through latent inhibition
  • Pre-exposure acts as form of training making it easier to discriminate between stimulus’s compared to those where the stimulus’s are new
  • Rats jumping through holes in stand srudy
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7
Q

What are the four basic effects associated with Pavlovian conditioning?

A
  • Stimulus generalisation
  • Extinction
  • Overshadowing
  • Blocking
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8
Q

What is stimulus generalisation?

A

-Same response from a stimulus slightly different to the original

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9
Q

What is Extinction?

A

-loss of the learned response

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10
Q

What is Overshadowing?

A

-Overshadowing is when two or more more stimuli are present, and one stimulus produces a stronger response than the often because it is more relevant, intense or salient

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11
Q

What is Blocking?

A
  • Pre-training can block learning
  • For example, rats who were exposed to noise =shock (condition 1) and then noise+light=shock (condition 2) showed little suppression to light on its own. Rats who only experienced condition (2) then shown light on its own showed greater suppression
  • This is because pre-training increases the associative strength of the stim used. The rat therefore expects the compound to be a result of the pre learnt stim (noise) and prevents the learning with the new paired stim (light). The control has equal associative strength for each stim as they are both novel
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12
Q

Name and describe three types of timing conditioning

A
  • Delayed condition, UCS shortly follows CS and easily establishes conditioning
  • Trace conditioning, UCS follows CS after certian amount of time, conditioning depends on the length of the trace
  • Simultaneous training , UCS and CS occur at same time, little conditioning occurs
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13
Q

What is the significance of Pavlovian conditioning?

A
  • Objective and underpins concept of association
  • Reliable with determinable rules
  • Practically useful (behaviour therapy)
  • May account for dysfunctional learning such as phobias
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14
Q

Describe human Pavlovian conditioning

A
  • Person has to be aware of conditioning for it to occur
  • Extinction can be consciously controlled, conditioning an electric response and then visibly turning off machine will remove response
  • However extinction cannot occur consciously if the response is fear relevant (
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15
Q

How does overshadowing explain contingencies

A

-Stimulus strength determines contingency, if response occurs without stimulus it gets overshadowed and reduces the strength of the association.

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16
Q

What is inhibitory conditioning?

A
  • That a stimulus paired with a response is paired with another stim omission of the response can be learnt
  • For example, light=shock and light+tone= no shock can be learned, tone is learnt to inhibit the action the response of light
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17
Q

What is excitatory conditioning?

A
  • That a stimulus is associated with a response

- For example, light= electric shock

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18
Q

What is the retardation test?

A

-See if inhibitor, after inhibitory learning slows the learning of said inhibitor now being an indicator of US (goes from inhibitory to excitatory)

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19
Q

What is the summation test?

A

-Testing to see if inhibitor from inhibitory learning can be transferred to a different stim that still gives same US

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20
Q

What is serial conditioning?

A

-That a sequence of more than one stim can be conditioned

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21
Q

What is second order conditioning?

A

-Conditioning of stim to another stim, that is conditioned with US, can elicit CR from the original stim despite never being paired with US.

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22
Q

Name three different conditioned response

A
  • Consummatory= A CR which is similar to the reaction elicited by US
  • Preparatory= A CR that shows preparation for the US
  • Compensatory= A CR that opposes the effects of US (drug tolerance, body compensates for effects of drugs)
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23
Q

How does US intensity effect conditioning?

A

-Stronger US increases strength of CR

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24
Q

How does CS intensity effect conditioning?

A

-Conditioning happens more rapidly if CS is strong, level of condition will ultimately be the same however

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25
Q

Outline how Rescorla Wagners explains compound conditioning?

A
  • Compound conditioning= conditioning with more than one stimuli
  • V-ALL determines the strength of the CR that can be expected in the presence of multiple stimuli (V-ALL= Va+Vb ect)
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26
Q

What is instrumental learning?

A

-Using reinforcement to establish a link between stimulus and response

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27
Q

Name and describe four types of instrumental conditioning

A
  • Positive reinforcement= positively reinforcing a behaviour (+ behaviour)
  • Punishment= punishing a behaviour (- behaviour)
  • Negative reinforcement= performing a behaviour to avoid a negative consequences (+ behaviour)
  • Omission training= taking away a reward as punishment for a behaviour (- behaviour)
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28
Q

What are schedules of reinforcement?

A
  • Not all responses a subject emits have to be reinforced to get a stbale conditioned response
  • A schedule of reinforcement decides which responses should be reinforced
  • Different schedules produce different highly predictable patterns of response each recognisable on a cumulative record
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29
Q

Describe 5 different schedules and there effects

A
  • Continuous reinforcement, CRF – reinforce every response
  • Fixed ratio, FR – reinforce every nth response. Pause after each reinforcement followed by fast responding
  • Variable ratio, VR – reinforce every nth response on average. Continuous fast responding
  • Fixed interval, FI – reinforce the first response after time t has elapsed since the last reinforcer. Pause after each reinforcement followed by gradually increasing response rate
  • Variable interval, VI – same as FI but with a variable time period. Continuous moderate response rate
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30
Q

What does ratio and interval schedules refer to to

A
  • Ratio= Number of responses reinforced with 1 = continuous

- Interval= Time interval of reinforcement

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31
Q

How is instrumental conditioning different to Pavlovian conditioning?

A

-Conditioned response learnt in guinea pigs with left head turn= reward when buzzer sounds. Turning right now gives reward and guinea pig eventually learns this (Omission based reinforcement). Therefore, not just Pavlovian conditioning as Guinea pig would always turn left

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32
Q

How do animals implement instrumental learning?

A
  • They have representations of the outcome of instrumental learning. If they know if the outcome is good/bad they will respond more/less
  • However, over training ,or creating a habit, maintained responses despite an adverse outcome. The value of the outcome became independent to the behaviour
  • Furthermore, learning based on representations requires knowledge about stimulus’s as shown in castaway dilemma studies (i.e sugar water is valued under thirst) incentive learning is needed to drive related actions based on available outcomes (choosing water vs food)
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33
Q

What is expectancy theory and reinforcer devaluation

A

-Behaviour is motivated by the expectancy of the reward and devaluing the reinforcer can reduce performance to the point where it is worse than a control who have only experienced the devalued reinforcer

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34
Q

What is simple discrimination?

A

-conditioning a discrimination between more than stim, for example two different coloured lights

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35
Q

Name three types of procedure for simple discrimination

A
  • Successive= present one stim and see how the animal responds
  • Simultaneous= present two stimuli and see which the animal approaches
  • Conditional= reinforce responses in the presence of different stimuli
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36
Q

Outline the six key phenomena of simple discrimination

A

-Generalisation= some response occurs to stimuli (1) that are similar but not the same as stim (2)
-Generalisation decrement= discrepancy between responding elicited by the original cue and the novel cue
-Peak shift= a phenomenon in stimulus generalization that occurs after discrimination training involving two stimuli along a common dimension (e.g., brightness). The peak response shifts
Transposition= The act of learning the relationship of stimuli rather than the stimuli itself. For example learning to choose 5cm circle over 3cm leads to an 8cm circle being picked over 5cm circle. 5cm circle has not been learnt but picking the larger circle has been learnt and thus tranposed onto picking the 8cm circle
-Transfer along a continuum= Teaching a easy discrimination can help an animal learn a more difficult one rather than just training it on the difficult one, known as TAC effect

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37
Q

Give an example of peak shift

A

-Train a rat to recognize the difference between a square and a rectangle. You present him a square and a rectangle with a switch in front of each. Every time the rat pushes the rectangle switch, you reward him with a piece of cheese. It won’t take long before the rat chooses the rectangle in every single trial.Now give the rat a choice between the original rectangle and a longer, skinnier rectangle. The rat will strongly prefer the longer, skinnier rectangle. The rat has been trained to do more than pick out one particular rectangle – it has been trained to be rewarded by the concept of “rectangularness” itself. So when it gets something that’s REALLY rectangular – a very long and skinny rectangle – it strongly prefers it. This is the peak shift effect – it occurs when the strength of a particular response is directly proportional to the magnitude of a somewhat simple perceptual cue. Exaggerate that cue, and you can exaggerate the response it elicits.

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38
Q

What is absolute vs relative discrimination?

A

-The issue of is the effective stimulus (stimulus that creates a response) absolute , black vs white, or relative, darker vs lighter.

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39
Q

What is continuity vs non-continuity theory?

A

-Is learning a gradual continuous process or a instant all or nothing process

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40
Q

Give an example of a complex discrimination

A

-Defining stimulus’s by category or artificial concepts (pigeons identifying “people” as being in or absent from photos)

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41
Q

Outline the theory behind category discrimination

A
  • Multiple feature model describes how objects are broken down in multiple features and these are focused on when trying to classify object, each feature has its own associative strength (humans will not do this and will look at whole picture)
  • Shown through matching task of same vs different
  • Struggle with more abstract categories and are highly focused around sensory perception
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42
Q

What is negative patterning/ configural theory?

A

-That while two stims with strong associative strength can increase lead to an excititory response the combination of them can be taught to be an inhibitor, thus the combined associative strength does not have to further increase an excititory response and they instead form a CONFIGURAL CUE which in itself becomes a stimulus (tone vs light vs tone+light)

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43
Q

What is acquired distinctiveness and acquired equivalence?

A
  • Distinctiveness= stims appear more different (different outcomes when conditioning)
  • Equivalent= Stims appear more similar and are harder to discriminate between (same outcome after conditioning)
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44
Q

What does learning in a single-layer network entail?

A
  • Change in the associative strength between a an input and an output (how much the CS effects the output in the absence of the US, Strong connection means a response is generated when US is not present)
  • Cannot explain negative conditioning
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45
Q

What does learning in a multi-layer network entail?

A

-Similar to single unit but with another layer (another layer between input and output known as the hidden unit)

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46
Q

What does learning in exemplar based networks entail?

A

-Similar to multi layer network but hidden unit has a more specific role (know becomes a configural unit) and is only activated by a certain pattern which then allows an association to be learnt

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47
Q

What is metacognition?

A

-Capacity to be aware of and report the state of our mental processes

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48
Q

What is the exemplar effect in discrimination learning?

A

-Individual training stimuli are learnt by subject and this is partially responsible for success (specifics on stim remembered rather than just a category) also explain why generate better performances against novel stim as they provide base for this comparison

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49
Q

What is prototype theory?

A
  • Exposure to members of the same category results in the formation of a prototype or average
  • Exemplars activate the prototype and elicit a response
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50
Q

How are categories and concepts different

A

-If a concept is learnt a subject should be able to identify stims as part of the concept despite sharing no psychical similarities

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51
Q

What are second order relationships?

A

-Ability to match the relationship between two stimulus’s to another set of stimulus’s (Two same colour = other pair that are same colour/ two different colour = other pair that are different colours)

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52
Q

What is analogical reasoning?

A

-Judging the equivalence of relationship to two other stimuli (dog = puppy, cow = ?, answer would be calf)

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53
Q

What is proactive and retroactive enforcement?

A
  • Pro= interference from old info

- Retro= interference from new info

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54
Q

How has proactive and retroactive interference been observed in animals as well as decay?

A
  • Delayed matching to sample (DMTS) experiments

- Radial arm mazes (more arms lead to more mistakes and also evidence decay)

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55
Q

How does retro/pro interference explain memory coding?

A
  • Retro= remembering arm visited
  • Pro= remembering arms you have yet to visit
  • Delayed symbolic matching to sample shows prospective code use as more mistakes are made when display symbols appear more similar (more confusion)
  • Radial arm mazes have shown though that animals switch between retrospective and prospective coding
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56
Q

-How have animal studies evidenced long term memory and reactivation

A
  • Shuttle box experiments show that ECS (electric shock) avoidance is higher after a longer time interval, ECS therefore interferes with short but not long term memory
  • Shuttle box avoidance was increased if rat (after 3 day rest period) was held in box for a short amount of time (compared to put straight in). Rats held for too long showed extinction and not reactivation
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57
Q

What is a savings measure?

A

-Faster learning of a stim that has already been learnt

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58
Q

What is dishabituation?

A

-The use of a distractor to prevent the habituation of a stimulus (S1 -> D -> S2 ,same as S1, prevents habituation as it disrupts memory of S1)

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59
Q

Explain two short term memory theories

A

Decay theory= forgetting occurs because, when an event is presented the information gradually and spontaneously decays, strength of trace not influenced by other short term traces (unlimited capacity), initial trace strength determined by duration and intensity of stim, cannot explain dishabituation
-Limited capacity theory= psychical restriction on the capacity of information that retained at any given time, therefore some events displace others causing forgetting, surprisingness a key factor in determining what traces are displaced, can not explain why only certian stims effect DMTS experiments (illumination only factor that effects animal performance)

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60
Q

What are serial position effects?

A

-The observation that the first (primary) items and last (recency) items are recalled better. Primary have more time to be rehearsed and recency items are still most prominent in memory store

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61
Q

What is metamemory?

A
  • The ability to remeber things and be able to comment on the strength of the memory (“it was on the tip of my tongue”)
  • Has been observed in animals to an extent in picture matching with rheseus monkeys
62
Q

What is active and inactive memory?

A
  • Active= info processed and encoded to be placed in inactive memory
  • Inactive= store of information to be retrieved and brought into active memory
63
Q

What are the two main schools of learning

A
  • Gradual= quantitative, the difference between humans and animals
  • Sharp= qualitative, instant learning
64
Q

What is insight learning?

A
  • Understanding of relationships not trial and error

- Not well evidenced in animals

65
Q

How has spatial learning been examined in animals?

A
  • Detour tests= idea of moving away from food to successfully obtain it (mazes)
  • Difficult to separate intelligence or instrumental learning over Pavlovian
66
Q

Explain tool use in relation to animal intelligence

A
  • Ability to use tools
  • Tool use can be taught but has not been show to be through insight and skills learnt are not transferable
  • Crows (1 crow) has shown tool construction
67
Q

Describe evidence of animals and rule use

A
  • Serial reversal learning tasks (learn discrim then reverse it) have shown consistent rule learning
  • Learning sets which contain consistently varying stim have shown one trial rule learning
  • However, some suggestion rules are not being used but is just the effects of recency and a reinforcer
68
Q

What is transitive inference and has it been evidenced in animals?

A
  • Idea of if A>B and B>C is A bigger than C (yes)
  • Has been observed but critiqued for being as a result of an associative assumption (symbolic distance effect). If A is always rewarded and B is linked to A it is assumed to be linked to a reward (think spectrum of cylinders linked A-E).
69
Q

What is analogical reasoning and has it been evidenced in animals?

A
  • Idea of puppy=dog so kitten=? (cat)

- No evidence except for Sarah the chimp

70
Q

What is gradient delay in instrumental learning?

A

-The response of animal is correlated which the speed in which they receive a reinforcer

71
Q

What is the molar theory of reinforcement?

A
  • The assumption that animals will respond at a equivalent rate to in which the reward can be delivered (increasing reward availability would increase responding) however, this also depends on the extent the response leads to reward (decreased response if food is delivered regardless of a response being made)
  • However, even if the mean amount of reward received (3 pellets in a min ect) is the same a rat will increase responses made, which contradicts the theory
72
Q

What is molecular theory of reinforcement?

A

-Alternative explanation to molar theory and focuses on the contiguity between response and reinforcer (the strength of association) known as the molecular analysis of instrumental learning

73
Q

What is Premacks principle?

A

-Argued that reinforcers were not stimuli but opportunities to engage in activity. An activity will reinforce another if that activity is more probable than the other activity (running in a wheel could reinforce drinking but only when the animal was not thirsty)

74
Q

What does equilibrium theory of behaviour refer too?

A
  • Outlines the shortcomings of Premacks principle (should not increase drinking of sweet liquid to access weak solution but did), animals will engage in a variety of activities at a certain rate and allocate different amounts of time to each, even ones not as desirable, this is known as the bliss point
  • Preventing an animal from achieving its bliss point will encourage it to restore equilibrium and will be driven to increase time allocation to certain activities to increase others (rats drinking sweet and normal water 10:1 ratio study)
  • Animals will comprise to get as close to bliss point as possible
75
Q

What is a conditioned reinforcer?

A
  • Pairing a stim with a reinforcer (which reinforces a reward, tone= food, lever press=tone which = food, lever becomes conditioned reinforcer)
  • These are often short lived but using token reinforces can sustain relationship (key presses = 1 token, 50 tokens =food, tokens act as conditioned reinforcers)
76
Q

What does distal and proximal refer too?

A
  • Distal= long range cues

- Proximal= short range cues

77
Q

What does egocentric and allocentric frames of reference refer too?

A
  • Egocentric= relative to individual

- Allocentric= (relative to the environment)

78
Q

What do beacons and landmarks refer too?

A
  • Beacons= Pavlovian approach, conditioned attractive stimulus
  • Landmarks= neutral stimulus used as a reference, van be single or multiple landmarks (Bees also take a snapshot of the landmark, if the landmark is increased in size they search a larger area and an area closer to the landmark if it is smaller)
79
Q

How do T-Mazes show spatial learning?

A
  • Enclosed T-Mazes show trail and error instrumental learning
  • Open mazes can show landmark or beacon or learning
80
Q

Outline animal study evidence for the use of landmarks in spatial learning?

A
  • Rotation of landmarks causes rats to follow their rotation
  • Transposition, where landmarks being moved effects performance, supports idea of hippo campus producing a visual map rather than using them as beacons to mark specific locations/ lesions to hippo-campus reduce performance (Morris water maze)
  • However, blocking worsens performance in MWM studies which contradicts the idea of visual maze (should increase performance)
  • Additionally rats released from novel starting point (with platform in same place as training) all started swimming in wrong direction before adjusting, something that would happen with a cognitive map (spatial learning is based on individual landmarks and not a big picture)
  • However, other studies have shown larger hippo-campus’s role in spatial learning (Maquire taxi study)
81
Q

Outline non-landmark based ways of navigation

A
  • Pheromone trail, magnetic field, sun position
  • Dead reckoning/ path integration= navigation by keeping track of ones position by keeping track of distance travelled and changes of direction (ants do not know where they unless they travelled there themselves)
82
Q

What is evidence is there for the use of geometric relation in spatial navigation?

A

-Has been observed in geometric relations where the target is halfway (only for two landmarks) but has not been well evidenced with more complex scenarios

83
Q

What is a geometric module?

A
  • A part of the brain dedicated to encoding the shape of an environment and where goals can be found in the shape of the environment (has been observed in many animals)
84
Q

-What are place cells

A
  • Hippo-campus place cells seen to be cells activated when learning spatial learning tasks, such as maze navigation
  • The activation of these cells has been seen to depend on the number of landmarks available
  • Activation also seen to depend on more than immediate cues, for example only activating if maze is in specific room
  • Landmarks only have to be shown briefly for activation and a correct response to be made
85
Q

How do animals use spatial navigation for extended travel?

A
  • Magnetic fields
  • Air pressure/ infrasound (generated by impact of air currents on environment, storms ect)
  • Polarized and ultraviolet light (allows for location of sun even in cloud cover)
86
Q

How do animals undergoing homing?

A
  • Use of landmarks (not essential)
  • Retracing outward journey
  • Map and compass hypothesis (possession of knowledge of their environment and the use of the sun, using the position and internal clock of the animal, to direct etc) clock-shift experiments have evidenced compass aspect (changing internal clock impacts navigation) but map aspect is poorly evidenced (pigeons fly home from unfamiliar locations)
  • Olfaction (not well understood but removing it affects navigation)
87
Q

What are the mechanisms of social learning and an example of each?

A
  • Observational conditioning (conditioning of phobias)
  • Stimulus of local enhancement (blue tits drawing attention to drinking milk which results in the behaviour, is not imitation)
  • Imitation (true imitation not well evidenced)
  • Tool use (monkeys using anvils to crack nuts)
  • Teaching (not well evidenced, closest is meerkats but is more help that allows young to educate themselves rather than explicit explanations)
88
Q

What is communication?

A
  • Intention to send message to the receiver with a reliable effect
89
Q

What is referential communication?

A

-Communication that gives varied information about external matters to the sender and receiver (alarm call etc)

90
Q

What is tactical deception?

A
  • Dishonest signals that can have intent which demonstrates the possibility of theory of mind
  • 3 levels of deceptive acts: 0= unintentional, 1= goal directed but is achieved when receiver is deceived (learnt, not understood), 3= “mindreading” understanding of attribution of intentions to others intentions (understanding of what others can and cannot see)
91
Q

Outline theory of mind in animals

A
  • Can learn Sally/Anne problems but do not understand them (no transfer)
  • Mirror test some evidence of self recognition but has not been well replicated
  • Overall little evidence for ToM
92
Q

What is the cephalisation coefficient?

A
  • The ratio of brain szie to body mass
  • Some evidence that tasks such as learning sets are correlated with coefficient. However, such tests are suited to animals such as monkeys that perform well (this is referred to as a contextual cue)
93
Q

What are some of the problems with measuring animal intelligence?

A
  • Not a one task fits all, some tasks more suited to different species
  • Hard to compare the findings from individual tasks
  • Need a battery of tests
94
Q

Outline the issues with contextual variables

A
  • Animals suited to different tasks, for example dolphins have difficulty learning learning sets with visual stims but not auditory ones
  • Animals with similar sensory and effector capabilities may only be able to be compared
95
Q

What is Macphail’s null hypothesis?

A
  • No cognitive differences between non-human animals (non-human and vertebrates)
  • Differences observed are a result of contextual cues
  • Some evidence in the shape that most animals learn simple forms of learning (classic and operant) at the same rate in the same way
96
Q

What is the comparability problem with animals intelligence?

A
  • Difficult to isolate all factors and scale accordingly all factors that are not learning: perceptual difficulty, mechanical difficulty of response, motivation, incentive value of reward
  • Leads to idea IQ can only be tested with comparable species
97
Q

What evidence is there against Macphail’s null hypothesis?

A
  • Different bird species have shown different levels of learning (pigeons vs corvids in learning sets) however, issues of receny effect
  • Speech trained monkeys vs Non-speech trained monkeys, however there are tasks that both do equally well on so suggests difference in intelligence
98
Q

Describe the nature of behavioural neuroscience

A
  • Focus on reductionism and generalisation of behaviour

- Uses laboratory models

99
Q

-Outline brief history of behavioural neuroscience

A
  • Balloonist theory (Descartes - 1590’s) that muscles moved by contracting when inflated by air or fluid (reactions)
  • Neural conductance (Galvani 1793) that natural electric currents generated in nerves cause activation of muscular cells
  • Neuron theory (Golgi 1843) nervous system made up of lots of individual cells (neurons) that form a network
  • Law of specific law energies (Muller 1835) perception is defined by the pathway of the nerves not the stimulus itself. For example pressing on the eye elicits flashes of light as the neurons in the retina signal the occipital lobe despite the sensory input being mechanical the experience is visual
  • Brain lesion studies (Flourens 1815) localized lesions of the brain in living rabbits and pigeons and carefully observing their effects on motricity, sensibility and behavior. Intention was to investigate localisationism, i.e., whether different parts of the brain had different functions
  • Cognitive neuroscience (Broca 1850) Broca’s area
  • Somatotopic organisation, arrangement of the somatosensory cortex. when a specific part of the body is associated with a distinct location in the central nervous system
100
Q

What is alien hand syndrome and describe the biology behind it?

A
  • Limbs performing meaningful acts without intention from the patient
  • Often caused by strokes (damage) to the anterior corpus callosum, this disconnects premotor and primary motor areas (disconnects planning and action)
  • Descending pathways from premotor and primary motor areas allow for other areas of transmission between the hemispheres allowing for general motor control to stay intact (through brainstem, midbrain, pons, cerebellum and back out to medulla into the spine)
  • Motor cortex preserved as descending motor pathway is somatotopically organised so different areas respond to different spinal vertebrae
101
Q

What is bioavailability and the effecting factors?

A
  • Availability of drug to a synapse
  • Route of administration
  • Dose
  • Rate
  • Absorption (transfer from site of administration into the bloodstream)
  • Elimination (irreversible loss of drug)
  • Kinetics (availability of drug over time)
102
Q

What is the blood brain barrier?

A
  • Specialised skin cells that surround the brain and prevents pathogens from entering it as well as other hormones and compounds which require active transporters. However, pharmaceuticals can passively diffuse across this barrier
  • Only water soluble molecules can pass through and the rate at which the drug reaches the active sites depends on its lipid solubility. For example Heroin is more lipid soluble than morphine so effects of it are more rapid creating more of a ‘rush’ which explain why it is preferred amongst addicts
103
Q

Describe an average dose-response curve for a drug

A

-S-shaped, increase with dosage but taper off due to the upper limit of neural firing rates

104
Q

What is the margin of safety or therapeutic index?

A

-Is the difference between the dose that produces the 50% maximum therapeutic effect, and the dose that produces the 50% adverse effect, expressed as a ratio. (lower ratio means greater chance of negative effects in the instance of an overdose/ toxic dose = 500mg and therapeutic dose = 100mg, therapuetic ratio = 5.0 )

105
Q

How do psychoactive drugs act on receptors?

A
  • Psychoactive drugs act on receptors on neurons, which open ion channels, which change the electrical potential of the membrane and so change psychological experience
  • Antagonist= prevents storage of NT in vesicles/ inhibits release of NT/ Blocks postsynaptic receptors/ inhibits synthesis of NT by deactivating synthetic enzyme/Stimulates auto receptors which prevents synthesis of NT
  • Agonist= Stimulates release of NT in vesicles/ Stimulates postsynaptic receptors (opens ion channels)/ Blocks auto receptors increases synthesis of NT/ Blocks reuptake of NT/ Inactivates antagonist
106
Q

Name the different types of agonist and antagonist drugs

A
  • Agonist (increase activity)
  • Partial agonist (partially increase activity)
  • Antagonist (neutral, prevent increased activity)
  • Inverse antagonist (reduce activity)
  • Indirect agonist/ antagonists have same effect as their direct counterpart but do not compete with target molecule (attach to other areas and effect ion channel)
107
Q

Describe Acetylcholine

A
  • Acetylcholine is a NT, produced CNS, found in the ganglia of the Automatic NS and target organs of the Somatic NS, in the pedunculopontine nucleus and the nucleus Basalis of Maynert, that causes muscles to contract, activates pain responses and regulates endocrine and REM sleep functions.
  • Increases the signal to noise ratio in the firing rate to specific stimulus linked to neuron (reduces noise)
  • Linked to Parkinsons
108
Q

Describe Dopamine

A
  • Involved in the nigostriatal system, mesolimbic system and meocortical system
  • Shown to be desired through self administration studies in rats and can be used to influence behaviour (ratbots)
  • Degeneration of dopaminergic neurons in the substantia nigra with caudate nucleus causes Parkinson’s
109
Q

Describe Norepinephrine (noradrenaline)

A
  • Located in the locus coeruleus but is projected across whole brain
  • Plays role two roles in attention; alertness and attention
110
Q

Describe serotonin

A
  • Cell bodies originate in Raphe nuclei in brain stem and project to spine, cerebellum, sub-cortex and cortex
  • Associated with depression and mood regulation, antidepressants often increase serotonin
111
Q

Describe glutamate

A
  • Used by 50% of brain cells and is responsible for changing synaptic weight (learning)
  • AMPA and Kainate= fast excitatory transmission
  • NMDA= synaptic weight change by modifying the number of AMPA receptors
112
Q

Describe GABA

A
  • Plays a role in inhibition, capping the upper limit of cell firing rates (+ = increased inhibition and prevents over activation)
  • Epilepsy is failure of GABA to constrain excitatory loops, meds often aim to increase GABA
113
Q

Describe Endorphins (opiates)

A
  • Endorphins inhibit transmission of pain signals in peripheral nervous system, and the central nervous system
  • Endorphins released by the pituitary form part of the fight or flight stress response, and act on presynaptic opioid autoreceptors on pain signalling neurons.
  • Endorphins microinjected into the nucleus accumbens (terminal of the mesolimbic dopamine pathway) increase hedonic facial reactions to sweet flavour, and decrease aversive reactions to bitter flavour (in rats) suggesting a role in subjective euphoria.
114
Q

Why do drugs vary in effectiveness?

A
  • Target different active sites, for example morphine and aspirin both have analgesic effects but morphine suppresses activity of neurons in brain/ spine while aspirin reduces production of chemical involved in transmitting info from damaged tissue to pain sensitive neurons (morphine more effective at same does as aspirin)
  • Affinity= equals readiness to bind with molecules, low affinity means high doses needed and vice versa. The affinity of drug for therapeutic and toxic effects also need to be considered (ideally high affinity for thera sites and low affinity for toxic sites)
115
Q

How does withdrawal symptoms occur

A

-Body compensating for effects of a drug (decreases affinity of receptors/ increases steps in coupling process making it less effective) when it is not present causing the opposite effect of the drug

116
Q

Describe early sexual development

A
  • Primary sexual characteristics formed (internal/external genitalia/gonads = testes or ovaries)
  • SRY gene causes male internal genitalia, absence of it causes female internal genitalia
  • Testes from male genitalia produce testosterone (an androgen) have organisational effect promoting masculinisation and defeminisation (sex hormones also effect activational effects later in life, as they decide what sex organs develop, such as ejaculation and ovulation)
  • External and internal genitalia can be non-linear supporting idea of non-binary genderisation
117
Q

How does puberty occur?

A
  • Hypothalamus arcuate nucleus releases kisspeptin which then activates the anterior hypothalamus to release GnRH
  • GnRH causes FSH & LH to be released in both sexes, in males it causes the testes to release testosterone and in females the ovaries to release estradiol. This drives sexual maturation
118
Q

Describe an instance of hormonal control of behaviour

A

-Menstrual cycle, estradiol and progesterone signal fertile phase of the cycle. This promotes sexual behaviour in females

119
Q

Describe an example of sexual behaviour and a study of hormonal control over it

A
  • rat studies
  • Proceptivity (female approaches)
  • Attractiveness (male engagement/mounting)
  • Receptivity (female willingness)
  • Lordos (penetration)
  • Gonadectomised rats (rats with removed genitalia) with no post birth hormones (m= testosterone/ f= estradiol+progesterone) show no genderisation and no sexual behaviour, those given respective hormone post birth did show genderisation and exhibit sexual behaviour. Therefore, there is a critical period for hormones to effect sexual behaviour
120
Q

Outline human sexual behaviour studies

A
  • Slight preference for human females during fertility period (photos study)
  • Counter evidence from this is that study has shown males have a consistent level of sexual initiation and females increase during ovulation and decrease afterwards. Male initiation would increase if women were seen as more attractive during fertility
  • Women during fertility are more likely to prefer masculine/ dominant traits/ genetic quality (symmetry which shows lack of virus during utera) when looking for “one off” sexual partners
  • Males who are given GnRH anatagonist have reduced sex drive but can be restored if given testosterone
121
Q

How can sexual orientation be determined?

A
  • The genderisation of the brain in accordance to the sex of the person
  • For example male heterosexual = brain masculinized and defeminized, male homosexual = neither masculinized or demfeminized
  • Some evidence from digit ratios (longer ring finger = masculine, longer index finger = feminine, het f & hom m)
122
Q

How can hormones influence sexual orientation?

A
  • Abnormal androgen (CAH) can cause ambiguous genitalia and lead to increased chance of homosexuality in females (33% compared to baseline 2%)
  • Androgen insensitivity syndrome= androgen insensitivity means testosterone does not cause masculinization and defeminization and males develop as females (complete or partial). Have external female genitalia with testes but no uterus or Fallopian tubes. Typically favour male partners
  • Some heritability evidence where identical twins have 50% chance of being homosexual if one is compared to 20% in non-identical twins
123
Q

Describe the neural basis of female and male sexual behaviour

A

-MPA (animals) and INAH3 (humans) in hypothalamus larger in males, homosexual men have been observed to have smaller INAH3 (like females) possibly evidencing lack of brain masculinisation

124
Q

What are the three categories of emotion?

A
  • Behavioural/somantic= voluntary muscular (species specific)
  • Autonomic= neural feed from brain
  • Hormonal= pituitary gland
125
Q

What are the three categories of emotion?

A
  • Behavioural/somantic= voluntary muscular (species specific)
  • Autonomic= neural feed from brain (increased heart rate etc)
  • Hormonal= pituitary gland (secretion of adrenaline etc)
126
Q

What are the somatic and autonomic nervous systems?

A
  • Somatic= sensory/voluntary muscle movement

- Autonomic= unconscious internal control over organs (has sympathetic and parasympathetic branches)

127
Q

Describe autonomic and somatic emotion

A
  • Somatic= voluntary muscular response such as bearing teeth
  • Autonomic= secretion of hormones to create a , often involuntary, response (para/symp branches can be separated by anatomical arrangement, symp= toracic and lumber spinal cord, para= cranial nerves and sacral spinal cord)
128
Q

What are cranial nerves?

A

-Emerge directly from brain stem and be sensory, motor or mixed

129
Q

How is hormonal emotion controlled

A

-Hypothalamus (controls both somatic & autonomic systems) controls pituitary gland which releases hormones into the blood stream via the circle of Willis. This acts on endocrine glands which themselves release hormones which effect organs

130
Q

What is the Amygdala’s role in emotion look to book for extras nearer exam

A
  • Receives all sensory input from cortex, thalamus and hippocampus
  • Detects emotionally salient stimuli and thus decides what we should emotionally respond too
  • Salinet stimuli is translated into somatic emotion via striatum, increases sensory and motor signal flow via thalamus, increased arousal via brain stem, autonomic activity via hypothalamus
  • Central nucleus of the amygdala projects to a wide range of nuclei which produce specific aspects of emotional response such as trigeminal, facial motor nuclei which creates facial expression of fear (lesions to amygdala effect somatic, autonomic and hormonal responses)
  • Mediates fear learning to neutral stimulus’s (such as “freezing”)
131
Q

Explain the relation between the amygdala and OFC

A
  • Amygdala activates during fear learning, OFC activates during extinction learning
  • OFC encodes expected outcome to be compared with actual outcome to generate prediction error signal which drives teaching signals to modify associative learning in the amygdala
132
Q

How is serotonin involved with emotion?

A
  • Low amounts increase impulsivity and aggression in humans (often observed in criminals who commit psychical crimes)
  • Also evidenced in animals where low serotonin has been observed to increase death due to partaking in more risky/aggressive behaviours
  • expected vs actual outcome discrimination is calculated by dopamine and serotonin systems to modify learning, low serotonin weakness this learning therefore, aggressive behaviour continues as individuals fail to learn to modify behaviour when it does not pay off (similar to effects of lesions in OFC)
133
Q

Outline the laterality of emotions

A

-Brain damage studies show right hemisphere (right somatosensory cortex) is more important in recognising and producing emotion (has mirror neurons which helps create and respond to the concept of an emotion)

134
Q

Outline support for mirror neuron hypothesis

A
  • Automatic mimicry of facial expressions of infants (can not see their own face but can copy parents facial expressions) neurons for recognition must be connected to expression also
  • Chimerical faces (mirrored image of one side of a face) show more emotion when image comprises of left side of face (linked to right hemisphere)
135
Q

What are the four primary symptoms of Parkinson’s disease and its demographics

A
  • Resting tremor
  • Muscular rigidity (stiffness)
  • Bradykinesia (slowness of movement)
  • Postural instability or impaired balance
  • 0.3% of pop affected and increases with age (1% at 60, 4% at 80)
  • 95% of cases are sporadic and thus suggest disorder isn’t solely genetic (some genes are related however) other causes are considered to be environmental toxins, metabolism and infection
136
Q

What causes Parkinson’s disease?

A
  • Caused by degeneration of nigrostriatal DA pathway (projects to striatum and basal ganglia nuclei)
  • Parkinson’s symptoms only show when 90% of neurons of this area have been damaged, making it difficult to treat/reverse the disorder
  • Surviving neurons express Lewy bodies which clog/ cause damage to other brain areas
  • Mutation of chromosome 6 causes production of defective Parkin which causes a loss of function as it allows high levels of defective proteins to build up and cause damage to celss (Parkin normally plays a role in ferrying these proteins to be destroyed)
  • Synthetic heroin where MPPP is synthesised with MPTP can cause PD. MPTP disrupts mitochondrial metabolism causing build up of free radicals and nigrostriatal apoptosis
137
Q

What is a Lewy Body

A
  • Dense protein core with radiating fibres made of alpha-synuclein protein bound to uniquitin
  • Chromosome 4 faulty genes create misfolded a-synuclein and produce a protein that is toxic to cells which forms the core of a Lewy body
  • Develop in substantia nigra, brain stem and basal forebrain and the cortex and cause particular damage to nigostrial cells
138
Q

How is Parkinson’s treated?

A
  • Remaining DA neurons (the 10-20%) are targeted to increase dopamine production. LDOPA (which can cross blood brain barrier as dopamine cannot) is administered but is not region specific.
  • Continued use increases overall dopamine levels resulting in dyskensia (involuntary movements) After 5 years of use 50% prevelance
  • LDOPA is often last resort
  • MOA-B inhibitors block dopamine breakdown and can help delay need for LDOPA in early disease but is less effective and also has side effects
139
Q

Outline how the treatments for Parkinson’s are administered

A

Standard treatment: Delay L-dopa for as long as possible

  • First line: MAO-B inhibitors (maximise what dopamine remains).
  • Then: Dopamine agonists (e.g. apomorphine) but floods system creating side effects: hallucinations delusions and compulsive behaviour.
  • Introduce L-dopa and disease worsens, and ↑ dose as needed.
  • Combine the 3 therapies.
  • DBS (deep brain stimulation) and continuation of other meds
140
Q

Describe Foetual transplants as a treatment of Parkinson’s

A
  • Targets cause not symptoms
  • Transplant (from fetal tissue) of substantial nigra cells give rise to dopamine producing cells which form connections
  • Effects short lived
  • Common side effect of dystonias (prolonged twisting contractions) due to excessive dopamine and aberrant connectivity
141
Q

Describe the role of DPS in Parkison’s treatment

A
  • Loss of nigrostriatal pathway decreases cortical activation and destabilises direct and indirect pathways blurring wanted and unwanted movements
  • DPS acts as pacemaker to steady firing in indirect pathway with stimulation of STN or steady stimulation of thalamus (overall controller of cortex)
142
Q

Outline motor circuitry in Parkinson’s

A
  • Cortex -> basal ganglia -> supplementary/primary motor cortex -> motor behaviour by projections to the spine (Plans arise in cortex and are moderated by basal ganglia before nuclei)
  • Two pathways= direct (activated cortex) activates wanted movement / indirect (inhibits cortex) inhibits unwanted movement
  • Direct pathway= striatum inhibits GPint -> inhibits thalamus -> reduces cortex excitation. This is the default state (inhibition of movement). When cortical cells excite striatal cells they inhibit GPint allowing for excitation of cortex
  • Indirect pathway= striatul cells inhibit GPext -> inhibits subthalamic nucleus (STN) -> excites Gpint -> Gpint inhibits thalamus -> reduces cortex excitation (default state). Cortical excitation causes striatal cells to indirectly inhibit thalamus and motor cortex
  • Nigrostriatal pathway excites direct pathway and inhibits indirect pathway causing dual effect of excitation in cortex
143
Q

How is ADHD characterised?

A
  • 6/9 inattention symptoms (cannot attend details, does not listen, fails to finish, loses things, forgetful, easily distracted) and 6/9 hyperactivity/impulsivity symptoms (blurting out, talk excessively, motor excess, fidgets, runs about, cannot wait for turn, interrupts)
  • Affects 8% of kids and is twice as common in boys
  • ADHD is co morbid with a range of other disorders which makes treatment more difficult
  • Strongly genetic with high concordance rates but does have some environmental causes (brain injury/ birth complications)
144
Q

What is the evolutionary theory of ADHD?

A

-Functional impassivity= risk taking etc may of been evolutionary beneficial

145
Q

How is ADHD medicated?

A
  • Use of Ritalin which blocks dopamine and noradrenaline reuptake transporter increasing dopamine in the synaptic cleft
  • This increase in dopamine is similar to the effects of cocaine
146
Q

What are the risk factors associated with ADHD treatment?

A
  • As Ritalin has similar effect to some recreational drugs it was suggested that does the use of Ritalin increase the rate of addiction in late life
  • Ritalin actually protects against addiction as it normalises activity in cortical regions and has a u shape effect on them (moderate dose is optimal, more or less impairs or does not facilitate function)
147
Q

What is ADHD’s relationship with addiction?

A

-High risk children with addict parents had higher dysregulation (ADHD + cognitive impairment) which encouraged early drug use resulting in adult addiction risk (cycle of addiction)

148
Q

How can addiction be explained through conditioning?

A
  • Positive reinforcement= Want rewards of the drug (evidenced by self administration in rats/ ratbots, medial fore-brain bundle is the hotspot where stimulation )
  • Negative reinforcement= Avoiding withdraw and consequences of target of drugs as well as self medication for mental disorders (pain and pain killers etc)
149
Q

How does withdrawal occur?

A
  • Creates opposite effect to the drugs and desensitises receptors, increased tolerance increases dosage and enhances withdrawal
  • Acute abstinence phase is immediate withdrawal
  • Protective defiant phase of withdrawal (days/weeks after) is where most relapse occurs
  • Withdrawal worse with longer use as chronic activation of cells breaches threshold leading to cell death, less recover with longer addiction
150
Q

Describe the insula cortex’s rule in addiction

A
  • Insula cortex is part of the primary sensory cortex and integrates emotional information from the amygdala as well as decision information from PFC (overall carries info about adverse internal and emotional states that then promote drug use)
  • Insula damage studies have shown ease increased ease of quitting (Blocks negative emotional states which prevents triggering of desire to use drug)
  • Involved in the motivation to use drugs