Midterm 3: Mar 14th, 16th,

What are some ways you can immediately increase your DOP?

1. check your phone
2. read a story
3. watch an advertisement
4. visualise something good happening

What are the 2 different ways that DOP is released?

1. fast error signal: short, large spike in the amount of DOP in a small region of the brain
2. slow motivational signal: all the time creating a constant, low concentration soup of DOP sitting around in many regions of your brain

When the media says “dopamine”, what kind of DOP release is it talking about? Is this the only place?

* DOP is released in many places in the brain (e.g., even in the eyeball!)
* media means:
* DOP releasing neurons in small groups in the middle of the brain
* also mean where those neurons release their DOP, big brain region tucked up under the cortex, the striatum

Describe how the short error signal of DOP works using 3 situations where you:

* expect something bad and get something good
* expect good and get good
* expect good and get nothing

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e.g., you wander into a strangers house and instead of being thrown out you get a biscuit, large spike of DOP would occur that signalled the error between your prediction and what you recieved

* prediction was in your favour, a positive error

e.g.., show up to a house to get a biscuit and you get it, no DOP release, no error

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e.g., show up to a house to get a biscuit but receive nothing, DOP neurons breifly pause their activity, signalling the error between what you predicted (a biscuit) and what you recieved (nothing)

* prediction not in your favour, negative error

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Fast DOP signals the error between what you predicted and what you got. That error can be positive, negative, or zero.

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Does DOP signal reward?

no! they fire when you get something good, fire when you get something unexpected, and sulk when you do not get something you expected

* rewards make you happy, DOP does not

Describe how the low and slow DOP works

signals how motivated you are to work

* high concentration of this soup the harder rats work for their food
* low concentration of the DOP soup and rats will not work

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DOP is for wanting, for signaling to your neurons to do this action, not happiness

Contrast our levels of understanding of fast and slow DOP release

fast: well known, solid theories

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slow: we have some ideas, but a broadly agreed upon theory is a long ways off

Discuss how studies related to Parkinson’s disease can cause problems for our fast sigalling DOP theory

there are some DOP neurons that use their fast firing to affect movement

* this could help explain why the loss of DOP neurons in Parkinson’s disease casues movement problems, but does not fit in with an error signal
* it seems that the error signal is carried by a separate set of DOP neurons

What did Humphries mean when he said “there is no getting away from the fact that there is nothing special about DOP”?

* it is on a list of tens, likely hundreds of different chemicals that the brain uses to convey information
* there is also a huge number that change that communication, making it easier or harder, slower or faster
* e.g., in a lobster’s stomach, its neurons use 2 chemicals to directly communicate, but 21 to alter this communication

What is the root of the crimes against DOP?

* writers have chosen to leave out the wrong words
* main research papers on DOP call its fast, large spike (and sulking pause) the reward prediction error system
* textbooks and population science articles shorten this to ‘reward system’
* from this word ‘reward’ the leap to happiness, pleasure, emotion and all the other crimes are easy to make
* DOP is the prediction error system

What did Sean Parker say about DOP’s role in facebook?

facebook’s leading question is “how do we consume as much of your time and conscious attention as possible”

* he explains: facebook exploits a vulnerabiliy in human psychology, whenever someone likes or comments we give them a little dopamine hit

What is one way that tech companies lure us in and create compulsion loops?

* most social media sites create irregularly timed rewards, a technique employed by the makers of slot machines
* BF skinner: found that this was the strongest way to reinforce a learned behaviour
* we compulsively check the facebook site because we never know when the delicious ting of social affirmation may sound
* other apps: implement a design where certain forms of encouragement (e.g., confetti) occur at random intervals

What is Dopamine lab?

it is a system that can be implemented into any app designed to build habitual behaviour

* e.g., running app that congratulates you at random intervals
* uses AI machine learning to tailor the schedule of rewards to an individual

How is attention related to addiction?

* a behaviour involved in perpetuating cravings linked to addiction is habitual and involuntary attention to cues signaling reward from the thing we are addicted to
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Connect addiction to Panksepp’s emotion systems

addiction is driven by seeking, and of Panksepp’s seeking system is implicated in the seeking component of addiction

* action tendency is approaching
* Panksepp: stimulus bound appetitive behaviour, a form of working toward the thing that makes you feel good

How is Panksepp’s seeking system related to the DOP system

it harness the DA system in search and goal direct behaviour to achieve a range of appetitive goals

What is meant when it is said that cues associated with reward have incentive salience? What is often the result of this?

incentive salience: means a cue stands out because of its associated with reward

* similar to emotional salience
* associations with this kind of cue trigger cravings
* feelings of cravings then turn to an automatic response
* in sum: cue → craving → automatic action

What is the reward system? What structures are associated?

group of structures that are activated whenever we expereince something rewarding like an addictive drug

* structures found along the major DOP pathways of the brain (DOP is released when we encounter something rewarding)
* pathway most associated with reward: mesolimbic DOP pathway: starts in the VTA (principle DOP producing region) and the pathway connects it to the nucleus accumbens (found in the ventral striatum, associated with motivation and reward)
* mesocortical DOP pathway is also associated: starts again in the VTA but projects to the cortex, particularily the frontal lobes

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What happens to the mesolimbic DOP pathway when we experience something rewarding?

* DOP neurons in the VTA are activated, projecting to the NA via the mesolimbic DOP pathway
* DOP levels in the nucleus accumbens increase

Describe the history of DOP as the pleasure molecule

* because it was released with addictive drugs, researchers originally thought it was associated with causing pleasure
* more recent research suggests that it related to motivation rather than pleasure
* e.g., it was found that DOP was triggered before a reward was even recieved, can thus could not be involved in the pleasure of that reward

What is the nucleus accumbens? What system is it a part of? What is it involved in psychologically? Under what circumstances does it interact with DOP?

region of the ventral striatum (which is in the basal ganglia

* key node of the mesolimbic DA system in the seeking system
* plays a role in motivation and addiction
* DOP is release onto neurons in the NAc either when you expect reward or when you encounter an unexpected reward

What are the caudate nucleus and putamen involved in? How do they work together? What specifically as the tail of the caudate nucleus been implicated in?

both are involved in:

* making decisions
* motivation
* motor control
* approaching things to get reward
* habit

they work together to transfer information from the cortex to the basal ganglia

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tail of the caudate nucleus has been implicated in motivational influences on attention

Where is DOP produced? Contrast tonic and phasic release of it? How is it related to incentive salience?

* produced in:
* substantia Nigra
* ventral tegmental area
* tonic (or slow and sustained DOP): motivates you to get up and out of bed and get out there to work for reward in general
* phasic (fast bursts of DOP): prediction error
* not just about prediction error though: also signals reward expectation and recent theories suggest its involvement in incentive salience

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What is incentive salience? How is it related to attention?

incentive salience: when a cue acquires association with reward and triggers a feeling of wanting or craving

* when a cue has incentive salience, we come to attend to it more in a habitual way
* habit, including habits of attention, are a key part of addiction

What determines whether a cue is habit forming? What occurs when a cue is unexpected?

a cue is habit forming if it predicts reward

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when a cue is unexpected you have learning

* there is a prediction error that we learn, we adjust our behaviour so that we are more likely to experience reward

What is Anderson et al.’s big picture question?

what is the role that of DOP in attentional biases to cues signaling reward?

What was Anderson et al.’s background? Specific question?

* background:
* DA is important for learning that certain cues predict reward
* cues signaling reward capture attention, even when not relevant to top-down goals
* specific question: what is the role of DOP in maintaining the attentional salience of reward cues when they no longer predict reward
* in relapse you crave a cue that used to be rewarding but now has wrecked your life and made you feel terrible

Describe Anderson et al.’s methods. Participants?

participants: 20 healthy young adults

* day 1 (training): creates incentive salience for certain colours
* report orientation of bars in red or green circles (report whether the bar inside the shape was horizontal or vertical), with specific colours predicting probability of either a high or low reward
* one colour predicted an 80% chance they would get a high reward of 1.50$ and 20% a low reward (0.25%)
* the other colour was the opposite
* after each search there was feedback on how much reward they got that trial and a running total of how much they had earned
* if they were too slow or were wrong they got nothing
* dat 2 (test)
* inject with tracer and put into a PET scanner
* task: report orientation in unique shapes (e.g., a diamond among circles or vise versa)
* scan A: distractors present (60 mins) - where in 50% of the trials one of the shapes that was not the target was in the colour that they had learned predicted high or low reward, but they did not get any reward
* idea was that it would still grab attention because it was now associated with reward (incentive salience)
* then a break for 75 mins
* scan b: distractors absent (60 mins)
* no salient distractors present, just did the task without any red or green circles
* this was so that they could compare the amount of DOP available when there were reward cues and when there were not

What were Anderson et al.’s independent variables? Dependent?

* IV training:
* different levels of reward associated with a specific colour
* IV test:
* distractors present versus no distractors present
* within distractor present: rewarding distractor absent, high reward distractor present, low reward distractor present
* region of interest
* looked at 10 but focused on the Putamen and anterior and posterior caudate
* DV:
* reaction time in indicating bar orientation
* PET measures of DA availability
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What psychological construct were Anderson et al. interested in? What is this a measure of? How was this implemented in their design?

* value driven attentional capture (VDAC): where you cannot help but pay attention to the cue that you have learned to associated with reward (just like bottom up attention). Capture indicates that it is not relevant to your task goals (e.g., tell the orientation of the bar in the unique shape) but you cannot help but pay attention to it
* form of reward-biased attention
* measure of incentive salience
* implemented in their design: if you are more distracted by the previously rewarded colour, you will be slower to report the orientation of the bar in the target shape

Describe Anderson et al.’s behavioural results

* in training they learned to be faster for high value targets, which is an index of appetitive conditioning
* test phase:
* before they learned that there was really no reward related to the distractors (extinction) they were slower to find the target when there was a high value distracter than when there was no distractor
* even further, there was no effect of the low value distractor, not different from the high value or the absent condition
* so the high value reward acquired incentive salience

In Anderson et al.’s paper, what was the measure of value driven attentional capture?

the difference between participant’s reaction times with a high value and distractor absent

* results showed that there was greater attentional capture initially by high value distractors

Describe Anderson et al.’s PET results

* positive values on the y axis indicates that the participants were slow for the trials with the distractors that had acquired incentive salience
* negative means they were slower for the trials with no distractors, looks more like no attentional capture
* larger numbers on x axis means more DOP release when high value distractors are present
* negative numbers means that there was more DOP when there were no distractors
* so: the more DOP increased when there were distractors, the more you showed the value based distraction
* for some people it looks like there is more DA release on distractor absent relative to distractor present, you can split the correlation into 2 groups
* high bias group: showed more DOP release for distractors and more attentional capture, or RT slowing, in the present of distractors
* low bias group: showed no evidence for attentional capture, DA release was lower on distractor present scans
* this split suggests a dissociation between groups:
* strong value driven attentional capture is associated with significantly elevated levels of DOP, whereas ability to ignore previously reward associated stimuli is associated with less DOP release in these same regions
* DOP release was NOT correlated with individual reaction time differences so the results are not differences in processing speedf

Evaluate the validity of Anderson et al.’s brain-behavioural correlations

* their results should be taken with all the caveats of small sample size correlations, but these patterns are very consistent and they worked hard to control for chance findings
* using a non-parametric randomization test in which the probability of each correlation was estimated by randomly shuffling the xy pairings 10,000 times
* so it is unlikely that the correlations are spurious

Draw a simplified plot for Anderson et al.’s DA release results

What regions were the differences in DA release seen in in Anderson et al.’s results? What do these regions have in common?

* regions
* right posterior putamen
* right posterior caudate
* right anterior caudate
* these regions are less about prediction arror than the ventral nucleus accumbens and more about voluntary motor behaviour, habits (learning and using) and motivation related to getting good things

Discuss the caudate's relationship with value driven attentional capture

* implicated in:
* shifting of covert attention
* responses of tail have been shown to be sensitive to learned value and play an important role in value based attentional capture
* tail communicates with the visual cortex
* Anderson et al.
* structure is involved in the representation of value and connected to the visual system, thus making it well situated to integrate these 2 sources of information into a value-modulated attentional priority signal
* specifically the role the caudate plays is habit
* AND affective and motivationally biassed attention is a habit

Describe the significance of Anderson et al.’s results

this is the first study linking individual differences in behaviour to differences in changes of DA with learning that builds attentional biases in the first place

* previous studies linked DA to pre existing individual differences in things like drug craving, impulsiveness, eating behaviour, or romantic excitement, but everyone has slightly difference experiences, so you never know whether your result is just due to differences in experience
* this is the first to link DA to differences in associations with reward that had just been acquired and were equal for everybody
* has important implications for who may be more likely to build associations that fuel anxiety on the one hand or addiction on the other

Summarise Anderson et al.’s results

* attention is captured by objects that previously predicted reward, even when they no longer do
* people who are more captured by cues of past reward show more DOP in the dorsal striatum in the presence of reward cues
* those who are not captured show less DA in the presence of reward cues: maybe they suppress?
* habit: DA signaling in the dorsal striatum is important for involuntary motivated attention linked to addictive behaviour

How is depression related to addiction?

it is on the other side of the spectrum, if DA driven systems are about seeking and predicting reward, depression is characterised by a lack of motivation to seek reward

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Discuss the results when Anderson et al. did the same paradigm but with depressed people?

* no difference in RT in the presence of a high value distractor in the depressed group
* they showed no value driven attentional capture
* BUT it could be that depressed participants just do not learn the associations between cues and reward
* not a good explanation, they learned just as well as the controls
* so depression was linked to lack of VDAC, not just a problem with reward learning
* ruling out differences in reward learning was imp

How did Anderson et al.’s training task create associations with reward?

participants indicated that orientation of a bar (vertical or horizontal) that is within either a red or green circle

* red was an 80% probability of a high reward, and a 20% probability of a low reward (if the task was done correctly)
* green had an 80% probability of a low reward (25 cents), and a 20% probability of a high reward (1.5$)

so after doing this for a long time, subjects associated the red colour with a high value reward and the green colour with a low value reward

* association with a high value reward was displayed in that participants responded faster to it than the low value reward

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How did the test task measure attentional capture by reward?

the test task was to determine the orientation of the bar (vertical or horiztonal) in the unique shape

* in 25% of the trials a high value distractor colour (red) was present
* in 25% of the trials the low value distractor colour (green) was present
* in the remaining 50% no distractors were present

using this set up they contrasted the reaction times for each condition, with a higher reaction time indicating that the distractors successfully captured your attention regardless of your goal (i..e to find the unique shape)

How did they use the task in 2 different scans to measure individual differences in DA release related to attentional capture by reward?

they took the difference in reaction time between high value distractors and low value distractors

* higher values indicate slower response for high value distractors, indicating more VDAC
* lower responses indicate slower responses for no distractors, indicating less VDAC

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they also took the percentage more DOP released in the distractor present versus no distractor present scan

* higher values indicated that most DA release was in the scan with distractors
* lower values indicated that the most DA release was in the scan without any distractors

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they then related these measures with one another, creating a correlation

Describe the main results illustrated in figures 2 and 3

* figure 2:
* 2A: from trial 121 onwards, participants were faster at reporting the target associated with the higher reward, indicating learning of the stimulus-reward associations
* 2B: attentional bias for the high reward stimulus is seen by a slowing of the response time compared to distractor-absent trials
* this then extinguished in the 2nd epoch, no difference between the 3 groups
* figure 3:
* y axis: difference in RT between high value and no distractors (positive indicates that the distractors achieved more incentive salience)
* x axis: % DOP release in the distractor present versus no distractor scan (higher values indicate more DOP release when high value distractors are present)
* correlations in these areas: right posterior putamen, right posterior caudate, and right anterior caudate
* as incentive salience of the distractors increased, so did DOP release when high value distractors were present
* so elevated levels of DOP in these areas is associated with robust value driven attentional capture
* correlation seem to be driven by DOP release that was greater on distractor absent scans in some participants
* this low bias group showed no evidence of attentional capture, DOP release was suppressed on distractor present scans
* ability to ignore previously rewarding stimuli is associated with the suppression of DOP in these regions

Discuss the controls that Anderson et al. put in place in their correlation analysis

* baseline RT (mean RT on distractor absent trials) did not correlate with the distractor-related DOP release in any of the 10 volumes of interest
* thus the findings are not confounded by individual differences in processing speed

What additional roles for striatal DOP do Anderson et al. describe? How do their findings fit into this?

1. representing expected reward signaled by a predictive cue
2. plays a role in voluntary motor behaviour
3. learning and execution of habits
4. cue-elicited motivation
5. when a cue is consistently paired with a reward, an automatic bias to orient attention to this view develops that is evident even when the reward is not expected


1. here they establish a relationship between DOP release in the dorsal striatum and involuntary preservation of an attentional bias

How do Anderson et al link their findings to previous findings of attention to drug cues? What is the relationship they describe between DA release and craving

* DOP release within the caudate and putamen is known to underlie habit learning and the expression of habitual behaviours
* DOP release within these same 2 structures is associated with craving elicited by drug cues
* their findings suggest that value based attention may be governed by similar neural mechanisms
* caudate has been implicated in (1) covert attention shifting and (2) learned value/value based distraction, making it well orientated to integrate these 2 sources of information into a value modulated attentional prioity signal

What connection do Anderson et al. make between normal value biased attention and addiction?

* abnormally high susceptibility to value driven attentional capture is associated with addiction
* AND DOP release within the dorsal striatum has been linked to cue-evoked drug craving
* here they make a neurochemical link that underlies both of these sources of individual variation
* DOP release within the caudate and posterior putamen predicts value driven attentional capture, and the suppression of VDAC is associated with the suppression of DOP in these same regions
* thus this study identifies a potential target for pharmacological intervention

How do the individual differences Anderson et al observe give us insight into what makes people vulnerable to addiction?

An individual could vary in their vulnerability to addiction based on their ability to suppress VDAC to rewarding cues (related to drug reward and craving), modulated by DOP release in the caudate and posterior putamen

Identify any methodological flaws in Anderson et al.’s paper

think of good answer!

Synthesize what Anderson et al.’s findings tell us about how the mind/brain works in relation to course readings and class discussions. Think of at least one broad follow up question that would lead to a greater understanding of this area of research

think of a good answer!

How can we explain amnesia for the past, yet retention of knowledge learned at school?

The hippocampus is critical for the retrieval of episodic memories. These are personal memories of events from your life. The hippocampus represents the spatial context in which the event occurred and thus acts to prompt recall of that event. This system is anatomically separate from the semantic system and so it is possible for a stroke to affect one but not the other.

Why do we begin to forget people’s names when we are in our fifties?

As we age we tend to forget names. This is not because they are arbitrary but because different people share many visual and semantic features but the name is attached to only one person. The perirhinal cortex is especially taxed when things are confusable in this way, and it is the perirhinal cortex that is most compromised in semantic dementia.

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Why do people with Alzheimer’s disease have difficulty in finding their way?

The fundamental role of the hippocampus is to represent the location of the person in space. It is engaged whether the person considers what route to take or conjures up an event from the past. In Alzheimer’s disease there is a loss of tissue in the hippocampus; and the result is that, as well as having trouble retrieving episodic memories, the patients can fail to know where they are or where they have been.

What pathway does information take in the brain to construct a scene?

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* There are distinct pathways for central and peripheral vision and the latter terminate in a structure in a structure called the parahippocampal cortex (lies on the inner surface of the temporal lobe)
* Parahippocampal cortex is activated if people are scanned while they view pictures of scenes or large objects such as houses that could serve as landmarks

Discuss the resting state covariance to the parahippocampal cortex

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* Parahippocampal cortex is connected with the inferior parietal cortex and with 2 areas on the medial or inner surface of the brain: retrosplenial cortex and the hippocampus
* These areas also receive direct input from the medial and inferior parietal cortex
* There are several parietal areas in which maps of external space can be identified

Describe Hassabis and Maguire’s hippocampal study

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* Hassabis and Maguire: scanned people while they learned their way around a virtual reality environment on the computer screen
* Multi-voxel pattern analysis: is it possible to tell where the person was in the environment?
* A: yes! This could be done from the pattern of activation in the posterior part of the hippocampus

Describe Spiers and Maguire’s study related to hippocampal surroundings recognition

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* Spiers and Maguire: recruited taxi drivers with many years of experience of driving through London, tested in a virtual reality set up, controlling the image of a taxi on the screen
* After the scans each driver was shown the video of the routes that they had taken and asked to remember what he was thinking about each stage on the route
* It was possible to relate the thoughts retrospectively to the dynamic brain images that were taken at the time that he was actually driving
* Only time hippocampus was activated: when the drivers were shown a familiar starting location and told the destination to which they had to drive
* I.e. when they had to plan how they were going to go from starting location A to destination B
* So hippocampal codes for where we are, and this knowledge serves as a context or reminder for a spatial direction or route
* Follow up study with taxi driver with hippocampal damage:
* After his stroke he was completely lost, even though he had 40 years of driving experience

Describe Vargha-Khadem’s patient Jon

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* Vargha-Khadem: had a patient Jon who suffered a small stroke, resulting in the loss of neurons in the posterior hippocampus
* Very poor at remembering past events
* however could still learn in school
* This is weird because if the specific role of the hippocampus is to enable memory retrieval, intuition tells us that damage would also interfere with school learning

What are the 2 notable situations when the hippocampus is activated?

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* When people think about how to get from A to B
* When they recall past events

Describe Clayton’s study investigating animal memory recall

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* birds were given email worms and peanuts to bury. If tested soon after they retrieved the mealworms, but if tested 5 days later they retrieved the peanuts
* Assumption: they did this because they knew the meal worms were perishable and the reason why they avoided them after 5 days was that they remembered when they had cached them
* Conclusion: they remembered what foods they had cached, where they had cached them, and when they had done so

Describe Burgess’s study related to memory recall

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* The more the same film was repeated, the greater the detail people could report
* Pattern analysis: compared the activations when viewing the videos and when recalling them a week later, checked to what extent the state of brian was more similar when viewing film 1 and recalling film 1 than when viewing film 1 and recalling film 2
* Many regions that were reinstated at recall
* Hippocampus
* Retrosplenial cortex
* Posterior cingulate cortex
* Degree of similarity in the posterior cingulate cortex was related to the amount of detail that was recalled
* Medial and inferior parietal cortex

What are some main differences between human and animal memory?

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* 1. We live in a technological world and this means that there is a much greater richness of things that we do
* 2. When trying to think where we left our keys, we are aware of letting our thoughts wander until simply imagining the kitchen unlocks a memory of what we did there
* Study: when people mind water in the scanner, there is extensive activation on the medial surface (posterior cingulate cortex and retrosplenial cortex, as well as medial PFC)
* Same occurs when chimpanzees are at rest, but there is no way to know what is happening in their minds
* 3. We can retrieve memories from the distance past and image the distance future
* Study: hippocampus and other medial areas are activated when people review events from the past or imagine ones in the future
* E.g., Chimpanzees cannot think about what they are going to have for breakfast tomorrow
* This is intuitively correct, but still unproven

Describe Bonnici and Maguire’s study related to memory recall

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* Bonnici and Maguire: asked people for their memories from 2 weeks or 10 years ago, during scanning, a MVPA was used to see whether it was possible to distinguish between different memories
* Proved possible when analyzing the activations in the hippocampus, retrosplenial cortex, and ventromedial PFC (in this area the degree of accuracy was better for more remote memories)

Why could patient Jon not remember past events but still learn in school?

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* There is a fundamental difference between remembering events in your life and remembering facts that you have been taught
* Episodic versus semantic memory
* One thing to remember where you put your keys, another to know what keys are used for

Describe Vandenberghe and Price’s study related to semantic knowledge

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* Vandenberghe and Price: scanned people while they were tested for their knowledge of the properties of things such as tools
* Individuals had to judge whether a spanner or a saw is related to a pair of pliers (answer is spanner because it can be used to grip)
* Irrespective of whether the problems were presented in pictures of words, there was activation in the middle inferior temporal cortex extending to the perirhinal cortex, lying at the temporal pole
* Also activation in the ventral PFC with which these are connected
* Activations common for the pictorial and verbal version were all in the left hemisphere
* Why? A: left hemisphere is the one specialised for language

Contrast the neural systems involved in remembering knowledge concerning objects versus events in your life

there is a clear distinction between a medial system for remembering events in ur life, and a ventral and lateral system for knowledge concerning objects

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* Within the latter:
* Perirhinal cortex plays a critical coll
* If MVPA is performed on the activations in the temporal lobe, it is the perirhinal cortex that object specific semantic information is represented
* Further, this area is increasingly engaged the greater the number of semantic features that object share

How does knowledge of meaning and words change in semantic dementia? What causes this syndrome?

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* Our knowledge of the meanings of words forms part of our semantic knowledge, and this degenerates in people who suffer from semantic dementia in older age
* Syndrome results from the loss of the temporal and prefrontal tissue, critically this includes the perirhinal cortex
* Damage to the perirhinal cortex leads to problems in naming things, but this problem is worse the more they are perceptually and semantically confusable

Relatively, how difficult is remembering personal names from all semantic tasks? What is the result of this?

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* Remembering personal names is one of the most taxing semantic tasks
* Different people share many visual features, and there are also many other properties that people share in common (e.g., both colleagues or in our list of email contacts)
* So all these people are confusable and we are supposed to remember something that is attached to only one of them
* Thus this form of cognition, remembering personal names, is particularly sensitive to ageing

What is Alzheimer’s disease? What are some of its symptoms?

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* Alzheimer’s disease: possible to detect a loss of volume in the hippocampus seven years or so before it becomes obvious that there is a severe memory problem
* Most obvious is that people are unable to retrieve memories of their life, also common to be confused about where they are or how they got there
* This is because the hippocampus represents location as well as autobiographical memories

Describe a study investigating route navigation in those with semantic dementia versus Alzheimer’s disease

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* Study: assessed ability to follow routes by showing a video of a car driving along the road taking a left or right turns at particular landmarks
* Person then shown the film again and asked which way to turn
* Alzheimer’s disease patients made many errors
* Patients with semantic dementia had little trouble
* 2nd test for what the road signs meant
* Here the reverse effect found, semantic dementia patients were the ones with the trouble
* Further emphasises that these are dissociable systems, one for what has been personally experienced and the other for what has been learned or told
* BUT as Alzheimer’s disease progresses the pathology becomes so widespread until it spreads to the perirhinal cortex and elsewhere, influencing both episodic and semantic knowledge

The ventral tegmental area:


1. Produces Dopamine
2. Projects to the cortex
3. Projects to the nucleus accumbens
4. Is part of the mesolimbic dopamine pathway

1,2,3,4

Dopamine is released in my  nucleus accumbens when:


1. I enjoy the flavour of a delicious ice cream cone
2. I find $20 I thought I lost
3. I’m walking to Rain or Shine for ice cream
4. I get my paycheck and it is exactly the amount I expected

2,3

The tail of the caudate nucleus has been found to play a role in:


1. Production of phasic dopamine
2. Motivational influences on attention
3. Prediction error
4. Production of tonic dopamine

2

Phasic dopamine is involved in:


1. Expectation of reward
2. Prediction error
3. Enjoying reward
4. Motivation to work for reward

1,2

What is the best description of the big picture question of the Anderson et al. paper?


1. What is the relationship between attentional capture by reward cues and dopamine release in the presence of cues that formerly predicted reward?
2. What is the role of dopamine in attentional biases for reward cues?
3. What is the role of dopamine in memory for cues that used to predict reward?
4. 1What is the role of dopamine in learning associations between cues and reward?

2

Which describes the way *value-biased attentional capture* was measured in the first test block?


1. When participants were faster to respond to targets when there was a distracting high reward colour than when there was no distracting colour
2. None of these
3. When there was the same amount of response time to respond to targets trials in which there were distracting high reward colours and no distracting colours
4. When participants were slower to respond to targets when there was a distracting high reward colour than when there was no distracting colour

4

How did they create reward-related “distractors” for the test phase?


1. Make the previously rewarded shape a non-target distractor in the display
2. Make the previously rewarded shape a target in the display
3. Make the previously rewarded colour a non-target distractor in the display
4. Make the previously rewarded colour a target in the display
5. Put a line that had a previously-rewarded orientation in one of the non-target shapes

3

What was the main finding of the Anderson et al., study? (DA = dopamine)


1. The more DA people released the faster they learned that cues that previously predicted reward no longer did
2. The more DA people released in the presence of tempting distraction, the more they continued to be distracted by cues that previously predicted reward
3. The more DA people released the faster they learned that a cue predicted reward
4. None of these

2

Which best describes the pattern of results in the dorsal striatum? 


1. None of these
2. The greater the increase in DA release between the scan with distractors and the scan with no distractors, the less of a difference in reaction time between trials with high reward distractors and those with no distractors
3. The greater the increase in DA release between the scan with distractors and the scan with no distractors, the longer the reaction times for trials with high reward distractors than trials with no distractors
4. The greater the decrease in DA release between the scan with and without distractors, the longer the reaction times for trials with NO distractors relative to those with high reward distractors

3,4

In the Anderson et al. PET study what was the purpose of having two scans?


1. To acquire enough trials to analyze the PET data
2. To torture the participants for longer
3. To make sure participants learned the red and green circles no longer predicted reward
4. To compare dopamine availability in the presence of previously rewarded distractors to the absence of previously rewarded distractors.

4

\[11C\] raclopride is


1. An excitatory dopamine receptor
2. A producer of dopamine
3. A radioactive tracer for measuring dopamine availability
4. An inhibitory dopamine receptor

3

What is episodic memory?

consciously recalled memory of past events

* one of many memory systems
* hippocampus is really important for it

Give a brief history on the discovery of multiple memory systems

* once psychologists thought there were only 2 types of memory: long and short term
* it was Endel Tulving who suggested that we have multiple memory systems in 1972
* very controversial, met a lot of resistance

Outline the different memory systems

1. implicit (unconsious)


1. procedural memory: performance of a skilled action
2. conditioning: memory for emotional relevance revealed by actions


1. can be consious
2. explicit (consious)


1. semantic memory: facts recalled


1. often do not know the event learning it
2. no temporal information, called up all in one piece
2. episodic memory: events, mental time travel


1. these unfold over time, consciously reliving it over the past, playing through it like a movie, rewinding, playing again
3. autobiographical memory: events in your life


1. mix of episodic and semantic memory
2. e.g., remembering the day of your graduation, and the date at which it occured
4. prospective memory: memory to do something in the future, performance of future action

What are place cells? Place fields? Contrast their orientation to the retinotopic maps in V1. What is remapping?

place cells: specific kind of cell in human an rat hippocampus thought to play a role in cognitive maps

place fields: e.g., rat video, some cells always fire when the rat goes around a particular bend in the track, and that area that this cell likes is called a place field

* there is no apparent topography to their pattern, meaning that the organisaiton of where the cells that fire for different places are does not map onto the relationship of the places the fire to out in the world


* contrasted with retinotopic map in V1, the cells of which literally map onto what is out in the world
* place cells next to eachother are just as likely to respond to areas close to each other as areas farther away from each other.
* and if you do a new experiment, about half of the place cells will fire to locations different from their original place field, they are quite flexible, can suddenly change their firing pattern (remapping)

What do we know about the hippocampus generally (as per lecture)?

* we need it to form and recollect episodic memories (memories played in a sequence like a movie, not scattered still pictures)
* need it to imaging future events (that have not happened yet)
* crucial for our ability to navigate
* hippocampus is key in creating these mental maps linking the role of navigating space and its role in navigating time

Describe the conundrum for a while present in hippocampus research

there were these parallel lines in research:


1. spatial navigation in rodents


1. place cells in hippocampus
2. grid cells in enhorinal cortex, rather than tagging specific locations like place cells they organise space into a grid like map to be used in any environment (do not remap like place cells)
3. head direction cells: track which direction you are facing in
4. border cells: track the edges of a spatial location
5. time cells in the hippocampus: track time
2. memory research in humans


1. key moment: research done on the famous HM, who had his hippocampus removed, completely losing his episodic memory.


1. we learned that the hippocampus played an extremely important role in episodic memory

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researchers have began to extend the idea of cognitive maps (established in relation to spatial nagivation) to episodic memory, or the ability to navigate through time as well as space

What is the cognitive map hypothesis?

hypothesis that the brain builds a representation, or mental map, of the spatial environment to support memory and `guide` future action

* introduced by Edward Tollen, to explain how rats learn the location of rewards in a maze
* he proposed that a cognitive map gave the rat a useful model of the environment emphasising what locations were important for what the rat needed to know to get the treat (not every detail in the maze, just the ones needed to navigate to reward)
* idea has been extended to the idea that both humans and animals use them to find their way and learn important features of their environment
* also been extended to include more metaphorical maps such as a schema: mental scripts of how certain situations tend to go as a rule
* seen as a way of organising memories as they are laid down
* e.g., restaurant schema, sit down, order, get food, you know how this interaction will unfold and you have these mental representations of how the interactions will occur
* \

How can schemas influence attention?

think about what we have learned with predictive coding → we attend to things minimising prediction error

influence attention and the absorption of new knowledge

* more likely to attend to things that fit into our schema, ignoring those that do not (some of the time, not when the stimulus is super suprising)
* so we reinterpret contradictions to the schemas as exceptions or we can distort our schema to fix them
* predictive coding: this is when we ignore the prediction error and go with our mental model

Are schemas unchanging? Concrete?

* schemas are thought to be flexible and can be reoriented
* not concrete things, they are much more of a theory rather something that we can prove we can have (consistent with how we lay out things though)

Describe the role of landmarks in the functioning of cognitive maps

landmarks: link mental map to sensory information

* allows you to know where you are in relation to something in the world you can percieve
* e.g., buildings, features in the landscape, anything that stands out

What type of information does the parahippocampal place area get?

* parahippocampal place area: region of the ventral visual cortex very sensitive to scenes
* gets a lot of information from the rods of the periphery, allowing us to perceive scenes as a whole (in contrast to object recognition)

What were the research questions in the study investigation the role of the human hippocampus in city navigation (taxi study)

1. when might the hippocampus be most required during an ongoing period of navigation
2. which specific navigation processes might it be most important for?

Describe the participants (what made them special?) and methods of the taxi driver study

20 london taxi drivers, mean age 49

* before GPS, they had to pass this test getting the knowledge, knowing the layout about 25,000 streets in london
* early structural MRI study found that these drivers had a way larger volume of hippocampus in the posterior region
* more experience, the larger it was

method:

* realistic VR of London, drivers had to navigate to a destination in response to customer requests
* specifically, each navigation block:
* customer request
* random dialogue from customers
* later on the customer would change their mind, prompting the driver to change their planned route (they had to consult their mental map!)
* 7 total of these routes
* after scan, watched video of route and reported what they were thinking
* watched a video replay while being interviewed about what their thoughts were

In the taxi study, how did they categorise the thoughts that taxi drivers had while conducting their route? What category were they most interested in?

some of the categories

* customer driven route planning: “please take me to Big Ben”, person things of the route
* spontaneous route planning: without the customer prompting them, replan route (e.g., I will use this shortcut)
* expectation confirmation: “just as I hoped this street is open”
* expectation violation: “they have blocked off this street”
* visual inspection: “this statue looks clean”
* action planning: in the moment, “I need to make a left hand turn”
* expectation based on what you know about the route: “I should see Bond street any moment”
* monitering traffic: “what will this bus do?”
* coasting: nothing particular happening

\
\
they were most interested in this customer driven route planning

Discuss the taxi study fMRI results. What conclusions were drawn from it?

hippocampal activation

* most when the customer gave their initial request (customer driven route planning)
* also activation when customer switched their route (customer driven route planning)
* less activation when customer said irrelevant things
* no other interaction for any of the other categories of taxi thoughts
* conclusion:
* brief activation in hippocampus is important for planning a route to a very specific destination
* did not see hippocampal activation when alternations to the route were made on the fly (when they were updating where they were in relation to that goal)
* more about generation the entire cognitive map
* lead to the theory: hippocampus retrieves relevant spatial information from a cognitive map

In the taxi study, why was hippocampal activation not required when making navigation decisions ‘on the fly’?

generating the initial vector, updating the most efficient route, and observing landmarks to update the current vector to the goal may be likely candidates for increased activation in the hippocampus

* results do not provide evidence for the first prediction, the latter 2 are not
* so more research is needed

How does the hippocampus play a role when you have to navigate a remembered route (follow up to taxi study)?

* Describe the methods.
* What would cognitive map theory predict?
* What were the results of this study?
* Conclusions?

case study of TT, \~40 years of experience as a London taxi driver

* lost hippocampus due to encephalitis , could not lay down new memories or retrieve pervious ones

\
cognitive map theory: predicts that flexible navigation in environments you have learned would be impaired with hippocampal damage

\
results:

* TT could identify landmarks and navigate main roads
* TT could NOT:
* learn new routes
* navigate smaller back routes
* verbally describe routes

summary/conclusions:

* hippocampus is NOT necessary for general orientation in London, detailed topographical knowledge of landmarks and the spatial relationships between them
* hippocampus required for navigating many routes learned long ago
* especially when detailed spatial representations needed