Learning & Memory Flashcards
1
Q
in what way is fear adaptive?
A
- keeps us away from harmful things
- some stimuli evoke an innate fear response with no learning
- snakes, spiders, big moving objects
2
Q
when do animals/humans display fearless-like behaviours?
A
- when we have lesions to the amygdala
- primates are innately scared of snakes, but lesions to amygdala remove this fear
3
Q
what is the amygdala’s role in fear?
A
- plays an essential role in learning to be afraid of potentially harmful things
- controls our ability to learn AND recall fear
4
Q
what are the four main elements of pavlovian (classical) conditioning?
A
- association of neutral stimuli with a biologically significant event (no control over what happens, organism can only react/prepare)
- unconditioned stimulus (US): biologically significant event
- unconditioned response (UR): normal response to significant event (salivation)
- conditioned stimulus (CS): previously neutral cue that reliably predicts significant event
- conditioned response (CR): body’s response to the CS alone
5
Q
what is required in order for classical conditioning to be successful?
A
- the conditioned stimulus must reliable predict the unconditioned stimulus (bell must predict food)
- delivery of conditioned and unconditioned stimulus are uncontrollable by the organism (food and bell)
- the conditioned response is uncontrollable
- in humans, the conditioned response appens in the absence of knowledge
- long last effects that can be suppressed but also reinstated very quickly with another CS-US pairing
6
Q
what is auditory fear conditioning? what happens when we use auditory fear conditioning in rats and damage the amygdala?
A
- when an organism is conditioned so that a tone triggers a fear response
- freezing is a natural defensive response for rodents
- made the rodents associate a tone (CS) with a shock (US)
- lesions to amygdala subnuclei removes freezing and autonomic response to the tone (CS)
- lesions made before and after the conditioning both disrupt conditioned response (amygdala responsible for learning and recalling fear)
- similar results in humans with amygdala damage
7
Q
how does the amygdala allow for fear conditioning?
A
- sensory input (tone) and pain information converge in lateral amygdala
- lateral amygdala sends signals to central amygdala
- central amygdala sends signals to areas that initiate autonomic, emotional, and freezing reponses
8
Q
what does firing in the lateral amygdala look like while learning?
A
- as we learn, neurons in lateral amygdala show changes in firing to CS that parallels emergence of conditioned response
- ex. more firing = more freezing
- human imaging studies found increased activation in amygdala to CS after conditioning
9
Q
how does the amygdala aid in appetitive conditioning?
A
- amygdala regulates pavlovian conditioning for rewarding stimuli as well
- in appetitive conditioning, the conditioned stimulus (CS) triggers approach behavior (CR)
- conditioned place preference: animal prefers an area and approaches it because it’s associated with rewards
- damage lateral amygdala: animals can no longer develop conditioned place preference, no matter the type of reward
- but lesions do not disrupt consumption of reward, they just stop the animal from responding to cues that predict the reward
10
Q
how was appetitive conditioning (reward learning) tested in humans using the red and black ball task? what did it tell us about reward-associated cues and behaviour?
A
- subjects did a “memory task” to find the red ball
- finding the red ball lead to a pleasant tone, with distinct patterned background, and a food reward
- black ball was paired with a buzzer, another pattern, and no reward
- subjects were shown different patterns (some previously linked with reward) and asked to say which they preferred
- they preferred the pattern associated with the red ball/reward, but had no conscious association with pattern and reward
- reward-associated cues can control our behaviour, sometimes without us being aware
11
Q
what is instrumental conditioning? what is a reinforcer?
A
- also known as operant conditioning
- association with a particular action/motor response and its consequences
- the organism can control what happens
- reinforcer: something that increases or decreases the likelihood of a response happening again
12
Q
what brain region is responsible for instrumental conditioning?
A
- regions of the striatum regulate action selection and instrumental conditioning
- striatum converges inputs from sensory/motor cortex and dopamine system
- both are activated when actions are reinforced, to facilitate learning
13
Q
what are the phases of instrumental learning?
A
- early in learning: behavior is new and the person/animal is still learning what actions lead to a reward
- responses are goal-directed, sensitive to levels of motivation
- late in learning: after the behavior has been repeated many times
- responses become more automatic (habitual), mediated by dorsal striatum
- dorsal striatum also mediates transition from goal-directed to habitual actions
14
Q
how does the amygdala work with the striatum in instrumental conditioning?
A
- amygdala sends input to the striatum and can influence instrumental action
- amygdala helps the striatum decide which actions are worth doing, especially when the action has an emotional or rewarding consequence
15
Q
what is an example of conditioned reinforcement in rats?
A
- CS light comes on that predicts reward (food)
- after learning, two levers are inserted to chamber
- one lever gives CS light that was associated with food, the other gives nothing
- rats press lever just for CS light, even though that never gives a reward
- light becomes reinforcing and animals with work for it
16
Q
what happens to conditioned reinforcement when the amygdala is damaged? what does this tell us about cues, reward, and behaviour?
A
- lesions to lateral amygdala disrupts preference for lever that produces CS (no conditioned reinforcement)
- but they consume reward normally and press levers for food normally
- cues associated with reward can control our behaviour, even though we may be unaware of their control
17
Q
what are the three key components of memory?
A
- encoding: getting sensory info into your brain by translating it into a neural code it can understand, requires attention
- storing: retaining information over time, biological memories tend to be more “fuzzy” and fragile (can be manipulated)
- retrieval: the active processes of locating and using stored information
18
Q
what is short-term memory?
A
- Information held for short periods while physiological changes needed for long-term memory are made
- Limited capacity (7 +/- 2 items)
- Susceptible to distraction, requires active rehearsal to maintain
synthesis - Patients with amnesia can still remember info they just hear (short-term intact) but cannot move the info to long-term
19
Q
how does information loss in memory occur?
A
- occurs through displacement (something new pushes it out) or through decay
- Info in short-term memory either gets discarded or moves to other stage of memory
20
Q
what is the primacy/recency memory effect?
A
· You tend to remember items at the beginning or end of a sequence better than items in the middle
21
Q
what is long term memory? what is the process of moving info from short-term to long term memory?
A
- Relatively stable, can last lifetime of organism, potentially unlimited capacity
- Consolidation - transferring of information from short to longer-term memory, can be active or passive
· Sometimes we study to remember information, other times just witnessing events ingrain it into memory
· Involves physical changes in the way neurons are connected and/or communicate with each other
· Requires new RNA or protein synthesis - Information can be forgotten or recalled inaccurately, can be hard to reactivate the pattern of neurons in the same way
22
Q
what is amnesia and what are the different types?
A
- Certain brain injuries or drugs can impair the encoding, consolidation, or retrieval of long-term memories
- Categorized by information lost relative to the time of the brain insult
- Retrograde amnesia - loss of memory for events just prior to an injury, info did not get from short-term memory to long-term
- Anterograde amnesia - inability to form new memories after an injury
23
Q
who was patient H.M?
A
- Henry Molaison had intractable epilepsy, seizures originating bilaterally in medial temporal lobes
· Seizure happens when cortex is firing synchronously- Surgeons remove both medial temporal lobes, included most of hippocampus, amygdala, and adjacent temporal cortex
24
Q
how was patient H.M altered after surgery?
A
- Post surgery - seizures mostly eliminated by the surgery, IQ increased from 104 to 118
- First and last patient to have bilateral temporal lobectomy, caused severe anterograde amnesia (couldn’t form new memories)
· Also showed retrograde amnesia for about 3 years prior to surgery - H.M. had normal short-term memory, but couldn’t transfer information to long-term memory
· He would forget everything once his attention shifted
25
what could patient H.M. not do?
**Digit Span + 1 Test:** present 5 digits, have subject repeat back correctly, then keep adding digits till they make an error
· H.M. could do up to 8 digits, shows his relatively intact short term memory
**Matching to Sample Task:** memorize a sample of images/items, then the cards were flipped back over to hide it
* Measuring a form of cued recall, tested a verbal and nonverbal version
* Verbal: longest delay used was 40 seconds and H.M. had no difficulty if he was allowed to repeat the letters, if we distracted him we'd see the impairment
* Non-verbal: impaired, intervals greater than 5 seconds disrupt his ability to do task, maybe because he cannot easily use repetition to remember
26
what could patient H.M. do?
* HM could learn motor skills (instrumental learning), but COULD NOT recall learning it
* Mirror Drawing Task - subject must redraw object from reflection in mirror, HM's performance improved but he didn't remember doing the task
* He could also gradually learn new facts (semantic memories) but could not recall learning them
26
how does damage to the striatum affect instrumental learning?
· Patients with damage to the striatum (related to instrumental learning and moving the body to obtain goals) show opposite trends as patient HM
· Cannot learn new skills, but remember the events
27
what did patient HM's case tell us about memory?
* Poor performance on long-term, but not on short-term memory tasks, **supports the two stage model for memory formation**
* Main problem was consolidating new memories from short term to long term storage
· Suggests that memories can be stored elsewhere, but hippocampus is crucial for converting memories to long-term storage
* HM could learn some types of tasks (skill learning), so...
1. Not all types of learning and memory are mediated by the hippocampus
2. Memory systems can be dissociated by the type of information being stored (as well as how long it lasts)
28
what are the different types of long term memory?
- declarative (explicit): episodic and semantic
- procedural (implicit): conditioning and skill learning
29
how does damage to the hippocampus affect memory?
causes selective deficit in declarative (explicit) memory but leaves procedural (implicit) memories intact
30
what brain areas mediate different types of procedural memory?
- striatum: skill/instrumental learning
- amygdala: conditioning
31
what is a radial arm maze? how does performance in the task change after hippocampus damage?
- rat navigates around maze to locate food using spatial cues around the room
- rats remember where they've been, they do not re-enter arms
- hippocampal lesions cause rats to make more error, re-enter arms that they've been to
32
what is a morris water maze? how does performance in the task change after hippocampus damage?
- pool filled with opaque water: escape platform hidden under surface
- rat must use spatial cues to navigate to platform, normal rats learn to find platform quickly
- hippocampal lesioned rats never learn to find hidden platform efficiently (but no impairment if platform is visible)
33
what does the performance of hippocampal lesioned rats in maze tasks tell us about the hippocampus?
the hippocampus is critical for learning about relationships between different stimuli, especially in the environment (spatial memory)
34
how do humans with and without hippocampal lesions perform through a virtual 3D environment?
- humans w/ hippocampal damage are impaired when navigating through space and remembering routes
- imaging in healthy individuals show increased activity in hippocampus when people learning routes in virtual environment
35
how do hippocampal neurons represent space and respond to cues?
Different neurons fire in specific locations—these are called place fields
Groups of neurons encode different locations, forming a mental "map"
When spatial cues are moved, place fields reorganize
Neurons fire relative to cue positions, not fixed spots
Place cells don’t associate with absolute locations, but with relationships between cues
36
what does place cell firing tell us, and why is it important?
Hippocampal firing reflects the relationship between stimuli (e.g., exit sign vs. door)
The brain needs to understand how cues relate to each other
Disrupting place cell activity impairs spatial memory and navigation
Recordings from many neurons show the hippocampus builds a spatial map
37
what experiment shows us how the hippocampus is not responsible for implicit learning?
- Tone-shock pairing in one context leads to fear response
- When tone is played in a new context, normal rats freeze
- Rats with hippocampal lesions still freeze (→ tone fear intact)
- Shows hippocampus not needed for tone (implicit) learning
38
How does hippocampal function affect contextual fear conditioning?
- Rats placed in the context that there were shocked in, but the CS tone that is associated with the shock doesn't come
shock context without tone...
- Normal rats still freeze (contextual fear, scared of the context)
- Hippocampal lesioned rats do not freeze → hippocampus needed for contextual fear
- hippocampus associates the context with the shock
39
What role does the hippocampus play in memory and fear?
- It links the shock to the context (not just the cue)
- Involved in remembering relationships between contexts and events
- Amygdala is needed for learning fear to both tone and context
- Hippocampus helps identify where the shock happened via its interaction with the amygdala
40
what role does the hippocampus play in episodic memory?
- Tracks what, where, when, and what stimuli were present during an event
- Records multiple pieces of info as distinct patterns of activity
- Keeps track of what sensory experiences happen at the same time
- Helps link and consolidate memory elements in the same cortical areas that first processed them
41
how does the hippocampus support memory retrieval?
- When remembering, hippocampus reactivates in the same pattern to trigger recall
- This can activate the same cortical regions used during the original experience
- Over time, a retrieval cue can trigger the cortex without the hippocampus
- Allows memory recall even if the hippocampus is no longer involved
42
what is dissociation of memory systems?
- when 2 or more brain regions are independently involved in separate forms of learning
- lesions to one area impair on one task but not on others
43
what is the Spatial Radial Maze and what brain region is required?
Task: Don’t revisit previously entered arms (uses spatial/relational cues)
Hippocampal lesion → Impairment
Amygdala lesion → No impairment
Dorsal Striatum lesion → No impairment
➤ Hippocampus is necessary for spatial memory
44
what is the Conditioned Place Preference task and what brain region is required?
Task: Return to arm where food was received before (Pavlovian/associative learning)
Hippocampal lesion → No impairment
Amygdala lesion → Impairment
Dorsal Striatum lesion → No impairment
➤ Amygdala is necessary for associative learning
45
what is the Locally Cued-Radial Arm Maze and what brain region is required?
Task: Go to arms with lights on to find food (stimulus-response learning)
No spatial cues (curtains block surroundings)
Hippocampal lesion → No impairment
Amygdala lesion → No impairment
Dorsal Striatum lesion → Impairment
➤ Dorsal Striatum is necessary for stimulus-response/habit learning
46
how do rats solve a maze, and how do strategies shift with training/impairment?
Rats can use:
- Place strategy (hippocampus): “Go to X place”
- Response strategy (striatal): “Turn left/right”
Early training (Day 8): Most rats use hippocampal/place strategy
- Inactivating hippocampus → rats switch to striatal strategy
Late training (Day 16): Most rats use striatal/response strategy
- Inactivating striatum → rats switch to hippocampal strategy
47
what does the maze task with place vs. response strategies reveal about memory systems?
1. different memory systems (hippocampus and striatum) can learn in parallel and independently
2. disabling one system reveals behavior controlled by the other
3. different systems learn at different rates (hippocampal = fast, striatal = more gradual)
48
how do emotions affect memory consolidation?
- strong emotional states can enhance memory consolidation
- may be mediated in part by noradrenaline
- normal subjects show better memory for emotional vs. neutral stories attributed to the same pictures
49
how do noradrenaline beta-receptor antagonists affect emotional memory consolidation?
- Reduce memory for emotional parts of the story only
- Subjects still feel emotional but don’t remember it as well
- This selective effect may help explain PTSD, where emotional memories are overly strong
- Beta blockers tone down arousal and don’t cross the blood-brain barrier
50
how do emotions enhance memory consolidation?
- emotional enhancement of memory consolidation is mediated by the amygdala
- train rats on memory task on day 1, test memory on day 2
- stimulating the amygdala right after training improves memory on day 2 for...
- Spatial learning (hippocampal)
- Instrumental learning (striatal)
- Aversive learning (amygdala)
- stimulation must be immediate to link the emotion to the event
51
why might emotional arousal enhance memory consolidation?
- Emotional events activate the amygdala
- amygdala can enhance consolidation across multiple memory systems
- likely works through stress-related mechanisms
- toning down emotional responses (e.g., in PTSD) can reduce over-consolidation of traumatic memories
52
what is synaptic plasticity and how does it relate to memory formation
- plasticity: the brain changes whenever you learn
- Short-term memory is carried out by cell assemblies (interconnected neurons)
- activity from an input can cause reverberatory circuits, a chain of activation to temporarily encode a memory
- if activity in the circuit is strong or lasts long enough, it leads to long-term changes in synapses to make memories more permanent
- these changes are called alterations in synaptic strength
53
how is synaptic strength measured and what causes changes in synaptic strength?
- synaptic strength is measured by changes in EPSPs (excitatory postsynaptic potentials)
- more synaptic strength = larger EPSP in the postsynaptic neuron
- changes can occur through:
1. Increased neurotransmitter release
2. Increased number or sensitivity of postsynaptic receptors
3. Both
- structural changes like dendritic growth can also contribute
Note: Synaptic strength can also decrease
54
what is Long-Term Potentiation (LTP) and what are the steps in seeing if LTP has occured?
LTP = a long-lasting increase in synaptic strength, linked to memory formation
Step 1: Stimulate axons at low frequency to establish baseline (small EPSP, no AP)
Step 2: Stimulate at high frequency (tetanus) → many action potentials (what happens when we form a memory)
Step 3: Return to low frequency → EPSP is now much larger
Conclusion: Input is stronger, synapse is potentiated, making postsynaptic neuron more likely to fire
55
where in the brain does LTP occur?
* LTP can occur anywhere in the brain where there are glutamate synapses
Hippocampus, Cortex, Amygdala, Striatum etc.
56
what are the two main types of ionotropic glutamate receptors? what are there similarities and differences? how do they work together for LTP?
AMPA and NMDA
- both allow Na+ to pass through and depolarize the neuron
- only NMDA allows Ca2+ to get into the neuron
- if neuron is hyperpolarized (at rest), NMDA receptor is blocked by Mg2+ ion, and it cannot be activated by glutamate
- AMPA receptors are not blocked, can always be activated by glutamate
- if AMPA receptors depolarize the neuron enough, Mg2+ block in NMDA is removed
- glutamate can now activate NMDA receptor and Ca+ can come into the cell
- calcium is responsible for LTP and long term changes in synaptic strength
57
what cellular mechanisms are responsible for the first phase of LTP?
- Ca+ enters the cell and activates enzyme pathways (kinases)
- kinases phosphorylates other proteins (adds phosphate group)
- Ca+ activates Calcium-Calmodulin (CaM) which then activates other kinases
- CaM Kinase hits latent AMPA receptor (floating inside cell) and inserts in membrane = more receptors
- protein Kinase C and Tyrosine Kinase can activate CREB = short term and long term effects
- CREB can lead to formation of retrograde messenger (molecule that goes from postsynaptic neuron to presynaptic terminal (Nitric Oxide)
- These messengers promote more transmitter release
increases synaptic strength by both pre and postsynaptic mechanisms
58
what are the two phases in LTP?
first phase: increase in receptors and glutamate release, occurs quickly (<1 hour), changes blocked by NMDA antagonists
second phase: CREB activates protein synthesis that causes long lasting changes (> 3 hours)
- changes dendrite shape and size, more ion channels
- changes are processed for hours after the initial memory was encoped
- second phase blocked by protein synthesis inhibitors
- both phases blocked by prevention of Ca2+ entry into the cell
- Ca2+ entry is localized, so only certain synapses/dendrites on a neuron will change synaptic strength
59
how have pharmacological studies shown us that LTP is a mechanism for memory?
- drugs that block LTP also disrupt learning
- blocking NMDA receptors during learning in...
○ Hippocampus = disrupt spatial learning
○ Amygdala = disrupt fear conditioning
○ Striatum = disrupt instrumental learning
- have to disrupt LTP before the learning in order to see impairment
- blocking protein synthesis disrupts other forms of learning
○ blocking protein synthesis immediately after training DOES disrupt memory formation
○ because longer term changes in neurons occur for some time after initial learning
60
how has behavioural electrophysiology shown us that LTP is a mechanism for memory?
- changes in neural activity resembling LTP that occur after learning
- lateral amygdala and fear conditioning: neurons fire more in response to CS+ after learning
* In vitro: train one group of rats on fear conditioning task, or the tone is not predictive of shock (unpaired), or no shock or tone
○ Remove brains 24 hours later: only rats that were trained on the task show increase in synaptic strength selectively amygdala pathways
○ Same amount of depolarization for the group with no tones or shocks, and the group with unpaired shocks/tones
61
what is the anatomy of the prefrontal cortex? what is different in rats?
* Involved in thinking, planning, coordinating between memories to retain goals, decision making
* Prefrontal cortex has very specific connections to the rest of the brain, we can differentiate it easily
* Medial and orbital regions = emotion regulation
* Dorsolateral regions in primates (humans) = working memory, flexibility, planning
* PFC functions develop late in humans (~2-3 years)
* The medial PFC in the rat shares some of the functions of the dorsolateral PFC in primates/humans
62
what is working memory?
Working memory = short term manipulation and retrieval of trial unique information
* Use info temporarily, manipulate it, then discard it
* Info is encoded in one form, but used to guide behaviour in another form
○ Ex. Remembering a sequence of digits: recalling digits forward = short-term memory
○ BUT recalling sequence backwards = working memory
* Can take information from long-term memory and manipulate it in working memory
63
how is the PFC related to working memory?
* PFC regulates executive functions, can be viewed as a conductor and commander of various cognitive skills
* Aids in selecting and successfully monitoring behaviours that facilitate the attainment of chosen goals
64
what is the delayed response task and how was it used on animals?
* "Delayed response" - classical PFC task that can be used across species
○ Animal acquires information, holds it over a delay and then uses it to guide a response
○ During "response" phase, animal must figure out where food may be based on what it saw
* Humans and primates: dorsolateral PFC lesions impair functioning in this task, even at the shortest delay
* Rats: medial PFC lesions impair delayed response
65
how was the delayed response task conducted on humans?
* Asked to look at fixation point and see where the black dot shows up, then point to where it was (after short delay)
* Trails are given in rapid succession with short inter-trial intervals
* On each trial, subject needs to distinguish the information to remember on that trial vs. previous ones
* This task taps into component processes of working memory that involve storage and manipulation of short-term information
66
what does neural activity look like during the delayed response task? what does this tell us about how the PFC helps with working memory?
* Record from PFC neurons: different neurons fire at different parts of task
* This activity is resistant to distracters (unlike similar activity in other brain regions)
* Brain activity during the delayed period predicts accuracy of response
○ Reduced delay activity = animal makes an error
* Multiple PFC neurons may “encode” different bits of information
* One theory is that activity of different groups of PFC cells “holds” different bits of information online
○ So that it can be manipulated to guide behavior
67
what is the wisconsin card sorting task? what does it measure?
Wisconsin Card Sorting Task: test behavioural flexibility (ability to change strategies)
1. Subjects must sort cards by one stimulus dimension (number of items on cards)
2. Then task switches, patients have to ignore old strategy and switch to new one (shape)
* When there is a new rule, patients are not told what they must do, or what the rule is
* Only given positive or negative feedback from experimenter (“yes, that is right”, “no that is wrong”)
68
how do patients with dorsolateral PFC damage perform on the wisconsin card sorting task?
* Patients with damage to dorsolateral PFC can learn first discrimination
* However they cannot switch strategies, keep sorting cards by first stimulus dimension (keep sorting by number) = perseveration
* Perseveration - not being able to switch tasks/rules, continuing to use the initial rule
69
how is the PFC involved in extinction learning?
* Give tone and shock pairings = rats freeze to tone
* KEEP giving tones with no shock = rats eventually stop freezing (extinction)
○ Extinction is not forgetting; it is a form of new learning that suppresses the old response
○ Fear memory doesn't fade away, it is actively suppressed
* PFC damage in rats does not disrupt learning of fear conditioning to cues or context
* However, rats with PFC damage take longer to extinguish fear response during extinction
* PFC is connected with the amygdala and PFC inputs can inhibit neural activity in the amygdala
○ Cortex tells the amygdala that it doesn't need to be scared of the stimuli anymore
69
how is behavioural flexibility tested in rats? what do we see when the PFC is inactivated?
* Day 1: rat learns Response Rule (always turn left)
○ Visual cue inserted in either left or right arm on each trial, rat must ignore cue (cue doesn't matter)
* Day 2: rat must now approach Visual Cue
○ Cue inserted in either left or right arm, rat must stop using old rule, engage in new one
* Reversible inactivation of PFC: infuse local anesthetic into PFC, lasts for ~1 hour
* Inactivate PFC during initial learning: no effect (PFC not involved in learning simple rules)
* Inactivate PFC during the shift: MAJOR impairment (PFC selectively involved in switching strategies)
69
how is the PFC involved in extinction learning and how do we know?
* Give tone and shock pairings = rats freeze to tone
* KEEP giving tones with no shock = rats eventually stop freezing (extinction)
○ Extinction is not forgetting; it is a form of new learning that suppresses the old response
○ Fear memory doesn't fade away, it is actively suppressed
* PFC damage in rats does not disrupt learning of fear conditioning to cues or context
* However, rats with PFC damage take longer to extinguish fear response during extinction
* PFC is connected with the amygdala and PFC inputs can inhibit neural activity in the amygdala
Cortex tells the amygdala that it doesn't need to be scared of the stimuli anymore
70
how is the prefrontal cortex responsible for planning?
* PFC keeps track of/helps plan sequences of action (Temporal Organization of Behaviour)
Ex. Cooking a meal, remember all ingredients and actions and put them together in a set sequence
71
how does PFC damage affect our ability to plan?
* PFC lesions = patient remembers particular items (long term memory in tact) but cannot order them correctly
ex. can remember all the ingredients, but cannot carry out various steps in proper sequence
* PFC damage impairs recalling the temporal order of events in memory
○ Ask patient "which movie did you see most recently", they remember what movies they saw but not where in time
72
what is the tower of london task and what does it measure? how does PFC damage affect our ability to carry out this task?
* assesses planning of a sequence of movements
* "move the balls from the start position to the final position in as few moves as possible"
* PFC patients need many more moves to reach goal positions, sometimes they don't reach the goal at all
73
what is the dinner party problem? how does PFC damage affect our ability to carry out this task?
* subject given a real world planning tasks
* Given 6 errands to run, also told to get answers to 4 questions (price of tomatoes)
* Explicitly told not to enter shops unnecessarily, and to finish as quick as possible
* PFC damaged patients are very inefficient, broke rules and failed on many tasks
* All patients remembered and understood rules and attempted to comply
* Not a memory deficit, but a deficit in integrating memory to form plan of action
74
what is the role of the hippocampus in learning and memory?
- critical for forming declarative (explicit) memories; episodic and semantic memory
- supports spatial and relational memory (navigating environments, encoding relationships between stimuli)
- contains place cells that encode specific locations based on spatial cues
- involved in memory consolidation — transferring info from short- to long-term memory
- shows long-term potentiation (LTP) — a cellular mechanism for strengthening synaptic connections and memory formation
75
what functions does the prefrontal cortex (PFC) serve in cognition? what do the different areas of the PFC do?
- directs executive functions: planning, decision-making, goal tracking
- supports working memory — short-term manipulation and use of trial-specific info
- organizes actions in time (remembering sequences like cooking steps)
- enables behavioural flexibility: adapting to rule changes (Wisconsin Card Sorting Task)
- regulates extinction learning by inhibiting fear responses via connections to the amygdala
Subregions:
* Dorsolateral PFC (humans) – planning, flexibility, working memory
* Medial/orbital PFC – emotion regulation
* Medial PFC (rats) – similar functions to dorsolateral PFC in humans
76
what is the function of the amygdala in memory and learning?
- mediates conditioning — learning emotional associations like fear responses
- LTP in the amygdala strengthens fear-related memories
- works with the PFC during extinction learning to suppress previously learned fear responses
77
what learning processes depend on the striatum?
- responsible for skill learning and instrumental learning (goal-directed movements)
- supports habit formation and learning through trial-and-error rewards
- damage to the striatum impairs new skill learning, but event memory may remain intact
