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Neuroscience 3 > Memory > Flashcards

Memory Flashcards

1
Q

Where are memories stored?

A
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2
Q

What was Kal Lashleys research (1920s)?

A

He wanted to see where memories are stored in rats, so removed bits of their cortex and tested their ability to remember a maze
found that
- the more cortex he removed the worse their memory was
- didn’t matter where the cortex was damaged, memory was still affected the same

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3
Q

What was Donald Hebb (1950s) research?

A

Investigated synaptic plasticity: thought that a stimulus activated a certain assembly of neurons, and that for as long as this assembly was active it = short-term memory. A longer stimulus strengthens the assembly to a point where if certains neurons in the assembly are activated, they activate the rest of the cells = long term memory

neurons that fire together wire together

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4
Q

Describe the case study of HM. What did we learn from him?

A

Had surgery to treat seizures where they removed his frontal lobe-> caused anterograde amnesia and partial retrograde amnesia
Learned that:
- damage to hippocampus/amygdala/cortex is not totally necessary for ALL memory; just consolidation
- suggested medial temporal lobe is not the site of long term memory since HM could remember stuff from childhood
- HMs short-term/working/non-declaritive memory was intact, just long term but was still able to drive a car and learn new skills, and priming was intact (aka non-declaritive) so medial temporal lobe not required for short-term/working/non-declaritive long term memory
- ability to make long term memories is unrelated to other cognitive functions since HM was normal except that

consolidation= converting new memory to long term

medial temporal lobe included hippocampus, amygdala, and entorhinal, perirhinal and parahippocampal cortex-> **HM tells us that these structures are needed for new long term declaritive but not short-term/working/new long-term non-declaritive memories **

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5
Q

What is anterograde amnesia? How is it tested?

A

Cannot form new memories after amnesia
Tested with recall and recognition of new words and pictures

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6
Q

What is retrograde amnesia? How is it tested?

A

Cannot remember long term memories (eg HM couldnt remember few years before surgery)
Tested with famous faces test, news events, autobiographical interview etc (questions that tap into semantic and episodic memory)

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7
Q

What is short term memory?

A

The process of storing small amount of info in brain for short amount of time
Rapid input and retrieval

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8
Q

What is long term memory? How is it divided?

A

Huge capacity to store information over long period of time
- Declaritive: explicit/represenational (eg semantic n episodic memory, consious recognition) aka WHAT
- Non-declaritive: implicit/procedural (eg skills, no consious recognition) aka HOW

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9
Q

What is working memory?

A

Temporary maintenance and manipulation of info
workspace for complex tasks like mental maths: combines storage and processing

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10
Q

What is a cell assembly and how could it support long term memory?

A

Cell assembly refers to Hebbs postulate, that cell assembly consists of all cortical cells activated by a certain stimuli, and that these cell connections strengthen over time and this provides long term memory

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11
Q

What evidence is there that declaritive and non-declaritive memory depend on different brain circuits?

A

HM case study: shows that declaritive memory is destroyed due to medial temporal lobe removal, but that non-declaritive memory works just fine

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12
Q

What is the difference between semantic and episodic memory?

A

Semantic: facts (eg words or capital cities)
Episodic: events (eg when? where? with whom?) and requires a lots more memory information than semantic

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13
Q

What tests would you use to test recognition memory?

aka declaritive memory

A
  • Delayed non-matching-to sample (DNMS) task: train monkey to pick up object it hasnt seen before-> exploits novel curiosity, and can test long term memory formation, then can test if lesions to brain affect this (eg lesions to medial temporal lobe made monkeys get it wrong after a longer delay)
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14
Q

What evidence is there that declaritive semantic memory is controlled by the perihinal cortex?

A
  • DNMS: only lesions to perihinal cortex (main) and hippocampus (a little) resulted in a delay dependent deficit-> means that perrihinal cortex is critical for object recognition memory, and hippocampus contributes but is not required
  • Jon: hippocampus was damaged at birth (semantic intact but episodic memory affected), but could recognise new objects just not by whom, where, and the order-> means that hippocampus is required for episodic memory (what when where) BUT not required for object recognition
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15
Q

How would you test episodic memory?

A

Virtual reality room: given different objects by different people in different rooms then asked questions abt what, who, where, and when:
- which object were you given
- who gave u the object?
- which of these objects were given to you in this room?
- Which of these objects were given to you first?

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16
Q

What evidence is there that the hippocampus contributes to declaritive episodic memories?

A
  • Virtual reality room test: Jon couldnt remember who/where/order of objects given-> means that hippocampus required for declaritive memory of episodic memory
  • Radial arm maze: tests spatial working memory, hippocampal lesions impairs memory of arms -> means that hippocampus required for declaritive memory of spatial information
  • Temporal odor task: two sand cups with diff smells, hippocampal lesions impaired ability to remember order of smell given-> means that hippocampus required for declaritive memory that involves temporal information

possible role of hippocampus in episodic memory is to provide the spatial and temporal features of events, and perhaps also to associate this info with the events themselves

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17
Q

What do PET studies in the neocortex tell us about priming?

A
  • activity in visual neocortex (lingual gyrus) is reduced when primed for word-stem completion task -> means less neural activity needed if it was previously presented
  • also indicates that changes in brain associated with priming occur v early in sensory pathway

aka testing non-declaritive memory

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18
Q

How do you test habit learning? What do habit learning studies tell us?

A

Radial maze arm test (rats): food is in illuminated arm, so rats built up habit of going into illuminated arms, found that striatal lesions impair habit but not spatial memory, whereas the reverse is found for hippocampal lesions-> means that the striatum is necessary for non-declaritive habit memory
Weather forecasting test (humans): humans try to predict the weather based on cards, and gradually approve over time (gut-feeling), amnesia patients are same as control but parkinsons patients cannot learn (bc they have loss of DA neurons into striatum)-> means striatum necessary for habit learning

hard to test non-declaritive in humans bc we use declaritive memory mainly
striatum (caudate and putamen) also important in skill learning

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19
Q

Which part of the brain controls short term memory? Evidence?

A

Prefrontal cortex: lesions to PFC in monkeys caused delay in remembering which object had a treat under it

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20
Q

What types of memory in rats are disrupted by lesions of the hippocampus?

A

Declaritive episodic memory involving temporal and spatial information

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21
Q

How is working memory tested? What did working memory tests tell us?

A

Wisconsin card sorting test: told to sort by color, number, shape; requires memory of previous cards, lesions to prefrontal cortex impaired ability to plan and organise->means that PFC needed for working memory

22
Q

What brain damage do children with developmental amnesia have? How does this affect their memory?

A

They have damage to the hippocampus due to deprived O2 at birth, this affects their declaritive episodic memory but not their ability to recognise objects and learn new tasks and skills (ie semantic memory is fine but their episodic is cooked)

23
Q

What is the role of the striatum in memory? How has this been demonstrated in rats and humans?

A

Needed for skill and habit learning
- sequence learning task (humans): learn to predict where the asterisk is going to show up; MTL lesion patients were unaffected, and PET scan showed that striatum is activated during this task
- radial maze arm task (rats)
- weather forecasting task (humans)

24
Q

What is the difference between small scale and large scale cognition?

A

Small scale= (eg mental rotation tasks)
- object based reference frames
- observer is stationary
- no long term memory used

Large scale= (ie navigation)
- multiple reference frames
- observer moves about
- short and long term memory used

25
Q

What is the difference between egocentric and allocentric reference frames?

A

Egocentric= centered on observer
- distances and directions are relative to observer, so when observer moves so does point of reference

Allocentric= world centered
- reference system is fixed and based on external coordinate system, so when observer moves only their position within reference changes

26
Q

What is path integration?

A

Tracking of ones position and orientation from a starting point based on self-motion cues

Eg: desert ants dont have any external clues on how to return home bc in desert, so use path integration to calculate a homing vector based on distance and directions travelled

27
Q

How can path integration be tested? What do these tests tell us

A

Feeder expt: Trained ants to go between nest and feeder, then removed the ants and put them in a different location, found: ants used same homing vector to try and return from transposed feeder

Triangle completion task: humans blindfolded and told to walk in a straight line back n forth, must rely on path integration since no environmental clues, over short distances humans r good but bad over long distances

Sahara desert (humans): set people off and they tended to walk in circles unless sun or moon was visible -> means that using self-motion cues (vestibular system, propioception, optic flow) is only good for short distances

28
Q

What is the role of the hippocampus and Medial Entorhinal Cortex (MEC) in spatial cognition?

evidence?

A

Path integration depends on hippocampus and MEC: rats follow a circular scented trail to food in the dark and return home by completing circle, rats with leisons to hippocampus and MEC have to turn all the way back on themselves to get home

29
Q

How is route learning tested and what does it tell us?

A

Tested with fMRI imaging: got people to memorize a pathway through a complex virtual environment, found that route retrival accuracy associated with activation of right caudate nucleus

30
Q

How is cognitive mapping tested? Which part of the brain is implicated?

A

Morris water maze: rats learn to swim to a hidden platform in middle of a pool, and use external landmarks to locate platform, rats with hippocampal lesions are impaired-> means that hippocampal computations are vital to allocentric place learning (aka cognitive mapping)

fMRI in virtual environment: trying to find shortest route between two locations, found that wayfinding accuracy associated with hippocampal activation

31
Q

Describe the evidence for hippocampal place cells in humans and in rats

A

In rats: put rat in black container with grey wall, when you moved the gray section the place cells followed area of grey wall so that they always fire in front of it

In humans: took intracortical recordings from patients in virtual environment, found that cells in hippocampus showed differential firing rates dependent on location-> first evidence for place cells in human hippocampus

32
Q

What is the difference between place, grid, and head direction cells?

A

Place= fires whenever an animal occupies a particaular location within its environment, controlled by visual cues (hippocampus)

Grid= individual cells firing at regular intervals along verticies of imaginary grid, controlled by visual AND self motion cues, may support path integration (MEC)

Head direction= fire when animal facing in a preffered direction, independent of its location, controlled by visual landmarks and self motion cues (postsubiculum and retrosplenial cortex)

medial entorhinal cortex= MEC

place cells- current location (you are here)
grid cells- distance info (scale of map)
head direction- directional information (current orientation)

33
Q

What aspects of spatial cognition do lesions to the MEC and hippocampus affect?

A
  • Path integration: lesions to MEC (grid cells) and hippocampus affected rats ability to generate homing vector (shown by winshaw and collegues)
  • Cognitive mapping: lesions to hippocampus affect spatial reference memory task (morris water maze)
34
Q

Describe three navigation strategies. What are their strengths and weaknesses?

A
  1. Path integration
    - weakness: not v good over long distances
  2. Route learning
    - weakness: inflexible
  3. Cognitive mapping
    - strengths: flexible (shortcuts)
35
Q

What cues provide self motion information?

A
  • optical flow
  • vestibular system
  • propioception
36
Q

Why is it important to start animals at different
locations in the water maze hidden platform task?

A

To ensure that they cannot follow a route back to the platform or swim towards a specific landmark, so it truely tests their ability to form a cognitive map

37
Q

How have fMRI studies enhanced our understanding of the neural basis of route navigation and cognitive mapping?

A

fMRI used in conjunction with virtual environment navigational testing
1) route learning (showed right caudate nucleus activation)
2) cognitive mapping (showed hippocampus activation)

38
Q

How do we study the brain mechanisms in emotion?

A
  1. Brain imaging (eg PET, fMRI scan)
  2. Pharmacological studies (eg NMDAR antagonist APV, inhibiting protein synthesis)
  3. Optogenetic studies (eg inhibiting amygdala)
39
Q

How is fear memory studied?

A

conditioning?

40
Q

What are the molecular mechanisms involved in fear conditioning?

A

Protein synthesis in amygdala

41
Q

Which brain regions are involved in fear learning?

A

Basolateral amygdala: inject APV (NMDAR antagonist) into it then freezing was reduced, this was not seen when injected into central amygdala

42
Q

What is memory reconsolidation and how can it be targeted for weakening fear memory?

A

Reconsolidation is when you reactivate a consolidated memory (aka comitted it to long-term), you can block protein synthesis during reconsolidation which blocks memory formation

  • Can weaken auditory fear memory (protein synthesis inhibitor reversed tone-shock conditioning)
  • Can weaken contextual fear memory (beta blocker reversed contexual-shock conditioning)
  • BUT does NOT work for weakening STRONG fear memories, only works in weaker fear memories
43
Q

How can fear memory be weakened?

A
  1. Extinction (inhibit it)
  2. Counterconditioning (counteract it)
  3. Blocking reconsolidation (blocking the restorable)
44
Q

How was the role of the amgldya in fear observed?

imaging

A

PET scan:
- fearful faces caused greater activation in left amygdala than happy ones

fMRI:
- amygdala more activated in response to the whites of fearful eyes
- amygdala much smaller in woman with Urbach-Wiethe disease

In vivo imaging:
- hypothalamus and lateral amygdala are more strongly activated in paired (tone&shock) than unpaired mice

45
Q

What can Urbach-Wiethe tell us about the role of the amgydla

A

Urbach-Wiethe is a disease resulting in defective social and personal descion making (aka no fear), and imaging of individuals brains with this disease shows that the amygdala is much smaller than normal- suggesting the amygdala controls fear response

46
Q

What can pharmacological studies tell us about fear learning?

A
  1. Applying APV (glutamatergic NMDA receptor antagonist) to the brain: blocking NDMAR in basolateral amydgala REDUCED freezing time (but not in central amygdala)-> means that NMDAR in BA is required in fear learning
  2. Protien inhibition in amygdala blocked long-term memory formation since % freezing was reduced
47
Q

How can optogenetics be used to study emotional memory?

A

Can use optagenetics to activate and inhibit neurons, so can selectively inhibit the amygdala in mice- did this and saw a reduction in freezing, suggests fear learning was inhibited

48
Q

Describe the information flow via amygdala in fear conditioning

A

Tone -> auditory thalamus -> lateral amygdala and auditory cortex

Shock-> somatosensory thalamus -> somatosensory cortex -> lateral amygdala

Lateral amygdala -> central amygdala -> periventricular nucleus (hormones) and lateral hypothalamus (blood pressure)

49
Q

How can you use extinction to weaken fear memory?

A

Give tone & shock to condition the animal, and then give a lot of tones with no shock (undoes condtioning)-> inhibits doesnt erase og learning
Lesions to rodent infralimbic cortex prevents the retention of extinction memories

HOWEVER
- og fear memory is temporarily inhibited but not unlearned at its source
- spontaneous recovery of fear learning over time

50
Q

How can you use counter conditioning to weaken fear memory?

A
  1. group told to focus on calming nature when blue stimulus (shock) is applied, and they have less response to stimulus than other group told to focus on the shock
  2. pair animal with scared or happy face, the happy face group show counterconditioning: reduce fearful memory in response to happy face

HOWEVER
- spontaneous recovery still occurs
- counterconditioning does not reduce the ‘return of’ fear

Neuroscience 3 (6 decks)

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