Memory Flashcards

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1
Q

What is memory?

A
  • The capacity to encode, store and retrieve information

- A lasting trace of past experiences that influence current or future behaviours

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2
Q

What does it mean to say that the different forms of memory appear to be separable?

A

One can be damaged leaving another in tact

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3
Q

What are the two divisions of long term memory?

A

Explicit (Declarative)

Implicit (Non Declarative) aka procedural memory

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4
Q

What does “implicit” (non-declarative memory refer to?

A

The memory/performance of things that takes place without our awareness e.g. skills that were learned with awareness but are now performed without thinking (procedural)

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5
Q

What is the Serial Reaction Time Task (SRT task)?

A

A common way to test procedural memory

  • A shape appears in one of 4 locations on a screen, Ps have to press corresponding button ASAP
  • This repeats with the shape appearing in different positions in random order
  • The first block of the task is in Pseudo-random order for 24 trials, AKA Baseline (B)
  • The second block of the task is an Implicit Learning Block (IL), shape follows a sequence for 12 trials
  • Baseline and Implicit Learning Blocks alternate
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6
Q

What happens to Reaction Times in the Serial Reaction Time (SRT) Task?

A

Implicit Learning block RTs decrease over time to a greater extent than for Baseline blocks

  • because when the IL sequence appears again, Ps motor responses are faster than the first time they saw it because its familiar (even though they don’t know)
  • RT for B is likely to decrease over time due to practice
  • RT for IL will decrease significantly due to implicit sequence learning
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7
Q

What did Rauch et al., 1997 find in their fMRI study with the Serial Reaction (SRT) task?

A

Found increased activation in the right striatum during sequence learning compared with baseline blocks
Found that in Ps who showed greatest amount of implicit learning, the magnitude of activation in the right putamen was correlated with the decrease in RT

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8
Q

Which form of long term memory is the Medial Temporal Lobe (MTL) crucial for?

A

Declarative memory

  • episodic
  • autobiographical
  • semantic
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9
Q

What happens to memories in the hippocampus?

A

Consolidation

they change from being short-term to long-term

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10
Q

What factors effect Consolidation?

A
  • depth of stimulus processing
  • distinctiveness
  • relevance
  • emotionality
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11
Q

How do stressful or emotionally exciting experiences effect memory consolidation & storage?

A

Adrenaline and cortisol secretion increase
- small to moderate amounts of cortisol activate the amygdala & hippocampus, which increases memory consolidation and storage

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12
Q

What is the benefit of greater processing of negative or threat related information?

A

Allows for better avoidance of dangerous situations

- clear evolutionary advantage

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13
Q

What is re-consolidation?

A

When a memory is reactivated (retrieved/remembered), it is brought into a labile state

  • in this labile state it is fragile/malleable
  • so the memory can be weakened or altered
  • OR the memory can be strengthened
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14
Q

What brain mechanisms are used to consolidate a long-term memory?

A
  • Specific axon repetitively stimulation another axon leads to growth/metabolic change that would connect them more strongly (Hebb)
  • Changes happening at the synapse between neurons of the hippocampus cause memories to be created
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15
Q

What is Long Term Potentiation (LTP)?

A
  • The way memories are consolidated
  • Changes that happen at the synapse between neurons of the hippocampus, when one or more axons bombard a dendrite with stimulation
  • Mainly depends on activity at Glutamate synapse
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16
Q

What is Long Term Potentiation called Long Term Potentiation?

A

Because the repeated stimulation leaves the synapse “potentiated” for a period of time, mean it is more responsive

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17
Q

What types of Glutamate receptor are important for Long Term Potentiation (LTP)?

A

AMPA

NMDA

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18
Q

Why are the AMPA and NMDA Glutamate receptors known as ‘inotropic receptors’?

A

Because when they are stimulated they open channels for ions to pass through

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19
Q

What is meant by ‘AMPA is a typical inotropic receptor’?

A

It opens sodium channels (Na+) when stimulated by Glutamate

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20
Q

What does NMDA’s response to Glutamate depend on?

A

The polarity of the membrane (the membrane potential)

- Sodium cannot enter until it is depolarised

21
Q

What happens when Glutamate attaches to the AMPA and NMDA receptors on a resting neuron?

A

At AMPA receptor: it opens a channel to let sodium ions enter
At NMDA receptor: it binds but usually fails to open channel, which is blocked by magnesium ion, because they are too big to get the NMDA receptor’s channel

22
Q

What does repeated Glutamate excitation of AMPA receptors do?

A

Depolarises the membrane
- because the AMPA receptor is letting positively charger sodium (Na+) into the cell, making the membrane potential more positive

23
Q

What happens to magnesium molecules (Mg) that are blocking NMDA receptors, when the membrane of a neuron is depolarised?

A

They are displaced

  • the Mg molecules were attracted to the cell because the cell was negative and the Mg molecules are positive
  • when the cell depolarises it is less negative, so the Mg molecules are not so strongly attracted and dislodge
  • the NMDA channel is now free for other ions, so Sodium (Na+) and Calcium (Ca++) flood into the neuron
24
Q

What happens to the neuron when Calcium (Ca++) floods into the cell through the NMDA receptor, once Magnesium (Mg) has been dislodged?

A
  • Calcium activates a protein called CaMKII
  • CaMKII begins a series of reactions that leads to the release of a protein called CREB
  • CREB goes to the cell’s nucleus & regulates the expression of several genes - this altered gene expression can continue for as long as a memory persists
  • new AMPA receptors are created as a result & there is an increase in the formation of new synapses
  • all of these changes make LTP modifications long lasting
25
Q

What magnifies the effects of CaMKII and CREB proteins?

A

A protein called BDNF

26
Q

When neurons are repeatedly activated, only those with the highest concentrations of what proteins will undergo LTP?
What results occur at the synapse when they do undergo LTP?

A

CaMKII, CREB, BDNF

  • dendrites make extra AMPA receptors, or move existing ones into positions
  • dendrites make more branches & spines - creating more synapses with same axon
  • phosphate groups attach to AMPA receptors, making them more responsive
  • neuron makes more NMDA receptors
27
Q

What changes in a presynaptic neuron can cause LTP?

A

Extensive stimulation of a postsynaptic cell causes the release of a retrograde transmitter that travels back to the presynaptic cell to cause:

  • a decrease in action potential threshold
  • an increased neurotransmitter release
  • expansion of the axons
  • transmitter release from additional sites
28
Q

What are the main properties of LTP?

A

Specificity
- only synapses on cells that have been highly active become strengthened, because activated CaMKII remains at the stimulated synapse
Cooperativity
- simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon
Associativity
- pairing a weak input with a strong input enhances later responses to a weak input

29
Q

What is the evidence for sleep improving both declarative and procedural memory?

A

Compared with a period of wakefulness of equal length, a period of post-learning sleep enhances retention of declarative information (facts) and improved non-declarative procedural performance

30
Q

What is meant by declarative memory?

A

Consists of facts and events that can be consciously recalled or “declared”

  • also known as explicit memory
  • type of long-term memory
31
Q

How are the beneficial effects of sleep on declarative memory enhanced?

A

If sleep takes place immediately after learning rather than after a delay (even just a 1hr nap).

32
Q

Sleep deprivation is associated with explicit learning and memory problems.
What did a review by Kreutzmann, Havekes, Abel & Meerlo (2015) find in regards to this being due the effects of SD on the hippocampus?

A
  • SD prior to learning inhibits hippocampal-dependant encoding
  • SD following learning inhibits hippocampal-dependant consolidation
  • SD appears to inhibit neurogenesis - the growth of new neurons - and long-term potentiation (LTP)
  • Chronic SD leads to a shrinkage of the hippocampus
33
Q

How does exercise improve the declarative memory?

A

Seems to cause an increase in the BDNF protein

34
Q

What can non-clinical forgetting be caused by?

A

Decay
- passive process
- simplest explanation for forgetting
Interference
- memories acquired on different occasions interfere with one another
- similarity of memories impacts interference

35
Q

What is meant by Retroactive interference?

A

Interference = an explanation for forgetting

retroactive inference = acting backwards (new memories affect old memories)

36
Q

What is meant by proactive interference

A

Interference = an explanation for forgetting
Proactive interference = acting forwards (previous memories affect the ability to form/keep new memories) e.g. trying to remember a new phone number instead of your old one

37
Q

How did McGeoch (1932) explain his belief of trace decay theories of forgetting being invalid?

A

Said time itself is not a causal agent

  • Iron rusts over time, but time does not cause the rusting, it is the process of oxidisation that does the damage
  • Therefore argued interference is the only true forgetting mechanism
38
Q

What is directed forgetting?

A

Phenomenon involving impaired long-term memory, triggered by instructions to forget information that has been presented for learning
- Allows us to see how we can intentionally control our memory, to look at neural differences in responding to intentionally compared vs unintentionally forgotten material

39
Q

What are the two phases in the Directed Forgetting (DF) Paradigm (MacLeod, 1989)?

A

Study phase
- Participants are shown a series of words or pictures which they are instructed to either remember or forget after each stimulus
Test phase
- Participants are tested on their recognition of study (indicate whether a word or picture is old or new) or their free recall of the study words

40
Q

How is the Directed Forgetting Effect (DFE) calculated after the Directed Forgetting (DF) task?

A

Take the number of to-be-forgotten words that were remembered (TBF-R), from the number of to-be-remembered words that were remembered (TBR-R)
DFE = TBR-R - TBF-R

41
Q

What does the Directed Forgetting (DF) Paradigm consistently show?

A

Significantly greater memory for the TBR words compared to TBF words

42
Q

What are the two Mechanisms of Directed Forgetting?

A
  1. Selective Rehearsal
    - TBR items are subjected to more elaborative processing and more repeated rehearsal than TBF items
  2. Active Suppression
    - TBF instruction leads to recruitment of inhibitory mechanisms which terminate further processing of TBF items, and suppress their memory to below-baseline levels
43
Q

What are Event-Related Potentials (ERPs)?

A

A measure of electroencaphalography (EEG)
- Can be used to examine remembering & forgetting
If we take a portion of activity at the beginning of each trial of an experiment, and average them together, we see a distinct waveform showing when and where different neural events happen

44
Q

What did Paz-Caballero et al., 2004 look at using Event-Related Potentials (ERPs) during the Directed Forgetting (DF) Paradigm?

A
  • Looked at brain activity happening in response to the “remember” and “forget” cues in Ps with high compared to low DFEs (Directed Forgetting Effects)
45
Q

What did Paz-Caballero et al., 2004 find in their study using Event-Related Potentials (ERPs) during the Directed Forgetting (DF) Paradigm?

A
Ps with high DFEs (who had been able to remember the TBR words and forget the TBF words) showed a very early difference between the cues at front regions: 
- showing more positive voltage activity by the Forget cue compared to Remember cue 
      - this shows frontal 
        inhibition mechanisms 
        being used by Ps that 
        were able to successfully 
        suppress the word when 
        given "forget" cue
- greater positive voltage in response to the remember cue 
      - shows activation of a 
        rehearsing or 'refreshing' 
        process
46
Q

What effect might emotional stimuli being processed more deeply than neutral stimuli have on Directed Forgetting (DF)?

A

Hauswald et al., (2011):

  • found there was significant DFE (Directed Forgetting Effect) for neutral photos, but they disappeared for negative photos
  • Suggesting showing negative information is harder to forget then neutral information
  • Mean ERP is response to negative pictures were more positive then neutral pictures - suggesting greater (deeper) processing of negative pictures
47
Q

Why do Hauswald et al., (2011) suggest negative information is immune to directed forgetting?

A
  • Negative images are processed more deeply than neutral

- Suppression of the memory trace is less successful

48
Q

What is Clinical Forgetting?

A

Injuries or illnesses of the brain can teach us a lot about the way they affect cognitive functions and behaviours
e.g. Amnesia