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BCB > S1W9Mem > Flashcards

S1W9Mem Flashcards

1
Q

Multi-store model (modal model) components and creators

A

Atkinson & Shiffrin (1968)

Sensory stores
STM
LTM

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2
Q

MSM Sensory Stores

A

Limited to one sense e.g. vision

Iconic store: visual

Echoic store: auditory

Attention moves info to STM or it decays

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3
Q

MSM Short term memory

A

Very limited capacity

Digit span tasks 7 (+/- 2)

Chunking info together improves capacity

Information held longer using rehearsal

Rehearsal moves information into LTM

Items can be lost through displacement (new items push out older items)

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4
Q

MSM Long Term Memory

A

Unlimited capacity

Semantic coding

Forgetting happens slowly

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5
Q

Support for MSM

A

Brain damage studies show distinction between LTM and STM (double dissociation).

Accounts for serial position (primacy/recency) effects

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6
Q

MSM Serial position effects

A

Primacy occurs as early items receive extra rehearsal which copies them into LTM.

Recency occurs as last items are available in STM immediately after before decaying.

Each item receives a fixed number of rehearsals: primacy drops.

30 second distraction delay: recency disappears.

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7
Q

Limitations of MSM

A

Oversimplified stores.

Assumes STM is a gateway to LTM and so info hasn’t had contact with LTM (chunking into meaningful groups means it must have done).

Assumes all info in STM is of equal status.

Assumes info gets to LTM through rehearsal.

Says that unconsciously processed info shouldn’t reach LTM but it does.

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8
Q

Working Memory Model parts and theorists

A

Baddely & Hitch (1974) argued for more complex STM.

Central Executive
Phonological Loop
Phonological Store
Articulatory Control Process
Visuospatial Sketchpad
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9
Q

Central Executive

A

Control centre that coordinates subsystems

Allows us to select actions and allocates attention.

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10
Q

Phonological loop

A

Two parts:

Phonological store

Articulatory control process.

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11
Q

Phonological store

A

Holds acoustic/speech-based information for two seconds

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12
Q

Articulatory control process

A

Produces inner speech

Allows us to sub-vocally rehearse information to ourselves to keep it in the phonological store

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13
Q

Visuospatial sketchpad

A

Allows us to maintain and manipulate visual/spatial images.

Two parts:

Visual cache: (VISUAL) stores information about visual form and colour

Inner scribe: (SPATIAL) and rehearses information in the visual cache and transfers it to the central executive (involved in body movements)

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14
Q

Dual-Task rationale for the WMM

A

WMM permits performance of more than one cognitive task at a time provided each one is processed by a different subsystem.

Evidence from dual-task experiments (people do two things at once).

If simultaneous processing hurts performance then the tasks use a similar subsystem.

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15
Q

Articulatory suppression

A

The process of inhibiting memory performance by speaking while being presented with an item to remember.

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16
Q

Word-length effect (WLE)

A

WMM suggests the number of items recalled depends on how often they can be rehearsed by the articulatory control process.

The shorter the words the more they can be rehearsed to prevent decay.

Word length effect: more short words recalled than long words.

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17
Q

Evidence for divide of visual spatial sketchpad

A

When a visual task and a spatial task are performed together there is little interference.

Some brain damaged patients show damage to visual but not spatial function

Imaging data suggests two components of visualspatial sketchpad in different brain regions.

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18
Q

Corsi

A

Assesses visuo-spatial working memory.

Involves mimicking a researcher as she taps a sequence of blocks (starts out simple but gets more complex).

Average Corsi span is 5.

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19
Q

DeRenzi & Nichelli (1975) (Corsi)

A

Found that Corsi span (visualspatial sketchpad) and auditory digit span (phonological loop) could be impaired independently in patients with different lesions.

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20
Q

Limitations of Central Executive

A

Unknown what controls the controller (homunculus problem).

Evidence shows that executive functions are not underpinned by a single mechanism.

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21
Q

Coherence and the binding problem

A

By assuming separate memory sub-systems the model creates a binding problem.

22
Q

Episodic buffer (Baddely)

A

Addressed binding problem.

A link between the WM subsystems and the LTM.

Limited capacity, temporary store that supports recall and integrates phonological, visual and other information to in STM.

23
Q

Neural basis of phonological loop

A

Left inferior frontal gyrus (IFG)

Bilateral parietal cortices.

The left IFG important for inner speech.

24
Q

Zimmer (2008) - review of brain imaging studies

A

Visual STM: Occipital and Temporal Cortices.

Spatial STM: Parietal cortex

25
Q

Neural basis of inner scribe

A

Neuroimaging doesn’t support the role of rehearsing visual information a messenger between the visual cache and the CE.

26
Q

Neural basis of CE

A

Prefrontal cortex

This is supported by rTMS to dorsolateral prefrontal cortex disrupting executive processes.

27
Q

Prefrontal Cortex+

A

Other regions other than prefrontal cortex used in CE.

Stuss et al. (2011): Patients with cortical damage have executive function deficits with no prefrontal damage.

Hedden and Gabrieli (2010): Found shared and distinct areas involved in inhibition and switching in and out of the prefrontal cortex.

28
Q

Processing levels

A

Deeper processing makes more elaborate, longer lasting and stronger memories.

29
Q

Incidental learning

A

Participants performed tasks involving a number of words, but were not aware that their memory for these words would be tested.

30
Q

Craik and Tulving (1975)

A

Incidental learning task.

Conditions differed in terms of processing level:

Shallow graphemic: decided whether word was uppercase or lowercase.

Intermediate phonemic: decide whether words rhymed with target word.

Deep semantic: decide whether word fits a blank in a sentence.

Memory 3x higher for deeper processing.

When sentence was complex memory was also better (elaboration).

31
Q

Distinctiveness

A

the more distinctive information is, the more likely it is to be remembered

32
Q

Relevance

A

more likely to remember informatio for something they know a lot about/something related to them.

33
Q

Emotionality

A

emotional stimuli are automatically processed more deeply than neutral.

34
Q

Memory of emotional stimuli

A

Activates the amygdala.

Greater processing of negative or threat related information has a clear evolutionary advantage.

Greater processing leads to better memory for emotional (especially negative) information.

35
Q

4 parts of neuron

A

Cell body (soma) - contains genes.

Dendrites

Axon

Presynaptic Terminals

36
Q

Endoplasmic reticulum

A

Synthesises protein in cell body.

37
Q

Action potentials

A

Axons convey action potentials from 0.1mm to 3m.

Rapid, transient and all-or-nothing nerve impulses.

Amplitude of 100mV and duration of 1ms.

Initiated at the axon hillock then travel down axon.

Presynaptic cells transmit signals from the axon branches (terminal buttons).

Terminals end on the postsynaptic cell’s dendrites, body or axon.

38
Q

Synapse

A

Point at which two neurons communicate.

39
Q

Post and presynaptic cells

A

Transmitting signal = presynaptic cell.

Receiving signal = postsynaptic cell.

Both are separated by synaptic cleft (don’t touch).

40
Q

Resting potential

A

At rest, cells maintain a difference in electrical potential on the outside and inside of the membrane.

Typically = 70mV.

Arbitrarily define the charge outside the cell as zero, so say that the resting potential is -70mV.

Positively charged potassium and sodium ions (K+ and Na+) and negatively charged amino acids and proteins cause resting potential.

Unequal distribution maintained by a membrane protein pumping Na+ out of the cell and K+ back in.

41
Q

Ions

A

Electrically charged particles (have an electrical charge due to an unequal number of protons and electrons).

42
Q

Stimulation = action potential

A

Alters the membrane potential.

If the stimulus is strong enough, it will cause action potential.

APs are generated by a sudden influx of Na+ ions.

When an input signal depolarizes the cell membrane, the change in potential opens Na+ channels.

Allows Na+ to flow from outside (Na+ concentration high) to inside the cell (Na+ low)

Activity of all synaptic potentials is summed and if the size of the input signal reaches threshold neuron fires AP.

If it doesn’t reach threshold it returns to resting potential.

43
Q

Absolute refractory periods

A

The membrane is not sensitive to stimulation.

An additional stimulus will not make the AP’s amplitude larger.

44
Q

Relative refractory periods

A

Additional AP can occur.

More difficult than usual as the membrane is hyperpolarised iso takes larger stimulus to depolarise.

45
Q

Long term potentiation

A

Reflects increased activity by presynaptic neuron and increased responsiveness by postsynaptic neuron.

Occurs when one or more axons bombard a dendrite with stimulation.

Leaves the synapse potentiated and the neuron more responsive.

LTMs are created by changes at the synapses in the hippocampus.

46
Q

Specificity (LTP)

A

only synapses onto a cell that have been highly active become strengthened.

47
Q

Cooperativity (LTP)

A

Simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon.

48
Q

Associativity (LTP)

A

When weak stimulation of a single pathway is insufficient for the induction of LTP, simultaneous strong stimulation of another pathway will induce LTP at both pathways.

49
Q

LTP in the hippocampus

A

Glutamate excitation of AMPA receptors depolarizes the membrane.

Depolarization displaces magnesium that were been blocking NMDA receptors.

Glutamate then able to excite NMDA receptors, opening channel so calcium enters the neuron.

Entry of calcium triggers further changes.

More AMPA receptors built and dendritic branching increases.

This potentiates the dendrite’s future responsiveness to incoming glutamate.

50
Q

LTP and presynaptic changes

A

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

Causes:

Decrease in AP threshold.

Increase neurotransmitter release .

Expansion of axons.

Transmitter release from additional sites.

51
Q

Long term depression (LTD):

A

Prolonged decrease in response at a synapse that occurs when axons have been less active than others.

BCB (19 decks)

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