S1W9Mem Flashcards
Multi-store model (modal model) components and creators
Atkinson & Shiffrin (1968)
Sensory stores
STM
LTM
MSM Sensory Stores
Limited to one sense e.g. vision
Iconic store: visual
Echoic store: auditory
Attention moves info to STM or it decays
MSM Short term memory
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)
MSM Long Term Memory
Unlimited capacity
Semantic coding
Forgetting happens slowly
Support for MSM
Brain damage studies show distinction between LTM and STM (double dissociation).
Accounts for serial position (primacy/recency) effects
MSM Serial position effects
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.
Limitations of MSM
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.
Working Memory Model parts and theorists
Baddely & Hitch (1974) argued for more complex STM.
Central Executive Phonological Loop Phonological Store Articulatory Control Process Visuospatial Sketchpad
Central Executive
Control centre that coordinates subsystems
Allows us to select actions and allocates attention.
Phonological loop
Two parts:
Phonological store
Articulatory control process.
Phonological store
Holds acoustic/speech-based information for two seconds
Articulatory control process
Produces inner speech
Allows us to sub-vocally rehearse information to ourselves to keep it in the phonological store
Visuospatial sketchpad
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)
Dual-Task rationale for the WMM
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.
Articulatory suppression
The process of inhibiting memory performance by speaking while being presented with an item to remember.
Word-length effect (WLE)
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.
Evidence for divide of visual spatial sketchpad
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.
Corsi
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.
DeRenzi & Nichelli (1975) (Corsi)
Found that Corsi span (visualspatial sketchpad) and auditory digit span (phonological loop) could be impaired independently in patients with different lesions.
Limitations of Central Executive
Unknown what controls the controller (homunculus problem).
Evidence shows that executive functions are not underpinned by a single mechanism.
Coherence and the binding problem
By assuming separate memory sub-systems the model creates a binding problem.
Episodic buffer (Baddely)
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.
Neural basis of phonological loop
Left inferior frontal gyrus (IFG)
Bilateral parietal cortices.
The left IFG important for inner speech.
Zimmer (2008) - review of brain imaging studies
Visual STM: Occipital and Temporal Cortices.
Spatial STM: Parietal cortex
Neural basis of inner scribe
Neuroimaging doesn’t support the role of rehearsing visual information a messenger between the visual cache and the CE.
Neural basis of CE
Prefrontal cortex
This is supported by rTMS to dorsolateral prefrontal cortex disrupting executive processes.
Prefrontal Cortex+
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.
Processing levels
Deeper processing makes more elaborate, longer lasting and stronger memories.
Incidental learning
Participants performed tasks involving a number of words, but were not aware that their memory for these words would be tested.
Craik and Tulving (1975)
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).
Distinctiveness
the more distinctive information is, the more likely it is to be remembered
Relevance
more likely to remember informatio for something they know a lot about/something related to them.
Emotionality
emotional stimuli are automatically processed more deeply than neutral.
Memory of emotional stimuli
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.
4 parts of neuron
Cell body (soma) - contains genes.
Dendrites
Axon
Presynaptic Terminals
Endoplasmic reticulum
Synthesises protein in cell body.
Action potentials
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.
Synapse
Point at which two neurons communicate.
Post and presynaptic cells
Transmitting signal = presynaptic cell.
Receiving signal = postsynaptic cell.
Both are separated by synaptic cleft (don’t touch).
Resting potential
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.
Ions
Electrically charged particles (have an electrical charge due to an unequal number of protons and electrons).
Stimulation = action potential
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.
Absolute refractory periods
The membrane is not sensitive to stimulation.
An additional stimulus will not make the AP’s amplitude larger.
Relative refractory periods
Additional AP can occur.
More difficult than usual as the membrane is hyperpolarised iso takes larger stimulus to depolarise.
Long term potentiation
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.
Specificity (LTP)
only synapses onto a cell that have been highly active become strengthened.
Cooperativity (LTP)
Simultaneous stimulation by two or more axons produces LTP much more strongly than does repeated stimulation by a single axon.
Associativity (LTP)
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.
LTP in the hippocampus
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.
LTP and presynaptic changes
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.
Long term depression (LTD):
Prolonged decrease in response at a synapse that occurs when axons have been less active than others.
