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Learning and Memory Flashcards

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1
Q

BRAIN CHANGES

A
  • some brain changes (BD/brain stimulation) can effect human beh/perception/cog/emotions/memory
  • other changes occur in brain/NS during prenatal development in early life
  • changes continue in later life w/ongoing experience/when aging/in dif contexts/environments as during early years
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2
Q

EXPERIENCE-DEPENDENT PLASTICITY

A
  • changes caused by previous experience can be observed at level of:
    BEHAVIOUR
  • actions/emotions/knowledge
    NEURONS
  • neural network activity
    SYNAPSES
  • interactions between individual neurons
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3
Q

HM

A
  • BD often causes memory loss for earlier events (retrograde amnesia) within limited time period of hours/days/years
    HM (1926-2008)
  • severe epilepsy; underwent bilateral medial temporal lobotomy; anterograde amnesia (LTM loss for new events/newly learned info) after surgery
  • most of HM’s hippocampus/amygdala/subcortical regions/entorhinal cortex = damaged; some probs spared
  • parahippocampal cortex fully removed
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4
Q

DIF BRAIN AREAS INVOLVED IN MEMORY FORMATION

A
  • HM’s cog abilities/STM/episodic memories/info learned pre-operation = largely preserved
  • could acquire new motoric skills (ie. tracing shape in mirror) BUT couldn’t recall performing same task before
    SCOVILLE & MILNER (1957)
  • provided first evidence for involvement of hippocampus in memory formation (confirming Bekhterev’s observations)
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5
Q

THE MEMORY ENGRAM

A

LASHLEY (1929/1950)

  • maze-learning exps w/rats w/parts of cerebral cortex surgically removed
  • unsuccessful in attempts to find memory engram (localised memory trace in cortex)
  • concluded that learning & memory not located in single area of rat cortex BUT distributed widely across brain
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6
Q

NEUROPSYCHOLOGY/PSYCHIATRY RESEARCH LIMITS

A
  • major limits for investigating causal relations between neural substrates/beh/psych processes in humans
  • ethical consideration of brain manipulations/measurements
  • number of patients w/lesions = small
  • cases don’t generalise
  • coarse damage across functional units
  • possible compensatory processes (beh change/functional reorganisation of brain circuits)
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7
Q

NEUROPSYCHOLOGY/PSYCHIATRY RESEARCH POSITIVES

A
  • (specifically animal models)
  • overcome some ethical limits
  • replication/precision of lesions
  • availability/sample sizes (2-3 pps in primates; more in rodents/non-mammalian models (ie. sea hare Aplysia/Drosophila flies/zebrafish larvae)
  • systematic study of wider method/beh/psych processes range providing circuit/synaptic level insights
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8
Q

SURGICAL LESIONS VARY IN PRECISION

A
  • rhinal cortex includes entorhinal/perirhinal cortex in medial temporal lobe
  • traditional method in experimental neuroscience to causally infer bran area function
  • neurons ablated applying physical (ie. suction)/pharmacological (ie. neurotoxin injections/pathologically high neurotransmitter concentrations) methods
  • neuron loss = permanent/significant damage of non-target tissues in surrounding areas
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9
Q

OPTOGENETICS: PRECISE TEMPORARY INACTIVATION OF NEURONS

A
  • ChR2 = channel-rhodopsin
  • NpHR = halo-rhodopsin
  • functional control of targeted cell types using light of specific wavelength
  • micro-stimulations during beh tests w/high spatial/temporal precision
  • reversible/temporary manipulations allowing in-pp comparisons
  • light-sensitive molecules inserted in membrane via genetic tools; animals selectively bred to generate transgenic lines to investigate specific brain circuits
  • genetically tractable models (ie. mice/Drosophila flies/zebrafish larvae)
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10
Q

EPISODIC-LIKE MEMORIES IN NON-HUMAN ANIMALS

A
  • episodic memory = recall of unique experiences explicitly located in past (“mental time travel”) as conscious experience; language based reports
  • delayed non-matching to sample task (DNMST)
  • test requirements = specific events/objects; familiarity/novelty; context/environment; time
  • ability to form/recall memories for personally experienced past events tied to specific context
  • novelty/familiarity judgements (delayed non-matching to sample)
    CLAYTON & DICKINSON (1998)
  • retrieval of when/where/what memories
  • learning of context-dependent tasks in scrub jays
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11
Q

TARGETED LESIONS IN MEDIAL TEMPORAL LOBE

A

SQUIRE & ZOLA-MORGAN (1991)

  • hippocampus involved in encoding specific items in context during LTM formation
  • perirhinal cortex important for familiarity sense
  • parahippocampus encodes context representations
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12
Q

DECLARATIVE LTM MEMORY

A

CLARK (2019)
FAMILIARITY/KNOWING WHAT
- declarative (episodic (events)/semantic (facts)) -> medial temporal lobe
- hippocampus (HM)
- mamillary bodies (NA/Korsakoff syndrome)
- neocortex (KC)

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13
Q

NON-DECLARATIVE LTM MEMORY

A 
CLARK (2019)
KNOWING HOW
1. PRIMING
- neocortex
- exposure to stimulus improves responses to same/similar stimulus 
2. NON-ASSOCIATIVE
- reflex pathways
- brainstem; medial cerebellum parts
- startle response
3. PROCEDURAL 
- striatum 
- basal ganglia
- acquisition of motor skills/habits
4. CLASSICAL CONDITIONING (EMOTIONAL/SOMATIC) 
- E = amygdala (fear conditioning)
- S = cerebellum (eye-blink conditioning/sensorimotor tasks)
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14
Q

NON-ASSOCIATIVE LEARNING: HABITUATION

A
  • response weakens w/repeated stimulus presentation due to repetition BUT not due to senses/fatigue adaptation
  • NOT extinction of associations acquired via learning
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15
Q

NON-ASSOCIATIVE LEARNING: DISHABITUATION

A
  • repeated tactile stimulation of siphon leads to reduced gill withdrawal response
  • response reinstated after stimulation via dis stimulus
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16
Q

LTM X NON-ASSOCIATIVE LEARNING

A

CAREW (2000)

  • training sessions over 4 days (T1-T4)
  • memory recall test on next day (R1)
  • test week later (R2)
  • memory retained for 3 weeks (R3)
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17
Q

PAVLOV’S DOG

A

PAVLOV (1849-1936)

- when dog receives food, it salivates (UR (unconditioned response)); dogs already salivating before given food

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18
Q

PD: CS-US CONTINGENCY

A
  • if sound (CS) always shortly precedes food (US) then dog will learn that sound predicts food SO starts to salivate (CR) on hearing sound
  • contingency = CS predicts occurrence of US meaning; its contingent on prior occurrence of CS
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19
Q

PD: APPETITIVE ASSOCIATION

A
  • degree of CS/US coincidence determines learning outcome
  • temporal contiguity = reinforcement most effective if reward coincides/follows CS shortly after (forward CS/US pairing)
  • US should be unexpected/surprising prior to conditioning; animal needs to attend CS
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20
Q

EYE-BLINK CONDITIONING

A
  • prior to training:
  • US = air puff; UR = eye blink
  • CS = tone; CR = tone alone elicits eye blink
  • neuronal circuit involves cranial nerves/nuclei connecting interneurons/cerebellum
  • sensory input US: trigeminal nerve (cranial nerve V)
  • CS input = auditory nuclei
  • motor output = cranial nerves VI/VII (fascial/eye muscles)
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21
Q

CONTEXTUAL/CUED FEAR CONDITIONING

A
  • mild foot shock elicits freezing/increased blood pressure/heart beat
  • cued conditioning (tone predicts punishment)
  • contextual conditioning (box alone predicts punishment)
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22
Q

STIMULUS-RESPONSE LEARNING

A

THORNDIKE (1898)

  • proposed animals learn based on outcomes of actions (Law of Effect)
  • when response followed by reinforcer, stimulus-response (S-R) connection strengthened
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23
Q

OPERANT CONDITIONING

A

WATSON/SKINNER

  • strongly influence ideas -> 1920s behaviourism emergence as research field dedicated to operant conditioning study
  • reinforcement learning = if beh reinforced, it’ll be repeated/extinguished
  • animals mainly tested in boxes (Skinner’s box)
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24
Q

TEMPORAL MEMORY FORMATION STAGES

A
  • shortest memories in sensory buffers (iconic memories) ie. during reading when eye makes saccade
  • STM/WM = few seconds to maximally few min long
  • intermediate memory = longer but not like LTM
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25
Q

ENCODING/RETRIEVAL/CONSOLIDATION

A
  • brain activation patterns differ when info encoded/acquired and later recalled (ie. recognition of visual stimulus)
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26
Q

CONNECTIVITY CHANGE DURING ENCODING/CONSOLIDATION

A

ENCODING
- hippocampus-dependent encoding of interconnected sensory attributes (stimulus/context)
RETRIEVAL OF MEMORY BEFORE CONSOLIDATION
- hippocampus-dependent retrieval of learned info
RETRIEVAL OF CONSOLIDATED MEMORY
- retrieval w/o hippocampus involvement

27
Q

STANDARD LTM CONSOLIDATION MODEL

A
  • connections between hippocampus/various cortical modules critical for encoding/consolidation BUT not later retrieval/reconsolidation
  • hippocampus inhibited by prefrontal cortex; time-limited role
  • strengthened cortico-cortical connections integrate new memories w/pre-existing ones
28
Q

BEHAVIOURAL MODELS OF SYSTEM CONSOLIDATION IN RODENTS

A
  • contextual fear conditioning (classical conditioning of freezing response); single trial training can generate life-lasting memory in same context
  • food preference learning (social conditioning of food preference)
  • hippocampus lesion causes temporally graded retrograde amnesia
29
Q

RECONSOLIDATION OF MEMORIES

A

SANDRINI et al (2018)

  • in unstable state memories can be degraded/strengthened but also modified (ie. false memories)
  • beh modifiers = interference/extinction
  • pharmacology (ie. protein-synthesis blockers)
  • NIBS = non-invasive brain stimulation techniques (ie. rTMS)
30
Q

ENCODING PROCESS

A 
ENCODING
-> new encoded memories (unstable)
CONSOLIDATION
-> stored memories (stable)
REACTIVATION (RETRIEVAL/REMINDER)
-> stored memories (unstable)
RECONSOLIDATION
-> altered memories (degraded/strengthened/updated) (stable)
MODIFICATION
- beh/stressor events
- pharmacological agents/NIBS
31
Q

SUMMARY

A
  • memory distributed across cortical/subcortical brain areas (ie. hippocampus/mammillary bodies/thalamus/cerebellum)
  • damage to brain areas causes amnesia
  • memories divided into declarative/non-declarative
  • animal research uncovers mechanisms at level of brain/neural networks/synapses
  • what/when/how memory depends on learning process (ie. associative/non-associative learning)/stimuli; sometimes rewards/punishments
  • memories differ in duration (sensory buffer/STM/ITM/LTM)
  • consolidation/reconsolidation of LTM
32
Q

HEBB SYNAPSE

A

RAMON Y CAJAL (1893)
- first proposed that site of contact between neurons could play role in memory formation
FOSTER & SHERRINGTON (1897)
- named them synapses
HEBB (1949)
- theory that some connections in neural networks could be strengthened if frequently activated/weakened if used less
- Hebb synapse concept implies strength of synaptic transmission can ^ if presynaptic cell repeatedly/persistently activates postsynaptic cell

33
Q

SYNAPTIC PLASTICITY IN LEARNING/MEMORY

A
  • synaptic plasticity = biological processes at synapse by which synaptic activity patterns change (increase/decrease synaptic strength)
  • when axon of cell A is near enough to excite cell B to repeatedly/persistently take part in firing it, some growth process/metabolic change takes place in one/both cells so that A’s efficiency (as a cell firing B) increases
34
Q

SEARCH FOR MEMORY ENGRAM +

A
  • fundamental principles of cellular/molecular mechanisms underlying learning/memory uncovered in Alysia
  • signals transmitted as few individually identified sensorimotor synapses control gill withdrawal response
    KANDEL et al
  • dissected whole neural network that steers motor-neurons of gill muscles
  • small number of neurons w/large-sized soma/axons
  • possible to measure/manipulate neural signals in single sensory/motor neurons (pre/postsynaptic sensorimotor synapse cells) during acquisition/memory formation/recall
35
Q

SYNAPTIC PLASTICITY IN LEARNING/MEMORY

A
  • changes in presynaptic neuron can include:
    1. short-term plasticity (enhancement/reduction)
    2. gain control (change in neurotransmitter amount released for given signal)
    3. temporal filtering (change in selectivity for frequency range of spikes arriving in axon terminal)
  • synaptic transmission enhancement (ie. presynaptic facilitation (Aplysia’s gill synapse))
  • short term facilitation (v brief/milliseconds)/potentiation (few seconds -> minutes)
  • short-term depression (opposite effect; decreases PSP)
36
Q

PRESYNAPTIC DEPRESSION

A
  • reduction of neurotransmitter release in STM

SHORT-TERM HABITUATION

37
Q

PD: SHORT-TERM HABITUATION

A
  • when siphon first stimulated by water squirt; Aplysia retracts gills to protect it; reflex mediated by sensory neurons synapsing directly upon motor neurons that withdraw gill
  • if squirted repeatedly, animal habituates to stimulus; no longer retracts gill; short-term habituation results as sensory neurons release less transmitter
38
Q

PD: LONG-TERM HABITUATION

A
  • if siphon squirted repeatedly over days, animal habituates faster each day; eventually shows almost no response
  • long-term habituation due to retraction of some synaptic terminals
39
Q

MODULATORY INTER-NEURONS

A
  • can influence how much/for how long neurotransmitter is released
  • presynaptic facilitation eg = changes involving inter-neuron modulation; modulation causes an increase in neurotransmitter release
40
Q

POSTSYNAPTIC NEURON CHANGES

A
  • evidence provided by studies investigating mechanisms of associative (classical/operant conditioning)/spatial learning
  • presynaptic neuron -> postsynaptic neuron changes -> both neurons
41
Q

SPATIAL LEARNING IN RODENTS

A

MORRIS (2008)

  • escape learning task in water maze by finding hidden platform in fixed location
  • dif training/testing protocols to investigate learning/memory/navigation mechanisms
  • lister-hooded rats have much better vision than white rats (common in research)
42
Q

HIPPOCAMPUS LESIONS PRIOR TRAINING

A

MORRIS et al (1982)
- don’t specifically impair working/reference memory BUT spatial memory; lesions after training have less strong effect on it
PHASE 1
- hidden platform
PHASE 2
- platform hidden but marked w/beacon (cue-based navigation); all rats show same escape latency
PHASE 3
- reversal to hidden platform; rats w/hippocampal lesions performed poorly again

43
Q

HIPPOCAMPAL FORMATION ENCODES SPACE LOCATIONS

A

MOSER et al (2015)

  • black lines show trajectory of foraging rat in 1.5m diameter wide square enclosure
  • each red dot depicts 1 spike fired via cell (microelectrode recordings in freely moving rats)
  • cyan triangles illustrate spatial regularity (hexagonal grid) of firing pattern characteristic for grid cells
  • colour-coded spiking rate map (blue = lowest activity; red = highest)
44
Q

HIPPOCAMPUS INVOLVED IN SPATIAL MEMORY FORMATION

A
  • neurotransmitter = glutamate
  • can take slices from hippocampus that preserve functioning network; can be kept alive; recordings performed ex vivo
  • 3 main pathways:
    PERFORMANT
  • entorhinal cortex input
    MOSSY FIBRE
  • dentate gyrus to CA3 pyramidal cells
    SCHAFFER COLLATERAL
  • CA3-CA1 pyramidal cells
45
Q

LTP = POSTSYNAPTIC MECHANISM

A
  • LTP = long term potentiation; can last hours
  • LTD = long term depression
    ANDERSSON (1966)
  • found in perforant pathway of hippocampus of anesthesised rabbits that during repetitive stimulation additional strong depolarisation w/many fast pulses during few seconds (tetanus) caused increase in neuronal firing of postsynaptic cell
    BLISS & LOMO (1973)
  • continued work; discovered LTP demonstrating frequency potentiations can be long-lasting
  • LTP found in other hippocampus paths too
46
Q

AMPA RECPTORS IN CA1 PYRAMIDAL NEURONS

A
  • AMPA receptors = ionotropic receptors (ligand-gated ion channels)
  • AMPA receptors open if glutamate binds to them; when open Na+ flow into postsynaptic neuron
  • synapse is excitatory as Na+ influx depolarises membrane (EPSPs)
47
Q

CA1 NEURONS

A
  • also have NMDA receptors in dendrites
  • NMDA receptors both ligand/voltage-gated
  • when cell at rest NMDA receptors blocked by Mg2+
  • binding of glutamate neurotransmitter necessary BUT alone insufficient to open them
48
Q

NMDA RECEPTORS ACT AS COINCIDENCE DETECTORS

A
  • open when both conditions met:
    1. binding of glutamate
    2. membrane depolarises above threshold expelling Mg2+ plug
  • leads to influx of Ca2+ ions into postsynaptic cell; also contributes to EPSP
49
Q

MORE RECEPTORS FOR STRONGER EPSPs

A
  • in dendritic spin vesicles contain AMPA receptors in membrane
  • if NMDA receptor opens it lets in Ca2+ from synaptic cleft; Ca2+ activates proteins that make those vesicles bind w/cell membrane in synaptic cleft
  • then ^ AMPA receptors in active zone; ^ Na+ will enter each time neurotransmitter released
  • ^ AMPA receptors in cell membrane lasts many hours
50
Q

STRONGEST LTM EFFECT

A
  • growth of new dendritic spines w/synapses
  • high Ca2+ influx activates intracellular enzymes (protein kinases)
  • PKA/PKC/CaMKII (calcium-calmodulin dependent protein kinase II) activate transcription factor CREB (cAMP response element binding protein)
  • CREB targets many genes that required for growing new dendritic spines/synapses
51
Q

INVESTIGATING ROLE OF NMDA RECEPTORS

A

MORRIS et al (1986)
- AP5 (APV too); selective NMDA receptor antagonist
- AP5 treatment of hippocampus cells suppresses LTP
TSIEN et al (1996)
- NMDA receptor knockout mice = using genetic tools to study brain functions
- LTP absent in NMDA knockouts; normal in wild-type animals/controls (also knockouts BUT w/intact NMDA receptors)

52
Q

MEMORY CONSOLIDATION REQUIRES PROTEIN SYNTHESIS

A
  • pharmacological agents used to dissociate dif stages of encoding/reconsolidation
  • drug manipulations relatively brief/accurately timed/usually reversible (in-pp control before/after treatment possible)
  • targeted intracranial drug delivery circumvents BBB (blood-brain barrier)
  • protein-synthesis blocker applied in LTM studies involving hippocampus/amygdala/prefrontal & insular cortex; anisomycin/rapamycin = amnesiac agents affecting consolidation/reconsolidation
53
Q

ROLE FOR ADULT NEUROGENESIS IN SPATIAL LTM

A

NOTTEBOHM (1985)

  • precise role of new brain cells born in adulthood unknown; presumable repair/plasticity
  • hippocampal neurogenesis (ie. DG (dental gyrus) found in many mammals)
54
Q

STRUCTURAL CHANGES IN HIPPOCAMPUS

A
  • associated w/extensive spatial learning/route following
    MAGUIRE et al (2000)
  • response to environmental stimulation under natural conditions
  • London taxi drivers have larger hippocampi
  • compared to bus drivers have greater grey matter volume in mid-posterior hippocampi; less volume in anterior hippocampi
55
Q

ENVIRONMENTAL ENRICHMENT ENHANCES BRAIN

A

STUART et al (2017)

  • enhanced opportunities for learning perceptual/motor skills/social learning
  • besides learning complex info ^ processing needs; changes in physio/activity rhythms
  • can influence experimental outcomes
  • evidence how function changes in specific brain areas ie. measuring synaptic density changes; correlate w/beh performance and other indicators for cog/physical health at dif ages
56
Q

VISUAL DEPRIVATION CAUSES STRUCTURAL CHANGES IN BRAIN

A

LE VAY, WIESEL, HUBEL (1980)

  • kitten/monkey exps reveal development/utilisation of V1 structures (orientation/ocular dominance columns) depend heavily on sensory experience during/after early crit period
  • brain functions compete for space; reorganisation takes time
  • alternating ocular dominance columns in layer IV of primary visual cortex (V1) receives input from either right (bright stripes after injection of radioactive dye)/left (dark stripes) eye
57
Q

RECRUITING NEW BRAIN AREAS WHEN A SENSORY SYSTEM DOESN’T DEVELOP

A

MERABET & PASCUAL-LEONE (2010)

  • cross-modal recruitment of occipital visual cortex in blind/auditory cortex in deaf reported
    1. occipital recruitment for tactile processing (ie. Braille reading/sound/localisation/verbal memory)
    2. recruitment of auditory/language-related areas for viewing sign language/peripheral visual processing/vibro-tactile stimulation
58
Q

AGE-RELATED MEMORY CHANGES

A

SPRENG et al (2010)

  • w/aging humans experience memory type decreases including spatial memory/navigational skills due to neuron/connection loss
  • memory impairment = neurodegenerative disease symptom
  • evidence for cholinergic inputs decrease to hippocampus/cortex
  • white matter can change in older subjects to allow task-dependent learning in specific regions dif to younger pps
59
Q

TEMPORAL PLASTICITY CONSTRAINTS

A
  • neural plasticity takes many forms
  • time courses differ over life span
  • important to find mechanism enabling/inhibiting it
60
Q

SUMMARY II: MEMORY FORMATION X PLASTICITY

A
  • Hebb proposed new approaches to understand beh via brain function perspective
  • Hebb synapse illustrates why/how signal transmission changes at synapse
61
Q

SUMMARY II: SYNAPTIC EFFICIENCY CHANGES OVER TIME

A
  • presynaptic facilitation/depression = changes underlying STM
  • LTP/LTD = stable/enduring change
  • plasticity in neurons at molecular level
  • structural changes in connectivity/synaptic density
  • pharmacological agents/genetic tools to dissect mechanisms of learning/memory
62
Q

SUMMARY II: SPATIAL LEARNING INVOLVES HIPPOCAMPUS

A
  • LTP can occur at several hippocampal formation sites
  • AMPA/NMDA receptors both present in postsynaptic membrane
  • NMDA receptor = coincidence detector; required for LTP
63
Q

SUMMARY II: PLASTICITY = DEFINING BRAIN FEATURE

A
  • prominent in neural development BUT also extends over life span
  • neurogenesis contributes to brain plasticity/repairs; may aid learning
  • some plasticity form limited to early critical/sensitive period
  • contributes to causes/treatments of psychopathology
  • sensory/motor systems show plasticity

Biological Psychology (21 decks)

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