Learning and Memory Flashcards

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
ENCODING/RETRIEVAL/CONSOLIDATION
- brain activation patterns differ when info encoded/acquired and later recalled (ie. recognition of visual stimulus)
26
CONNECTIVITY CHANGE DURING ENCODING/CONSOLIDATION
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
STANDARD LTM CONSOLIDATION MODEL
- 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
BEHAVIOURAL MODELS OF SYSTEM CONSOLIDATION IN RODENTS
- 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
RECONSOLIDATION OF MEMORIES
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
ENCODING PROCESS
``` 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
SUMMARY
- 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
HEBB SYNAPSE
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
SYNAPTIC PLASTICITY IN LEARNING/MEMORY
- 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
SEARCH FOR MEMORY ENGRAM +
- 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
SYNAPTIC PLASTICITY IN LEARNING/MEMORY
- 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
PRESYNAPTIC DEPRESSION
- reduction of neurotransmitter release in STM | SHORT-TERM HABITUATION
37
PD: SHORT-TERM HABITUATION
- 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
PD: LONG-TERM HABITUATION
- 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
MODULATORY INTER-NEURONS
- 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
POSTSYNAPTIC NEURON CHANGES
- evidence provided by studies investigating mechanisms of associative (classical/operant conditioning)/spatial learning - presynaptic neuron -> postsynaptic neuron changes -> both neurons
41
SPATIAL LEARNING IN RODENTS
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
HIPPOCAMPUS LESIONS PRIOR TRAINING
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
HIPPOCAMPAL FORMATION ENCODES SPACE LOCATIONS
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
HIPPOCAMPUS INVOLVED IN SPATIAL MEMORY FORMATION
- 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
LTP = POSTSYNAPTIC MECHANISM
- 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
AMPA RECPTORS IN CA1 PYRAMIDAL NEURONS
- 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
CA1 NEURONS
- 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
NMDA RECEPTORS ACT AS COINCIDENCE DETECTORS
- 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
MORE RECEPTORS FOR STRONGER EPSPs
- 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
STRONGEST LTM EFFECT
- 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
INVESTIGATING ROLE OF NMDA RECEPTORS
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
MEMORY CONSOLIDATION REQUIRES PROTEIN SYNTHESIS
- 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
ROLE FOR ADULT NEUROGENESIS IN SPATIAL LTM
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
STRUCTURAL CHANGES IN HIPPOCAMPUS
- 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
ENVIRONMENTAL ENRICHMENT ENHANCES BRAIN
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
VISUAL DEPRIVATION CAUSES STRUCTURAL CHANGES IN BRAIN
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
RECRUITING NEW BRAIN AREAS WHEN A SENSORY SYSTEM DOESN'T DEVELOP
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
AGE-RELATED MEMORY CHANGES
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
TEMPORAL PLASTICITY CONSTRAINTS
- neural plasticity takes many forms - time courses differ over life span - important to find mechanism enabling/inhibiting it
60
SUMMARY II: MEMORY FORMATION X PLASTICITY
- Hebb proposed new approaches to understand beh via brain function perspective - Hebb synapse illustrates why/how signal transmission changes at synapse
61
SUMMARY II: SYNAPTIC EFFICIENCY CHANGES OVER TIME
- 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
SUMMARY II: SPATIAL LEARNING INVOLVES HIPPOCAMPUS
- LTP can occur at several hippocampal formation sites - AMPA/NMDA receptors both present in postsynaptic membrane - NMDA receptor = coincidence detector; required for LTP
63
SUMMARY II: PLASTICITY = DEFINING BRAIN FEATURE
- 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