Karteikarten
Chapter 17 - Learning & Memory
Karten in diesem Stapel (42)
- 1Definition of learningRelatively permanent change in behaviour due to experience
= Acquisition - 2Definition of memoryAbility to recall/recognize previous experience / mental representation of previous experience
Reflects change in brain
= Retention + retrieval - 3Classical conditioningAssociation of neutral stimulus with biologically relevant stimulus
In humans: eye blink reflex - pair tone with airpuff - mediated by cerebellum, stopped by GABA-blocking drugs - 4Fear conditioningPair shock with tone -> tone = fear
Involves amygdala
Different brain areas for different types of stimuli/responses - 5Operant conditioningAnimal learns actions -> consequences
Learning shown in response rate & speed of task performance
Thorndike's box (cat)
Skinner box (can be operant or classical)
Morris Water maze (find platform, can include learning set or landmark learning) - 6Types of memoryExplicit/declarative - conscious memory of learned task - facts & info - includes episodic & sematic
Implicit/procedural - unconscious learning - memory about perceptual/motor procedures - 7Forms of implicit memorySkill learning - ex. perceptual, sensorimotor & cognitive (basal ganglia (all) + motor cortex & cerebellum (S))
Priming - change in processing due to prior exposure to same/related stimulus (L frontal cortex)
Conditioning - learning simple associations (hippocampus, cerebellum, ventral V1 & cortex) - 8Gollin figure taskPresent progressively clearer images until they can ID object
Gets better with trials - 9Testing explicit memory in animalsWater maze - retest after day
Go to platform = explicit knowledge of location
Search for platform = implicit knowledge of learning set (task) - 10Encoding of explicit memoryTop-down manner
Cortex makes mental representation of goal - impacts how info is processed by ignoring info not matching representation
Internal cues can initiate recall - 11Encoding of implicit memoryBottom-up (how info is perceived)
Passive role - no recall of encoding
Processed by different areas vs. explicit - less cortical involvement - 12Encoding ST vs LT memoriesST = frontal lobes
LT = temporal lobes needed for storage (but actually stored in area of cortex where originally processed) - 13Stages of memoryIconic - fleeting impression
ST/working - last 30 sec with rehearsal - phonological loop (auditory) + visuospatial sketch (visual) + episodic buffer (integrated) - supervised by executive control - recency effect
Intermediate - not permanent
LT - days to years - primacy effect - 14Patient HMSurgery for epilepsy - bilateral hippocampus, amygdala & associated cortical structures
Anterograde amnesia, no explicit memory
Normal ST memory & implicit memory
Learned: memories NOT stored in hippocampus, medial temporal & frontal cortex for explicit memory - 15Patient NADamaged thalamus & mammillary bodies
Anterograde amnesia (esp verbal) = explicit
Normal ST & long-term implicit memory - 16Korsakoff's diseaseCan't recall previous experience, no familiarity with re-presented items
Damaged mammillary bodies & dorsomedial thalamus
Normal temporal lobes & hippocampus
Confabulation to fill in memory gaps
Caused by lack of thiamine - 17Patient JKParkinson's -> lack of dopamine to basal ganglia
Normal explicit memory
Damaged implicit memory - couldn't remember everyday tasks (turn on light) - 18Patient KCDamage to L fronto-parietal & R parieto-occipital cortex
Good general knowledge & could make semantic memories
No autobiographical memories & couldn't make new episodic memories (retro & anterograde episodic amnesia) - 19Explicit memory circuitCortex ->
Parahippocampus (visuospatial)
+ Perirhinal (visual)
-> Entorhinal (integrates)
-> Hippocampus
Info is bidirectional - 20Role of hippocampusEncodes spatial memory
Decreases performance on water maze
Causes deficits in place-recognition tasks (monkey)
Correlation study: bigger in seed caching chickadees > sparrows, taxi drivers - 21Role of frontal lobeDamage -> can't remember temporal orders/sequences
Gets input from all sensory systems - role in ST sensory memories
Active while "holding" something in memory - 22Radial arm maze testMust select initial arm when given option to go elsewhere
Deficit with hippocampal damage - not caudate nucleus or extrastriate visual cortex - 23Task that is caudate dependentTests response recognition memory
Start in 1 arm, leave & turn L or R - must turn same way next time for reward
Impaired with caudate nucleus damage (not hippocampus or visual cortex) - 24Extrastriate visual cortex-dependent taskPresented with 2 objects - must push aside new (not old) one to get reward
Needs extrastriate visual cortex (not hippocampus or caudate) - 25Model of explicit memoryBasal forebrain - maintains right arousal for info processing
Prefrontal - maintains ST memories, chronological order
Medial temporal - forms LT memories
Hippocampus - final stage of convergence before storage - 26Implicit memory circuitsCortex -> Basal ganglia -> Ventral thalamus -> premotor cortex
Neocortex gets little feedback - 27Emotional memory circuitsAmygdala - for coding emotion memories
Lesion -> eliminates fear conditioning - 28Types of info processingEncoding - info from sensory channels -> STM
Consolidation - STM -> LTM (hippocampus for explicit)
Retrieval - of stored info - 29Brain region summary
- 30PTSDStress/emotion enhance memory via opioids, GABA, epi & norepi -> influence amygdala (esp BLA)
Outputs to many regions - 31Changes in brain in environmental enrichmentIncreased brain weight
Increased dedendrite length
Increase in astrocytes
Increased vascularization
Increased synaptic density
Increased mitochondria
Increased cortical thickness - 32Cortical mapsVary by experience
Studied in humans viai fMRI & TMS + special experiences (musicians, Braille) - 33Changes in communication between neuronsTRANSMISSION - more NT release (pre), more sensitive receptor (post), larger synapses (pre & post), change in inactivation of NT
MODULATION - increase/decrease in NT release
SYNAPTOGENESIS - formation of new synapses
STRUCTURAL CHANGES IN SYNAPSES - existing synapses sprout collateral terminals or eliminated for more effective synapses (long term) - 34Changes in dendritesSpines can be added (filopodia formed & look for new connections - become spines if useful connection)
or eliminated - 35AplysiaSimple ganglia with visible neurons
Exhibits simple learned behaviours
HABITUATION: touch siphon -> withdraw gill - withdrawal amplitude decreases bc learns stimulation is harmless
ST change in synapse bt sensory & motor neuron + LT change from repeated stimulation = physical change in number of synapses
Also SENSITIZATION - touch siphon then shock tail, next siphon touch = more intense withdrawal - 36Plasticity in hippocampusCell assembly – group of cells that tend to be active at same time due to past successive activation – linked by Hebbian synapses
LTP occurs in hippocampal formation in synapses using glutamate - 37Long term potentiationStable & enduring change in effectiveness of synapse
Mechanism in memory form/storage
Stimulate synapse at high freq -> PSPs bigger after
Long-term changes: new synapses, enhancement of existing synapses, new dendritic spines
Affects presynaptic cell via retrograde chemical messenger -> inc glutamate release - 38LTP & glutamatePostsynaptic cells have NMDA + AMPA receptors - glutamate doesn't always activate NMDA (always binds but normally blocked by Mg unless depol is big enough = -35) -> Na & Ca can enter
Don't need NMDA for PSP but do for LTP
Ca influx via NMDA -> more depol + activation of Ca-sensitive enzymes (calmodulin & calcium-calmodulin kinase)
NMDA is important for LTP but also back-up system - 39LTP & CaMKCaMK enhances excitability via: 1) mobilizes new AMPA receptors, & 2) phosphorylates existing AMPA receptors -> increased conductance
Ca-dependent protein kinase
Affect early responsivenss = early LTP - 40Other Ca biochemical cascadesEARLY LTP:
Nitric oxide synthase -> produces NO -> enhances presynaptic NT release
Production of arachidonic acid & endocannabinoids
LATE LTP:
Activates CREB -> binds DNA -> triggers gene expression -> new proteins & receptors - 41Manipulations of intracellular pathwaysBlocking kinases/CREB -> interfere with learning & LTP
Increase activity of CREB -> smarter, instant memories
Block protein synthesis -> prevent late LTP & LT memories (early LTP & ST unaffected) - 42AgingWorking & explicit memories & tasks of executive function decline
Existing memories are stable
Some spatial memory & navigational decreases
Causes: encoding/retrieval impairment, loss of neurons/connections (esp frontal cortex), cholinergic NT problems (Alz)
Treatment: anti-cholinesterase drugs, ampakines, stimulating activities
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- Final stuff (P375) Karteikarten am Chapter 17 - Learning & Memory, erstellt von Megan Willerth am 20/11/2014.
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- Megan Willerth
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