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44 Cards in this Set
- Front
- Back
4 sequential steps in memory
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1. encoding
2. consolidation 3. storage 4. retrieval |
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Describe encoding
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newly learned info integrated w prior knowledge
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Describe consolidation
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encoded info converted into a form that can be permanently stored.
Associated with structural changes in the brain |
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Describe storage
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actual deposition of memory into final location
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Describe retrieval
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accessing stored memory
-subject to distortion. dependent on working memory |
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2 Primary classifications of memory are associated w/ diff circuitries. What are they?
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1. declarative (explicit) memory
-available to consciounsness -expressed by language (telephone number, etc) 2. nondeclarative (implicit) memory -cannot be retrieved consciously (riding a bike, etc) |
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2 types of declarative (explicit) memory
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1. semantic
-knowledge of objects, facts, concepts -words & their meanings 2. episodic -events |
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What neural circuitry is assoc w/ Declarative memory
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1. encoding: sensory systems via association cortices
2. consolidation: hippocampus & surrounding areas (temporal lobe) 3. storage: association cortex 4. retrieval: brain regions involved in sensory percept |
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What lesions would create declarative memory deficits?
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medial temporal lobe lesions
(usually bilateral to notice symptoms) |
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What would medial temporal lobe lesions cause?
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inability to consolidate info into long term memory
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____________ lesion would cause a greater deficit in memory for spatial representation
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right hippocampal
(declarative memory deficit) |
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___________ lesion would cause greater deficits in memory for words, objects or people
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left hippocampal
(declarative memory deficit) |
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__________ lesions would cause greater deficits in memory storage for object recognition
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surrounding cortices
(declarative memory deficit) |
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_______________ degeneration due to Alzheimers is associated w/ loss of short term declarative memory
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Entorhinal cortex
(CA 1 area) |
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________________, _________, & __________ degeneration due to Korsakoff syndrome (prolonged thiamine defic, alcoholics) is assoc. w/ loss of short & long term declarative memory
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hippocampal formation, mammillary bodies, & thalamus
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4 types of non-declarative (implicit) memory
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1. priming cues
2. procedural -skills & habits -sensory-motor adaption 3. associative learning classical & operant condition - skeletal musculatural - emotional response 4. non-associative learning habituation & sensitization |
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T/F
Non-declarative memory circuitry involves the temporal lobe & midline thalamic nuclei |
FALSE
involves basal ganglia, prefrontal cortex, amygdala, sensory assoc cortex, cerebellum, & reflex pathways |
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2 forms of associative learning (non-declarative)
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1. Classical (Pavlov) conditioning
-learning relationship btwn 2 stimuli (fear involves amygdala) (eye blink involves cerebellum) 2. Operant conditioning -relationship btwn behavior & reward/punishment (involves nucleus accumens) (food aversion, trial & error, addictive behaviors) |
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2 forms of non-associative learning (non-declarative)
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*both involve one stimuli
1. habituation- repeated (harmless) stimulation decreases response 2. sensitization- repeated (harmfull) stimulation increases response *responses involve sensory & motor pathways involved in motor reflex |
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What is the amygdala involved in?
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association of sensory input (via cortex/subcortical) & emotional ouput (via HPT axis & autonomics)
*also has output responsible for emotional arousal to modulate memory processing (PTSD) |
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Procedural memory is composed of 2 subsystems. One involves the striatum & is assoc w/ ___________
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habit & skill
*dorsal striatum (basal ganglia) required for learning skilled movement sequences (loops, tonic activity, etc) |
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The second subsystem of procedural memory involves the cerebellum & mediates ______________
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sensory-motor adaptations
(ex: vestibulo-ocular adaptions) |
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Damage to the _____________, Huntingtons, Parkinsons, are accompanied by inability to learn motor skills
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basal ganglia
(non-declarative memory damge) |
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Damage to the ___________leads to failure to develop fear conditioning
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amygdala
(non-declarative memory damage) |
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_____________ damage can also interfere w/ conditioned reflex learning (eye-blink reflex)
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cerebellum
(non-declarative memory damage) |
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The process of converting working (short term) memory to long term memory is _____________
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consolidation
(inability to convert diff types of memory= forgetting) |
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What areas are assoc w/ working (short term) memory
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hippocampus
prefrontal cortex & neocortical areas (more complex tasks of working memory, problem solving, etc) |
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Declarative long term memory:
Semantic (factual) knowledge is stored in a distributed fashion in the __________. |
neocortex
(Damage to a specific area can lead to loss of specific info & fragmentation of knowledge (agnosia)) |
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Declarative long term memory:
Episodic (autobiographical) knowledge about time & place involves the ___________ |
prefrontal cortex
(Frontal lobe damage assoc/ w tendency to forget how info was acquired (amnesia)) |
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Non-declarative long term memory:
For habituation/sensitization, fear cond., reflex, etc cortical storage is NOT required. Learning is supported by what structures? |
subcortical structures, spinal pathways (habituation & sensitization), amygdala (fear cond), & cerebellum (reflex)
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What is priming (non-declarative/implicit)?
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memory effect- exposure to a stimulus influences a response to a later stimulus (list of words, see later if any are familiar)
(demonstrates continual transfer from short to long term memory) |
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Diff btwn anterograde & retrograde amnesia
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anterograde- inability to form new memories
retrograde- inability to retrieve stored memory *both due to pathology |
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Describe neural changes involved w/ habituation
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presynaptic neurons less sensitive
(decreased strength of synaptic connection) (decreased NT vesicles available for release) |
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Describe neural changes involved w/ sensitization
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presynaptic neurons more sensitive
(post tetanic potentiation) (increased Ca in presynaptic terminal, brings closer to threshold for next stimuli) facilitory interneuron enhances NT release |
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short term sensitization in presynaptic sensory neuron occurs by.......
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-activation of metabotropic receptor & second messengers (cAMP & PKA, DAG & PKC)
--broadened AP via K+channel inhibition ---increase Ca influx & vesicle release or --more vesicles mobilized by MPK (PKA activated) phosphorylation of Synapsin = activation of motor neuron |
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long term sensitization in presynaptic sensory neurons occurs by.........
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-MAPK (PKA activated) phosphorylates CREB (transcription factor)
--CREB changes gene epression ---leads to new protein synthesis ----makes facilitation more permanent |
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What are the long term effects in the postsynaptic cell?
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gene expression changes
changes in physical connections (necessary for memories to persist long term) |
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Long term potentiation depends on ________ increase in the postsynaptic cell
How does this occur? |
calcium increase
NMDA ((glutamate) receptor & Ca channel) is activated by Mg+ & causes Ca influx |
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Ca release is only possible when the postsynaptic membrane is 1st depolarized by ______________
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glutamate binding to AMPARs
(occurs due to increase Ca in synaptic cleft) |
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Increased activity in the postsynaptic cells results in activation of ________________.
What does this do? |
nitric oxide synthase (generates NO)
NO produces permanent changes in presynaptic terminal to enhance glutamate release w/ APs |
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Pre & postsynaptic changes leads to what?
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ability to activate synapses normally silent under same conditions (silent synapses)
*sensitization (mechanism for forming new circuitry in memory) |
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The (early/late) phase of memory formation requires de novo proteins synthesis
For what? |
formation of new synapses
(via CREB-1 binding to genes & regulation transcription) |
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what is the primary modification to postsynaptic cells?
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modification of spines on dendrites
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How can long term depression occur?
Where does it occur? |
-by long term low freq stimulation
--depresses excitatory potential --lowers Ca stores ---decreased AMPA receptors (# (via internalization) & sensitivity (via depohsphorylation)) *occurs in cerebellum |