Learning and Memory Flashcards

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1
Q

What is the Information processing model

A

Theory that memory consists of multiple components and processes.

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2
Q

What are the components and processes of the Information Processing Model?

A

Sensory input -> Sensory Memory -> Short Term Memory -> Long Term Memory

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3
Q

What is sensory memory?

A
  1. Immediate, initial recording of sensory info.
  2. Large capacity
  3. very short duration (~1-2 seconds)
  4. reflects residual activity of sensory neurons.
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4
Q

What is short term memory?

A
  1. active “workspace” for conscious thought and reasoning
  2. requires encoding from sensory memory and/or retrieval from LTM
  3. Small capacity (~ 7items)
  4. short duration (~30 sec)- longer with rehearsal
  5. prefrontal cortex
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5
Q

Long term memory

A
  1. potential infinite capacity & duration
  2. accessed via working memory (retrieval)
  3. requires consolidation by limbic system (enhances REM sleep)
  4. strengthened by frequent rehearsal (although details may change)
  5. different subtypes distributed throughout the brain.
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6
Q

What are some key questions concerning memory?

A
  1. how is sensory information encoded into STM? (Attention)
  2. Where and how does consolidation (STM to LTM) take place?
  3. Where an how is LTM stored?
  4. WHere and how is LTM stored?
  5. Are there different types of LTM?
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7
Q

What is retrograde amnesia?

A
  1. Loss of memory for past events (i.e. prior to injury), typically limited to a short time period.
  2. a temporary interruption of consolidation from STM to LTM (or ITM)
  3. Caused by concussion, loss of consciousness, alcohol
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8
Q

Anterograde Amnesia

A
  1. loss of ability to retain new information (a permanent impairment of consolidation from STM to LTM)
  2. Dues to bilateral damage to the limbic system, especially the hippocampus (medial temporal lobes). e.g. strokes, korsakoff’s syndrome
  3. famous cases: H.M., Clive Wearing
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9
Q

What have studies shown on anterograde amnesia?

A
  1. amnesic show improvement on implicit skills- (mirror tracking, fragmented pictures)
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10
Q

What is declarative (explicit) memory?

A
  1. info acquired through learning
  2. memory we are aware of accessing
  3. requires intact limbic system
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11
Q

Procedural (implicit) memory

A
  1. memory shown through performance rather than conscious recollection
  2. memory we are not aware of accessing
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12
Q

Declarative Memory (semantic memory)

A
  1. generalized memory of information
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13
Q

Declarative Memory (episodic memory)

A
  1. autobiographical memory

2. memory for events in time and place

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14
Q

How does damage effect Declarative Memory

A
  1. Frontal-parietal damage can selective impair episodic memory (source amnesia)
  2. Semantic memory appears to be more widely distributed. (focal cortical lesions impair ability to name objects from specific categories)
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15
Q

Procedural (non-Declarative memory

A
  1. Stored in sam areas responsible for carrying out the behavior
  • sensorimotor skills = basal ganglia, cerebellum, motor cortex
  • classical conditioning = cerebellum
  • emotional memory = amygdala
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16
Q

Animal Lesions

A

general consistent with finding from humans

  • hippocampal lesions impair performance , especially spatial memory
  • cannot easily discriminate and explicit memory in animals
17
Q

What is Hebbs view on synaptic plasticity?

A
  1. learning is dues to increases in synaptic strength
  2. existing connections between simultaneously active neurons are strengthened (“Hebbian synapses”)- Neurons that fire together wire together
18
Q

What are the 4 mechanisms of synaptic plasticity

A
  1. Changes in existing synapses (amount of NT or # of receptors)
  2. changes in interneuron modulation (axo-axonal connections)
  3. more or fewer synaptic contacts between neurons
  4. rearrangement of synapses.
19
Q

What are the effects of behavioral intervention on synaptic plasticity (environmental condition)

A

Enriched environments produce:

  • better learning & problem solving
  • faster recovery from injury or malnutrition
  • less age-related declines in memory
20
Q

What are the effects of behavioral intervention on synaptic plasticity (neurological changes)

A
  1. increased amounts of AChE (more neural activity)
  2. larger cortical volume & thickness
    - larger cell size
    - more dendritic branching
    - larger synaptic contacts
21
Q

What are the effects of behavrioal intervention on synaptic plasticity ( Habituation in aplysia)

A
  1. a decrease in response to repeated presentation of a stimulus.
  2. short term habituation- decreased release of NT at sensorimotor synapse.
  3. Long term habituation- retraction of some synaptic terminals at sensorimotor junction.
22
Q

How was Long Term Potentiation discovered?

A
  1. repeated high intensity stimulation of neurons in the perforant pathway of the rat hippocampus results in a prolonged pattern of elevated EPSPs in the mossy fibers (receiving neurons)
23
Q

What is the role of NMDA receptors on long term potentiation

A
  1. at least 2 types of glutamate receptors:
    - AMPA: ionotropic Na+ channels
    - NMDA: ionotropic Ca++ channel blocked by Mg+
24
Q

What are some more roles of NMDA receptors on long term potentiation

A
  1. repeated stimulation of AMPA receptors (Na+ channels) by Glu produces depolarization of post-syaptic cell
  2. knocks Mg+ block out NMDA receptors, allowing Ca++ inside (when Glu is present)
  3. Ca++ triggers activity of protein kinases.
25
Q

What is protein kinases?

A
  1. cause increase in # of AMPA receptors on post-synaptic cell
  2. trigger second-messenger system that enhances release of Glu in pre-synaptic cell
26
Q

What are conclusions we can draw from the role of NMDA receptors on long term potentiation?

A
  1. synapse is strengthened

2. effects can last a long time

27
Q

What are other LTP mechanisms?

A
  1. in some brain regions, LTP can occur when NMDA receptors are blocked by an antagonist
  2. this LTP likely involves other types of Ca++ channels- LTP does not occure when all Ca++ channels are blocked
28
Q

What is classical conditioning?

A
  1. a form of non-declarative learning in which as association is formed between two stimuli, such that they both produce the same (or similar) responses.
29
Q

What are eye blink conditioning in rabbits?

A
  1. unconditioned stimulus (US): puff of air
  2. unconditioned response (UR): reflexive eye movement
  3. conditioned (learned) stimulus (CS): tone (paired with US)
  4. conditioned (learned) response (CR): eye blink in response to CS (tone), timed to protect eye against puff of air
30
Q

What procedure was most effective in eye blink conditioning?

A

delay conditioning (CS precedes & overlaps US)

31
Q

What are the effects of brain lesions on eye blinking conditioning?

A
  1. hippocampal lesions have negligible effects on delay conditioning.
  2. cerebellar lesions prevent &/or abolish conditioned eye blinks, although the reflex is still present