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Bio Psych 210 > Learning and Memory > Flashcards

Learning and Memory Flashcards

1
Q

What is Habituation?

A
  • response to stimulus gradually gets smaller over time
  • ex) if you turn on the fan in a room, you will initially hear it and eventually you don’t hear it anymore
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2
Q

What is sensitization?

A
  • the opposite of habituation
  • response to a stimulus increase over time
  • ex) after a bumpy plan ride, you may be a little jumpy for a while
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3
Q

Neural Mechanisms of learning

A
  • larger neurons and fewer neurons make it a good animal to study
  • largely studied in aplysia californica
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4
Q

What is the gill-withdrawal reflex?

A
  • the gill is used for breathing
  • the gill is covered with the mantle shelf
  • waste and seawater are released through siphon
  • touching the siphon leads to a retraction of the gill
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5
Q

What is the habituation in the gill-withdrawal reflex?

A
  • touching the siphon repeatedly leads to less of a reflex/retraction of the gill
  • what would this be?
  • either sensory neurons are becoming less responsive
  • motor neurons are becoming fatigued or changes occur between the sensory and motor neurons
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6
Q

What is habituation explained?

A
  • single cell recordings show that sensory neurons do not decrease activity with each touch of the siphon
  • electrical stimulation of the gill’s motor neurons show that it can still contract after being habituated
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7
Q

Changes in hibituation explaned

A
  • so, changes must be occurring between the sensory and motor neurons
  • repeated siphon touches leads to less calcium into the sensory neurons which means less neurotransmitter is being released into the synapse
  • smaller EPSP’s occur in interneurons and motor neurons ~ leads to a smaller gill withdrawal
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8
Q

What is sensitization in siphon?

A
  • after an electrical shock to the head or tail, aplysia show an increased gill-withdrawal response
  • sensory neurons release more neurotransmitter onto the interneurons and motor neurons which to leads to the larger response
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9
Q

Long term changes observed

A
  • normal aplysia showed 1300 axon terminals synapsed with sensory neurons
  • those that experienced sensitization had 2800 terminals
  • those that experienced habituation had 800 terminals
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10
Q

long term potentiation

A
  • a long lasting strengthening of a synapse
  • more NT is released with any input
  • thought to be associated with memory formation
    LONG TERM DEPRESSION: a weakening of a synapse that lasts hours or days ~ thought to be associated with learned
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11
Q

What are the cellular mechanism for LTP?

A
  • NMDA and AMPA receptors
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12
Q

What does NMDA and AMPA receptors do?

A
  • they both are receptors for glutamate
  • normally just NMDA receptors are available to depolarize the postsynaptic membrane
  • when the connection is strengthened, AMPA are added to the membrane
  • allows for the postsynaptic membrane to be depolarized easier ~ leads to LTP
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13
Q

Is LTP the mechanism for long term memory?

A
  • both can last indefinitely
  • both can result from very brief input
  • LTP is consistent with models proposed by Donald Hebb
  • LTP is found in cells thought to be associated with memory formation like the hippocampus and the cerebellum
  • MNDA receptors (that have been linked to memory) are also linked to LTP
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14
Q

What about brain structures in learning?

A
  • Hippocampus and the temporal lobe
  • thalamus ~ Papez’s Circuit
  • prefrontal cortex
  • basal ganglia
  • cerebellum
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15
Q

What happened with patient H.M.?

A
  • large areas of H.M.s hippocampi and temporal lobes were surgically removed
  • personality and IQ were not impacted and experienced profound anterograde amnesia
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16
Q
  • What is amnesias?
A
  • retrograde: loss of memories of the past
  • anterograde: inability to form new memories
  • H.M. had issues with both
17
Q

What else happened with patient H.M?

A
  • His short term memory was ok ~ “working memory”
  • he could learn procedural tasks ~ mirror drawing
  • his deficits were in explicit memory tasks
18
Q

What were the conclusions of H.H?

A
  • the ability to store memories and the ability to access previously stored memories are in different brain areas
  • procedural memories are dealt with in different brain areas than explicit memories
19
Q

What are the different parts of the hippocampus?

A
  • the right hippocampus is active during spatial memory processing
    ~ may include a 3D representation of the world around
  • the left hippocampus is more active during verbal memory tasks
20
Q

What is Korsakoff’s syndrome?

A
  • caused by a thiamine deficiency due to alcoholism
  • damage to the thalamus and the mammillary bodies
21
Q

What else about the thalamus?

A
  • patient N.A. : a fencing foil produced a lesion to their left thalamus ~ N.A’s amnesia was similar to H.M’s
22
Q

What is the DNMS task?

A
  • delayed non-matching to sample task
  • requires the ability to transfer memories from short term systems into long term systems
23
Q

What is the Papez’s Circuit?

A
  • a network that connects the thalamus, mammillary bodies, and hippocampus
    ~ it is believed to be key to forming long term memories
24
Q

What about the prefrontal cortex?

A
  • patients with PFC damage have issues with the Wisconsin card-sorting tasking ~ short term memory issues
  • object permanence studies: adult monkeys with prefrontal damage don’t seen to grasp object permanence
    ~ prefrontal cortex is constantly developing throughout youth/childhood - object permanence usually develops in the first year of life
25
Q

What about the bsala ganglia?

A
  • lesions of the basal ganglia impact procedural memories, but not explicit memories ~ the opposite of H.M’s problems
  • diseases that lead to damage to the basal ganglia typically also have procedural memory deficits like Huntington’s and Parkinson’s Disease
26
Q

What about the cerebellum?

A
  • possibly key to procedural memories as well ~ motor learning
  • unclear if damage upon the cerebellum leads to deficits in motor learning or simply the performance of that learned task
27
Q

What about stess and memory?

A
  • that stress impacts the amygdala ~ has connections to the hippocampus
  • cortisol may damage the hippocampus ~ repression and flashback/flashbulbs memories

Bio Psych 210 (9 decks)

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