Lecture 17 Review Flashcards

1
Q

What’s the difference between short-term and long-term memory?

A

short term
- aka working memory
- close to sensory information, active information buffer
long term
- relatively permanent
- requires consolidation (long lasting change in neuron function)

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2
Q

What are the types of amnesia?

A
retrograde = before the event 
anterograde = after the event 
global = both
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3
Q

What’s the difference between declarative memory and non declarative memory?

A
  • Declarative memory is something you can consciously report
  • nondeclarative memory is something you learned about but do not remember the events that cause the plasticity in circuits to change for learning
    • i.e. classical conditioning, procedural memory, etc.
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4
Q

How does synaptic modification play a role in learning?

A
  • learning involves mostly with changing synaptic connectivity
  • coincident neural connectivity is key in wiring the brain
    •neurons that fire together will wire together
    •out of sync will lose the link
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5
Q

What role do glutamate receptors play in synapse plasticity

A
  • AMPA, NMDA, and metabotropic glutamate receptors are key to plasticity
  • they must be coincident with extracellular glutamate and internal depolarization
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6
Q

Describe HM and how he was significant to learning and memmory

A
  • epileptic man who was cured by removing the foci
  • had declarative memory deficits
    •could not form new memories
    •short term memory intact but long term memory lost
    • specific disruption of consolidation
    •implicit memory was normal, procedural memory was normal
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7
Q

Describe the role that the medial temporal lobe has in declarative memory

A

Critical for declarative memory

  • delayed non-matching example monkey experiment. memory decreased over time
  • hippocampus receive input from the entorhinal cortex, outputs through the fornix
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8
Q

What structure is central for amnesia?

A

Peri-rhinal (PR) cortex

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9
Q

What role does the hippocampus have in memory?

A
  • very involved in remembering places, navigation, and specific places
  • roles in emotional regulation
  • navigation requires interaction with entorhinal cortex
  • closest link is to relational memory - linkage between stimuli
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10
Q

How is long term potentiation produced?

A
  • Produced by high frequency stimulation of CA3 projections in CA1
  • synapse must be active at the same time that a postsynaptic CA1 neuron is depolarized
  • repeated coactivation of synapses = firing together makes them linkes = cooperativity
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11
Q

How is long term depression produced?

A

Low frequency stimulation of CA3 projection in CA1

- produces weaker synapses

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12
Q

How does AMPA and NMDA receptors affect LTP?

A

AMPA
- LTP can be produced either by increasing function of existing AMPA receptors through phosphorylation or by adding more AMPA receptors to the membrane of the synapse
NMDA
- the amount of NMDA receptors can determine if LTP or LTD will occur
- weakening/strengthening is input specific

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13
Q

How does calcium affect LTP

A

high [Ca] favors LTP

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14
Q

What role does CaMKII playin neural plasticity?

A
  • it is critical for neuroplasticity
  • it can autophosphorylate NMDA-mediated efflux of Ca for long periods of time
    •this allows for long-term changes in cellular function to occur
  • acts as a molecular switch for long term changes
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15
Q

What role does protein synthesis play in memory in the hippocampus?

A
  • all long term memory requires protein synthesis
  • transcription factors like CREB seem to be involved
    •CaMKII can phosphorylate CREB which induces transcription
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16
Q

What is AMPA trafficking? what is the role of PSD-95

A
  • AMPA trafficking is a common mediator of increasing and decreasing synaptic strength
  • PSD-95 is a scaffolding protein that allows for more AMPA in the membrane
17
Q

Where else foes LTP and LTD occur?

A

It occurs not only in the hippocampus but also the neocortex in the medial temporal lobe
- cortical structure are dependent on NMDA receptors

18
Q

What is the importance of the dorsal striatum?

A

Procedural learning is associated with plasticity in the dorsal striatum
- NMDA antagonists and decreases in DA can block learning

19
Q

What is the importance of the cerebellum?

A

it is involved in procedural learning, fine-tuning motor functions

20
Q

What are the cells of the cerebellum? What are their function?

A

Purkinje cell (PC)
- major output of the cerebellum
- receives excitatory input from climbing fibers from the medulla
- carries information about what is going o
- PC receives input from granule cells through parallel fibers
Granule cells
- receives input from mossy fibers (neocortex structure)
- tells us what we want going on

21
Q

What is the PFC’s role in memory?

A

involved with working memory or “info in mind”
- critical for regulation of memory
- damage to PFC = confabulation
•person makes stuff up but actually believes it

22
Q

When is the amygdala activated

A
  • highest activation when mixed emotions are present

- sensitive to both positive and negative expression

23
Q

what are the inputs and outputs of the amygdala?

A
  • inputs from the association cortex and the hippocampus

- outputs to PFC, nucleus accumbens and hippocampus

24
Q

Describe the pathway of learning conditioned fear. Describe neuroplasticity

A
  • Basolateral amygdala is the site that mediates association of US and CS. this projects to the cerebral cortex, nucleus accumbens, and hippocampus
  • central nucleus projects to the brainstem and hypothalamus to produce ANS response
  • plasticity works the same as LTP in hippocampus
    • NMDA critical for acquisition
    • AMPA mediates long term change
25
Q

What is the hippocampus’ role in fear?

A

Hippocampus encodes context information and spatial information
- how environmental clues determine context
• i.e. a snake in a zoo vs the wild

26
Q

What is the PFC’s role in fear?

A
  • regulates the degree to which the amygdala expresses fear response
  • involved in executive function and provides cognitive control
  • critical for relearning during extinction training