Higher Cortical Function: Memory Flashcards

1
Q

Define learning

Define memory

A
Learning = acquisition of knowledge 
Memory = retention of knowledge
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2
Q

How can memory be classified?

A
  • nature of memory e.g. declarative vs non-declarative

- duration e.g. short vs long term

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3
Q

For how long are the following stored?

  • sensory memory
  • short term memory
  • long term memory
A
  • sensory memory = <1 second
  • short term memory = >1 min
  • long term memory = lifetime
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4
Q

Define the following

  1. explicit vs implicit memory
  2. declarative vs procedural memory
  3. episodic vs semantic memory
A
1. explicit = conscious 
implicit = unconscious 
2. declarative = facts and events 
procedural = skills, tasks
3. episodic = events and experiences 
semantic = facts and concepts
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5
Q

Draw the memory tree

A

see lecture notes

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6
Q

Describe the nature of declarative memory

What are the two types of declarative memory?

A
  • explicit
  • consciously aware
  • able to describe in words
  • fades with type
    Two types
  • episodic = events, experiences
  • semantic = facts, concepts
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7
Q

Describe the nature of non-declarative memory

Give two examples of conditioned responses

A
  • implicit
  • skills, habits, behaviours
  • procedural memory e.g motor tasks, acquiring experience
    Conditioned responses:
  • associative reflexes e.g Pavlov’s dog
  • emotional response –> strengthens declarative memory
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8
Q

What is the functions of sensory memory?

How long is it stored?

A
  • sensory processing

- lasts for fractions of a second

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9
Q

What is meant by working memory? What is its function?

A

Working memory is a cognitive system with a limited capacity that is responsible for temporarily holding information available for processing. Working memory is important for reasoning and the guidance of decision making and behavior.

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10
Q

What are some causes of amnesia?

A

TBI
neurodegeneration
resection
stroke

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11
Q

What are the two types of amnesia and how are they different?

A

Retrograde amnesia = can’t remember anything before the insult
Anterograde amnesia = can’t form new memories after the insult

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12
Q

What is Ribot’s law?

A
  • Retrograde amnesia is not usually complete

- Ribot’s Law = recent memories are more likely to be lost than remote ones

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13
Q

What is the anatomical location for declarative memory?

What disease provides evidence for this?

A
  • medial temporal lobes
  • evidence for this is lesions
  • the pathology of alzheimers disease –> lose episodic, then semantic memory
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14
Q

What is the declarative memory pathway?

A

sensory info –> rhinal cortices and hippocampus –> neocortex

hippocampus –> hypothalamus (MB’s) –> thalamus –> neocortex

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15
Q

What memory is lost in Korsakoff’s?

A

episodic memory

- mamillary bodies in hypothalamus key step in memory formation

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16
Q

What is the anatomical location procedural memory?

What disease provides evidence for this?

A
  • supplementary motor area, basal ganglia and cerebellum
  • ## parkinsons disease, difficult to acquire new procedural skills
17
Q

What is the anatomical location of working memory?

What is the evidence for this?

A
  • prefrontal cortex

- evidence in ADHD and schizophrenia

18
Q

Describe the HM case study?

A
  • bilateral temporal lobectomy –> severe anterograde amnesia for declarative memory
  • childhood memory intact
  • temporal lobe required for new declarative memories but not old
  • no effect on procedural memory
19
Q

How do neurones store memories?

A
  • change in neurotransmission
  • change in synaptic structure
  • neuronal plasticity = dynamic synapse formation/retraction
  • long term potentiation
20
Q

Where was long term potentiation first shown?

A
  • hippocampus in vitro
21
Q

What is long term potentiation?

A
  • neurones in the hippocampus have a baseline level of activity
  • if you stimulate the hippocampus with lots of afferent input, then remove the input
  • the baseline activity of the neurones has increases
  • the nature of these neurones has been changed
22
Q

What kind of memory is LTP shown in?

A

declarative memory

23
Q

What is happening at the synapse during LTP?

A

Glutamate transmission critical in LTP
- glutamate normally binds to AMPA receptor
- if stimulated, you unblock NMDA receptors and so get AMPA and NMDA activity
- NMDA allows calcium entry
- leads to changed gene expression and altered kinase activity especially CAMKII
- CAMKII affects cellular processes = biological equivalent of memory
LTP also triggers physical transformation of neurones
- spine formation

24
Q

What are key theories for the biological basis of memory formation?

A

Long term potentiation

  • changes in baseline activity
  • changes in receptor activity on postsynaptic knob
  • calcium entry –> changes to cellular processes
  • enzyme CAMKII activity
  • physical changes e.g. spine formation in response to glutamate
25
Q

How can be manipulate memory?

A

Pharmacological
- enhancement by nootropics, NMDA agonists enhance memory formation in animals, other mechanisms target ACh transmission e.g. ACh loss in Alzeheimer’s
- suppression by NMDA antagonists e.g. ketamine
Non-pharmacological
- CBT - changes in network activity