LECTURE 7 - memory and learning Flashcards

1
Q

What is the difference between implicit and explicit memory?

A

Explicit (declarative) = facts or events, easy to learn easy to forget, available for conscious recollection

Implicit (non-declarative) = things you learn to do, less likely to be forgotten, requires repetition, not available for conscious recollection

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2
Q

How is declarative memory split?

A

Long term memory: recalled after a long time

Short term memory: last for a short time, vulnerable to disruption

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3
Q

What are the two theories of memory consolidation?

A
  1. Sensory information –> short term –> long term
    consolidation occurs together
  2. Sensory info –> short term +
    sensory info –> long term
    occurs separately

Some believe first you have STM then it is consolidated, others believe consolidation are parallel processes occurring independently

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4
Q

What is amnesia?

A
  • loss of memory and learning ability

- can be caused by concussion, tumour, stroke, alcoholism, encephalitis

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5
Q

What is the difference between the different types of amnesia?

A

Retrograde = forget things before event

Anterograde = cannot form new memories

Transient global amnesia = lose memory of everything for a short period of time

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6
Q

What experiment did Lashley perform and what were the results?

A
  • surgically induced brain lesions by damaging or removing cortex of rat’s brain either before or after maze training
  • He concluded the severity of the deficit was related to the size but not the location of the lesion
  • He concluded all cortical areas involved equally in memory storage
    HOWEVER
  • He damaged interconnecting areas in brain because the brain is so small so he was not right
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7
Q

What role does the cortex have in declarative memory?

A
  • Information from sensory modality stored in cortical region that serves that modality
  • Visual memory: extrastriatal cortex
  • Temporal lobes : complex memories
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8
Q

What role does the medial temporal lobe have in memory processing?

A
  • consolidation of declarative memory
  • temporary memory storage in the MTL - consolidation in cortex

Hippocampus

  • spatial memory - place cells
  • working memory - related to ongoing behaviour
  • relational memory - ties together things happening at the time of memory storage
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9
Q

What are the consequences of a temporal lobectomy?

A
  • loss of STM (declarative)
  • loss of anterograde and retrograde memory
  • maintained procedural memory
  • maintained some LTM (childhood)

Why have one?
some forms of epilepsy can only be treated by removing the temporal lobe

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10
Q

What is Hebb’s theory?

A

(1949 - Organisation of behaviour)

  • claims that an increase in synaptic efficacy arises from a presynaptic cell’s repeated and persistent stimulation of a postsynaptic cell
  • attempts to explain synaptic plasticity, the adaptation of brain neurones during the learning process

When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased

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11
Q

What is the engram of an object?

A
  • assembly of cortical cells activated by the external stimulus

(engram = memory trace)

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12
Q

Describe cell assembly in the brain

A

Reciprocally interconnected: STM

Fire together wire together: LT consolidation

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13
Q

What is the new model of learning that comes from Hebb’s theory?

A
  • modifications of synaptic transmission
  • synaptic transmission triggered by neuronal activity
  • alterations of existing synapses
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14
Q

How can synapses become stronger?

A

‘Neurones that fire together, wire together’

When strong activation of synapses leads to firing of the postsynaptic neurone (in time with the presynaptic neurone), this leads to potentiation of the postsynaptic response

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15
Q

What is LTP?

A

Long term potentiation = persistent increase in synaptic strength following high-frequency stimulation of a chemical synapse

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16
Q

What is required for LTP?

A
  • glutamate release first activates AMPA receptors (found near NMDA receptors)
  • NMDA do not activate from a small amount of glutamate due to Mg+ block
  • frequent stimulation of AMPA receptors causes depolarisation which eventually removes Mg+ to allow Ca2+ ions to flow through NMDA receptor
  • influx of Ca2+ activates cellular mechanisms that cause more AMPA receptors to be inserted into membrane
  • these new receptors are more responsive to glutamate and allow more +ve ions to enter
  • now the postsynaptic cell is more sensitive to glutamate due to the increased number of receptors
17
Q

How is AMPA receptor conductance altered?

A
  • receptor conductance increased through CaMKII-dependent phosphorylation
18
Q

How are cytosolic AMPA receptors inserted?

A
  • inserted through CaMKII activation
  • phosphorylation phenomenon inserts AMPA receptors into membrane
  • amplifies ability of postsynaptic membrane to receive glutamate messages
19
Q

What is LTD?

A

Long term depression = activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus
- for occasionally coinciding firing

20
Q

How is LTP used for learning?

A
  • neurone activation => production of neurotrophins that feed neighbouring synapses
  • the synapses have a chance to grow in morphology, release more NT and increase post-synaptic response
  • -> modification of synaptic transmission and connectivity
  • neurotrophins = molecules that feed neurones
21
Q

How is plasticity associated with LTP?

A
  • leads to visible changes

- experiment in newborn animals, dendrites physically branch out within a few hours of LTP

22
Q

Describe the plasticity in the pathways associated with learning and memory

A
  • the cortical association areas that send messages to hippocampus and receive LTM storage have the plasticity
23
Q

Explain the variation of synaptic plasticity

A
  • plasticity is not equal in all brain areas
  • the limbic system (with hippocampus), the hub of memory info has the nightly plastic synapses which can change rapidly and drastically
  • primary sensory and motor areas have rigid synapses as they shouldn’t change
  • depends on how integrative the function is
24
Q

Is it possible to make cognitive enhancers?

A
  • do we know enough about learning and memory?
  • cognitive enhancers, smart drugs = nootropics

Possible effects?

  • increased brain metabolism
  • increased cerebral circulation
  • protection of brain from physical and chemical damage

–> all depends on neurotrophins