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Systems Neurobiology > Memory > Flashcards

Memory Flashcards

1
Q

What is learning?

A

a change in behaviour as a result of experience

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2
Q

What is memory?

A

the changed behaviour resulting from learning

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3
Q

Where do the IT and prefrontal cortexes signal?

A

the medial temporal cortex (not part of the neocortex)

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4
Q

What surgery did HM undergo?

A

a bilateral medial temporal lobectomy to surgically resect the anterior two thirds of his hippocampi, parahippocampal cortices, entorhinal cortices, piriform cortices, and amygdalae in an attempt to cure his epilepsy

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5
Q

What were HM’s symptoms after surgery?

A
  • unable to recognise hospital staff
  • recalled nothing of the day-to-day events of his hospital life
  • partial retrograde amnesia
  • unable to form new memories but early memories were intact
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6
Q

What is partial retrograde amnesia?

A

a condition where a person loses some, but not all, memories from before the onset of amnesia, typically affecting more recent memories while sparing older ones

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7
Q

What is the first major lesson from HM?

A
  • some MTL structures are needed for forming and storing new long-term declarative memories
  • some remote (oldest) memories are independent of the MTL structures needed for forming new declarative memories and for recalling more recent declarative memories
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8
Q

How are declarative memories tested?

A

by asking simple questions e.g. what did you have for breakfast?

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9
Q

How does the MTL relate to memory?

A

it is required to form new memories but as the memory gets older, it is no longer required to recall

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10
Q

What is cellular consolidation?

A

a quick process at the synaptic level that stabilises memory traces

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11
Q

What is systems consolidation?

A

a slower process that reorganises and transfers memories from the hippocampus to the cortex for long-term storage

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12
Q

What happens in the initial stage of memory consolidation?

A
  • strong connections exist between the hippocampus and various cortical modules
  • the hippocampus plays a central role in linking different cortical modules, acting as a hub for integrating and retrieving memories
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13
Q

What happens in the intermediate stage of memory consolidation?

A
  • over time, the connections between the hippocampus and the cortex begin to weaken, while connections within the cortical modules - - this represents a transitional phase where the hippocampus still contributes to memory retrieval, but the cortical modules are starting to form direct connections with each other
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14
Q

What happens in the final stage of memory consolidation?

A
  • eventually, the memory becomes primarily stored in the cortex, with strong interconnections between the cortical modules and significantly reduced dependence on the hippocampus
  • the cortical modules are now sufficiently interconnected to support memory retrieval independently of the hippocampus
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15
Q

What is the second major lesson from HM?

A
  • procedural learning is independent of the MTL structures needed for forming new declarative memories
  • different types of memory involve different parts of the brain
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16
Q

What structures are responsible for declarative memory?

A

hippocampus and parahippocampal region

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17
Q

What structures are responsible for procedural memory?

A

brainstem and spinal motor outputs, striatum and cerebellum

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18
Q

What structures are responsible for emotional memory?

A

hypothalamus, autonomic and hormonal outputs and amygdala

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19
Q

What are possible reasons for HM still being able to acquire some declarative memories?

A
  • spared MTL structures e.g. posterior parrahippocampal cortex
  • sufficient repetition may overcome loss of some MTL structures
20
Q

What is one possibility of learning being due to changes in the brain?

A

learning is due to a change in the strength of connections between neurons

21
Q

What is the Hebbian idea?

A

pre and post synaptic neurons must be active at the same time to have LTP

22
Q

What is LTD?

A

a form of excitatory synaptic plasticity defined as a persistent decrease in synaptic strength, and like LTP, can be NMDA receptor-dependent and independent

23
Q

What is LTP?

A

a persistent strengthening of synapses based on recent patterns of activity

24
Q

What synapses on CA1 neurons?

A

glutamate

25
Q

What are CA1 and CA3 regions?

A

principal excitatory neurons involved in the hippocampal circuitry

26
Q

What is the function of CA1 and CA3 respectively?

A
  • CA1 - integrates signals from CA3 and entorhinal cortex
  • CA3 - involved in pattern completion
27
Q

Describe the perforant pathway

A

it originates from the entorhinal cortex and projects to the dentate gyrus and serves as the primary input to the hippocampus, bringing in information from the cortex

28
Q

What do granule cells in the dentate gyrus do?

A

project to the CA3 region via mossy fibres characterised by high synaptic specificity, important for pattern separation and encoding distinct memories

29
Q

How do neurons in CA3 project to CA1?

A

through Schaffer collaterals which are crucial for associative learning and the consolidation of information within the hippocampus

30
Q

What does high and low frequency stimulation of CA3 cause respectively?

A
  • high - LTP
  • low - LTD
31
Q

What happens when neurons in CA3 release glutamate?

A

they excite neurons in CA1 of the hippocampus

32
Q

What are the 2 types of glutamate receptors?

A
  • AMPA
  • NMDA
33
Q

What are commonalities between the 2 glutamate receptors?

A

both require glutamate to open and when open, they drive the membrane potential towards 0mV

34
Q

What are AMPA and NMDA receptors permeable to respectively?

A
  • AMPA - Na+ and K+, but not Ca2+
  • NMDA - Na+, K+ and Ca2+
35
Q

What do NMDA receptors require to allow ion flow?

A

glutamate and postsynaptic depolarisation

36
Q

What happens to NMDA receptors at hyperpolarised and depolarised potentials respectively?

A
  • hyperpolarised - extracellular Mg2+ sits in the pore, blocking the flow
  • depolarised - Mg2+ is repelled from the pore which allows ion flow
37
Q

What does LTP/LTD require at CA3-CA1 synapses?

A

NMDA receptors

38
Q

What are the 4 steps of plasticity occurring at NMDA receptors?

A
  1. several presynaptic APs cause more glutamate release
  2. more postsynaptic AMPA receptors open causing greater postsynaptic depolarisation
  3. greater postsynaptic depolarisation repels Mg2+ out of the NMDA channel, allowing positive current and Ca2+ to enter
  4. sufficiently high postsynaptic Ca2+ leads to more AMPA receptors being inserted into the postsynaptic membrane, strengthening the synapse
39
Q

What is the calcium control hypothesis?

A
  • LTP and LTD require Ca2+
  • low Ca2+ → LTD
  • high Ca2+ → LTP
40
Q

How can LTP associativity be described?

A
  • when only the weak synapse is activated, the small postsynaptic depolarisation does not open NMDA receptors at the synapse, so the weak synapse does not strengthen
  • when the weak and strong synapses are activated together, the depolarisation caused by the strong synapse spreads to the weak synapse, sums with the depolarisation caused by the weak synapse, resulting in sufficient depolarisation to open postsynaptic NMDA receptors at the weak synapse, allowing the weak synapse to strengthen
41
Q

What is the most precise localisation of memory?

A

to say which synapses or neurons were changed to produce new behaviour

42
Q

What are hippocampus dependent memories?

A

memories that are lost when the hippocampus is silenced

43
Q

How are memory functions mapped to different brain regions?

A

by observing activity patterns or studying the effects of brain damage using fMRI and PET scans

44
Q

Describe the involvement of the hippocampus and striatum in habitual behaviour

A

during initial learning, both the hippocampus and striatum are involved, but with continued training, the striatum’s role becomes more dominant

45
Q

What is a common shift in habitual learning?

A

tasks initially performed using deliberate, spatial strategies eventually become automatic and routine, facilitated by the striatum

Systems Neurobiology (10 decks)

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