Memory And Forgetting Flashcards

1
Q

What types of memory are there (+associated brain regions)?

A

Short-term memory
- prefrontal cortex
Working memory
- prefrontal cortex, parietal lobe, temporal lobe, hippocampus
Long-term memory
- declarative memory (explicit memory): hippocampus, neocortex, amygdala
- non-declarative memory (implicit memory): basal ganglia and cerebellum

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2
Q

Hippocampus

A

= situated in mesial temporal lobe within the inferior horn of the lateral ventricle

  • seahorse-like appearance
  • three parts:
    -> head = mesolateral axis
    -> body = anteroposterior axis
    -> tail = mesiolateral axis
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3
Q

Long-term potentiation (LTP)

A

pyramidal neurons in rodent hippocampus:

  • high frequency stimulation of synapse makes the post-synaptic neuron more responsive to future stimulations at this synapse
  • effect can last hours to years
  • specificity:
    -> no general increase in responsiveness of the post-synaptic neuron (= synapses that are inactive during the high-frequency depolarisation are not reinforced)
  • will arise both when the pre-synaptic and the post-synaptic neuron are depolarised in synchrony (= within approx. 100ms)

–> Cells that fire together, wire together

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4
Q

Activation of NMDA receptors

A

NMDA receptors = ligand-gated cation channels activated by glutamate

  • at resting potential (post-synaptic cell not depolarised): no NMDA receptor activity
  • during post-synaptic depolarisation: depolarisation activates NMDAR –> Ca2+ influx
  • Ca2+ activates proteins that contribute to expression of AMPA receptors on surface –> locally amplifying glutamate effects or activating ‘silent synpases’ (=previously not expressing AMPA receptor)
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5
Q

How to study memory: Behavioural experiments

A

1) memory tests
- recall tasks to measure woking and short term memory
2) eye witness memory studies
- to examine how people recall events, often focusing on how memories can change over time or be influenced by suggestion

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6
Q

How to study memory: Neuroimaging

A

1) fMRI
- measures brain activity by detecting changes in blood flow to see which areas of the brain are activated when people form or recall memories
2) PET
- measure glucose metabolism in the brain to see which regions are more active during memory tasks
3) EEG
- measure electrical activity in the brain

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7
Q

How to study memory: lesions

A
  • examine people or animals with brain damage to see which parts of the brain are involved in memory
  • for example: damage to the hippocampus is associated with problems in forming new memories (patient HM)
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8
Q

How to study memory: TMS

A
  • temporarily disrupt or enhance activity in specific areas of the brain to see how disrupting these areas affects memory performance
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9
Q

How to study memory: pharmacological studies

A
  • using drugs to investigate memory processes (drugs that modulate acetlycholine, glutamate, dopamine systems)
    –> how different neurotransmitters or receptors affect memory formation
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10
Q

How reliable are our memories?

A

memory is reconstructive
- based on a combination of the original experience and external information
- each time we retrieve a memory, it can be altered and re-stored with new details

false memory
- false memories can be created –> people can vividly recall events that never happened, especially when they are given misleading information or are asked leading questions

Loftus’s research: suggestive questions leading to people remembering details that were never part of the original event

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11
Q

What affects memory?

A
  • emotion and stress
  • attention
  • age-related memory decline
  • neurodegenerative diseases (AD, dementia)
  • cognitive bias (stereotypes, ideologies)
  • sleep
  • drugs
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12
Q

Influence of LTP and LTD

A
  • LTP and LTD cannot happen at the same time (mutually exclusive)
  • dopamine is used as a neuromodulator in both
  • LTD provides necessary balance for fine-tuning neural signals
  • LTP alone would result in all synapses becoming maximally strong
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13
Q

LTD versus forgetting

A

LTD ≠ forgetting

LTD
- single synaptic mechanism
- induced within minutes
- can sometimes result in forgetting

Forgetting
- multiple mechanisms
- occurs in minutes to years

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14
Q

Forgetting: Passive forgetting

A

Passive forgetting:
- natural decay of memories over time
- loss of retrieval cues/context

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15
Q

Forgetting: Two mechanisms

A

Two mechanisms:
- memory inhibition: direct suppression of memories
- process inhibition: general suppression of memories

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16
Q

Forgetting: Benefits

A

Benefits:
- emotional resilience
- reduced cognitive conflict
- allows for adaptation to current goals

17
Q

Forgetting: Practical implications

A

Practical Implications:
- useful in organisations (?) for training
- clinical applications
- emotional regulation

18
Q

Unwanted forgetting

A

= Amnesia (pathological forgetting)

1) anterograde amnesia = difficulty forming new memories

2) retrograde amnesia = difficulty retrieving old memories

Can have various causes:
- head injuries
- strokes
- neurodegenerative diseases

19
Q

Dementia and (early) symptoms, types of dementia

A

= ‘loss of mind’, more than normal memory loss due to ageing

  • characterised by memory loss, decline of other cognitive functions and personality changes

Some common features:
- dyslexia
- dyscalculia
- receptive dysphasia
- prosopagnosia
- agnosia
- episodic memory loss
- mood changes
- expressive dysphasia
- alternations of behaviour and personality
- executive dyfunction

Types of dementia:
- Alzheimer’s disease
- dementia with Lewi Bodies
- vascular dementina
- frontotemporal dementia

20
Q

Alzheimer’s Disease

A

most common form of dementia (60-80%)

early symptoms include:
- short term memory loss (particularly episodic memory)
- spatial disorientation

diagnosis can only be confirmed post-mortem

three characteristic pathological changes:
- intraneuronal neurofibrillary tangles
- extracellular amyloid plaques
- diffuse loss of neurons

21
Q

Dementia with Lewi Bodies

A

makes up 20% of dementia cases

Characteristic symptoms include:
- visual hallucinations
- fluctations in cognitive performance
- Parkinsonism

22
Q

Vascular Dementia

A
  • makes up 10% of dementia cases
  • more prominent mood changes
  • bigger fluctation in symptoms