Theme 5: Memory and the changing brain Flashcards

1
Q

hebbian learning

A

learning through strengthening connections

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2
Q

neurons that fire together, wire together –> explain

A

if neurons often fire together –> increased probability than when neuron A is activated, neuron B will become active too

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3
Q

long term potentiation

A

more effective synapse transmission = stronger response to same stimulus –> lasts a long time

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4
Q

long term depression

A

synaptic transmission becomes less effective as a result of recent activity = weaker response to similar stimulus

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5
Q

role hippocampus in memory

A
  • critical for episodic memory (rats weren’t able to form episodic memory about a maze)
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6
Q

prediction of recall using fMRI

A

incidental learning task –> found more activity in medial temporal lobe for words that would be recalled

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7
Q

levels of processing effect in brain areas:

A

same brain areas are active in different levels of processing, however stronger activation during deep processing

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8
Q

distinguishing true from false episodic memories

A

parahippocampal cortex responds more strongly to ‘true’ episodic memories

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9
Q

robots gradient

A

in retrograde amnesia: more memory loss for events that occurred shortly before the damage than a longer time before

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10
Q

standard consolidation theory

A

first hippocampus & medial temporal lobe structures are involved in consolidation –> over time cortex become independent in retrieval

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11
Q

subcortical structures involved in episodic and semantic memory

A

-basal forebrain produces acetylcholine –> help hippocampus word effectively
-basal forebrain connects to diencephalon (thalamus, hypothalamus, mammillary bodies) through the fornix
-basal forebrain receieves oxygen from ACoA (anterior communicatory artery) –> aneurysm in ACoA causes anterograde amnesia (because hippocampus doesn’t receive neuromodulators anymore)

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12
Q

confabulations + possible cause

A

highly detailed false memories (basal forebrain damage) –> seems to be a source monitoring error

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13
Q

korsakoffs

A

-deficiency in thiamine (b vitamin) commonly seen in alcoholics
-causes confabulations and disorientations

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14
Q

dementia

A

impairments in thinking, commonly memory but no impairment to consciousness

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15
Q

alzheimer’s
-causes
-symptoms
-brain damage?

A

-neuronal loss, neurofibrillary tangles (inside) & amyloid plaques (outside)
-symptoms: problems with central executive, ribots gradient in memory loss, usually most damage to episodic but also semantic in the end

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16
Q

parkinson’s

A

-damage to neurons in basal ganglia + substantia nigra + disruption in dopamine processing
-motor problems + WM problems, ribots gradient for EM + issues with locating events in time /correct sequence of information

17
Q

huntington’s

A
  • basal ganglia & caudate nucleus damage
  • motor movement impairment, problems with central executive more uniform memory loss over time
18
Q

multiple sclerosis

A
  • demyelination of neurons, damage to hippocampus
  • muscle control problems and possibly memory loss
19
Q

amnesia

A

memory loss

20
Q

organic amnesia

A

amnesia as a result of organic brain damage

21
Q

retrograde amnesia

A

loss of memories prior to incident

22
Q

anterograde amnesia

A

loss of ability to store new memories / memory loss after incident

23
Q

transient global amnesia

A

complete memory loss for a short period of time

24
Q

semantic amnesia

A

inability to retrieve semantic knowledge

25
Q

anomia

A

difficulty recalling word meaning (can be specific category of words)

26
Q

apraxia

A

difficulty with how objects are used

27
Q

aphasia

A

loss of ability to use language (comprehend/produce)

28
Q

prosopagnosia

A

failure to recognise faces

29
Q

psychogenic amnesia

A

amnesia with a psychological cause

30
Q

dissociative amnesia

A

inability to remember segment of life

31
Q

dissociative fugue

A

forgetting fundamental aspects of identity

32
Q

Maguire et al: London taxi drivers & bus driver mri study

A

-goal: investigating effects of self motion, driving experience, stress on grey matter volume in taxi/bus drivers
- hypothesis: difference in grey matter volume is indicative of plasticity due to spatial demands placed on hippocampus
- method: MRI scan, loads of tests, using VBM to analyse grey matter volume
-RESULTS: more grey matter volume in posterior hippocampi, less volume in anterior hippocampi
-