Learning & Memory 1 Flashcards

1
Q

Define the term ‘learning’?

A
  • Acquisition of new information or knowledge

(active process of acquiring information)

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2
Q

Define the term ‘memory’?

A
  • Retention of learned information

(keeping them in store)

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3
Q

Why is ‘retrieval’ needed?

A
  • Necessary to recall stored information

(need access to recall memory)

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4
Q

What three components could affect memory?

A
  • Learning
  • Memory
  • Retrieval

(e.g. sometimes you can learn something but cannot retrieve the memory)

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5
Q

What is meant be ‘declarative’ memory?

A
  • Memories for facts & events
  • These can be accessed for conscious recollection

(e.g. my first bike was a present on my sixth birthday)

(these memories can be recalled & explained to someone else)

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6
Q

What are the three different types of declarative memory?

A
  • Episodic Memory
  • Semantic Memory
  • Working Memory
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7
Q

What is meant by ‘episodic memory’?

A
  • Recollecting specific events in time
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8
Q

What is meant by ‘semantic memory’?

A
  • Remembering familiar objects or facts
    (e. g. the capital of france - learnt it at some point but cannot remember the event where you learned it so not episodic anymore but semantic)
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9
Q

What is meant by ‘working memory’?

A
  • Has qualities of both episodic & semantic memory (combination)
    Memories for a short-period of time
  • They are not held forever (just for few minutes/hours)

(e.g. parking a car in the supermarket carpark)

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10
Q

What is another name for ‘working memory’?

A
  • Short-term hold memory
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11
Q

What is meant by procedural memory?

A
  • Memories that do not require conscious recollection
  • These include habits (e.g. riding a bike)

(relatively long-term memory - these habits such as riding a bike need to be ‘learned’)

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12
Q

What is short-term memory?

A
  • Lasts for a few minutes
  • Usually involved mental rehearsal
  • Easily disturbed

(e.g. initial stages of learning a telephone number - need constant rehearsal at first)

These can become long-term memory –> where they no longer need to be continued rehearsed –> they are resistant to disturbance

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13
Q

What is long-term memory?

A
  • More permanent
  • Does not require continued rehearsal
  • Has a greater capacity
  • Resistant to disturbance

(e.g. memory for familiar telephone numbers)

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14
Q

What are the two methods that process long-term memory called?

A
  1. Serial Process
  2. Parallel Process
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15
Q

Describe briefly the serial process of memorisation?

A
  1. Sensory information comes into system
  2. Held in the short-term memory
  3. Via consolidation (usually requires sleep) –> becomes stored in long-term memory
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16
Q

Describe briefly the parallel process of memorisation?

A
  1. Sensory information enters & held in short-term memory
  2. At the same time –> information is being consolidated over a longer period of time –> to acheive storage in long-term memory storage

Difference –> long-term memory is not a consequence of short-term memory –> but its own independent pathway

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17
Q

What is amnesia?

A
  • Memory loss due to brain insult

(can range from minor to serious)

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18
Q

Name four potential causes of amnesia?

A
  1. Concussion (usually between 20-30 minutes)
  2. Chronic Alcoholism
  3. Tumours
  4. Strokes

(patients usually wake up confused with no recollection of event & no awareness of location)

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19
Q

What occurs with the memory of the event?

A
  • Loss of Memory (amnesia) –> is permenant for that specific period of time
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20
Q

What is retrograde amnesia?

A
  • Loss of memory for events prior (before) to the trauma
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21
Q

What is anterograde amensia?

A
  • Inability to make or retrieve new memories after the trauma (event)
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22
Q

When can you not use the terms anterograde & retrograde?

A
  • To describe memory (not such thing as anterograde memory)
  • It is anterograde or retrograde amnesia
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23
Q

What is a clinical presentation of someone with retrograde memory loss?

A
  • Able to recall early childhood memories
  • Unable to recall a certain time window before the trauma (event) - no recollection

(this can range from minutes/days/weeks)

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24
Q

What are the clinical presentations of someone with anterograde amnesia?

Is isolated anterograde amnesia common?

A
  • Usually serious anterograde amnesia is not seen alone
  • Inability to form new memories from the date of event (trauma)

(usually patients present with both anterograde & retrograde amnesia)

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25
Q

What is the physical storage of memory called?

A
  • Engram
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26
Q

How has memory circuitry been studied?

A
  • Brain lesions
  • Lashley (1920s) –> studied maze learning in rats with cerebral cortical lesions
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27
Q

Where is memory stored generally?

A
  • Memories are distributed

(sizes of lesions correlated to memory impairment)

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28
Q

Is the cortical areas equipotential for learning?

A
  • No
  • Cortical areas are not equipotential for learning (some areas are more important than others)
  • Lesions in certain areas have a more profound effect
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29
Q

What happens if there are large bilateral lesions of the temporal lobes?

A
  • Psychic blindness

(animals will repeatedly put the same inedible objects into their mouth even having tried it before - usually animals learn from the first time)

Temporal lobe has specific regions involved in recognising specific objects (memory system for recognising visual objects)

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30
Q

What happened to patient HM?

A
  • To treat severe epilepsy
  • Received bilateral, medial temporal lobe resection
  • Improved epilepsy
  • Profound amnesia
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31
Q

What four areas are near or in the medial temporal lobe?

A
  • Hippocampus
  • Entorhinal Cortex
  • Pernihal Cortex
  • Parahippocampal Gyrus
32
Q

Describe the medial temporal lobe area involved in memory.

A
33
Q

In terms of amnesia, what happened to patient HM?

A
  • Partial Retrograde Amnesia (could recalled early childhood but not years before surgery)
  • Profound anterograde amnesia (no new declarative memory ever again - despite memory test experiments)
  • Retrieval mechanism undamaged (could recall early childhood still)
  • Short-term memory was normal (six numbers fine)
  • Procedural memory (mirror writing) was normal
34
Q

What areas in the temporal lobe are important in memory?

A
  • Rhinal Cortex
  • Perirhinal Cortex
  • Amygdala
  • Anterior Hippocampus
  • Parahippocampal Area
35
Q

Describe the loop involved in memory.

A
36
Q

What is a good test for temporal lobe?

A
  • Delayed non-match to sample (DNMS)
  • Test of recognising object that have been seen recently (over seconds to minutes)
  • Tests for declarative memory amnesia (seen in patient HM)
37
Q

Particularly what part of the brain is implicated in declarative memory amnesia and therefore difficulty with DNMS task test?

A
  • Temporal Lobe Lesions
  • specifically Perirhinal Cortex damage

(monkey able to remember within a small amount of time –> but after 1 minute of screen going down the rule is forgotten - only have short-term memory)

38
Q

Name the four critical areas for declarative memory loss (name the 2 most critical).

A
  • Rhinal Cortex
  • Perirhinal Cortex
  • Hippocampus
  • Amygdala
39
Q

How does the associative circuitry work?

A
  • There are a lot of reciptical connections
  • These allow for additional output pathways from associative circuitry
40
Q

What is less damaging to memory than parahippocampal & rhinal area damage?

A
  • Lesion in Hippocampus

(those others were more improtant as they are in the middle of reciprical connections)

41
Q

Describe the declarative memory circuitry.

A
42
Q

What is the diencephalon involved in?

Which structures specifically?

A
  • Memory
  • Thalamus & Mammillary Bodies
43
Q

How is memory located in the brain?

A
  • Different structures are involved at different times
  • Depends on memory type & time the memory is at (minutes or weeks from start)
  • Memory constantly moves & distributes (does not remain)
  • Stored in different brain regions
  • System must work together to recall memory properly
44
Q

What occurs when there is damage to either?

  • Anterior Nuclei of the Thalamus
  • Dorso-Medial Nuclei of the Thalamus
  • Mamillary Bodies
A
  • Distruption to Memory
45
Q

Describe pathway 1 invovled in memory.

A
46
Q

Describe pathway 2 involved in memory.

A
47
Q

What test is affected with midline thalamic lesions in monkeys?

A

DNMS Test Deficits

48
Q

What occured with patient NA?

A
  • Stabbed with fencing foil
  • Went up through right nostril –> into left dorsomedial thalamus
  • Severe anterograde amnesia & retrograde amnesia (2 years up to accident) - difficult reading books & TV

(strong similarities in deficits with patient HM –> related to temporal lobe - diencephalic connections)

49
Q

What causes Korsakoff’s syndrome?

A
  • Chronic Alcoholism
  • This depletes thiamine (vitamin B1) reserves
50
Q

What happens in Korsakoff’s syndrome?

A
  • Anterograde amnesia
  • Limited retrograde amensia
51
Q

What is damaged in Korsakoff’s syndrome?

A

Degeneration of:

  • Mammillary Bodies
  • Dosomedial Nucleus of the Thalamus
  • Cerebellar Anterior Lobe Vermis
52
Q

What are the neurological signs of Korsakoff’s syndrome?

A
  • Anterograde amnesia
  • Limited Retrograde amnesia
  • (maybe) Confusional State
  • Ataxia (especially gait ataxia - cerebellar anterior lobe vermis)

(gait is affected but distal limb control is not)

53
Q

What is the treatment of Korsakoff’s Syndrome?

What can we expect?

A
  • Treatment with Vitamin B1
  • Leads to remarkable & rapid recovery of the motor & confusional problems
  • Amnesia usually persists

(confusional state can be helped a lot but damage to memory such as to mamillary body is permenant)

54
Q

What does chronic alcoholism do to the cerebellum?

A
  • Damage to anterior lobe vermis
  • Causes gait ataxia
55
Q

Name three causes of dementia?

A
  1. Vascular Dementia
  2. Senile Dementia
  3. Alzheimer’s Dementia
56
Q

What causes Alzheimer’s Disease?

A
  • Neurofibrillary tangles (phosphorylated tau)
  • *Neuritic plaques** (amyloid)
57
Q

What does AD severity correlate with?

A
  • Increase in neurofibrilary tangles (phosphorylated tau)

(not plaques/amyloid)

58
Q

What are the two structures first affected by AD?

A
  • Hippocampus
  • Posterior Parieto-Temporal Cortex
59
Q

Secondly, what does AD affect?

A

Degeneration of:

  • Basal Nucleus of the Forebrain (nucleus of Meynert)
  • Cholinergic Neurones
  • Noradrenergic neurons (locus coeruleus)
  • *Serotonergic raphe neurons**
60
Q

What neurological sign is seen in AD?

A
  • Retrograde amnesia
  • Spreads back in time as the disease progresses
61
Q

Which type of memory is affected the most & least in AD?

A
  • Episodic memory (affected most & early on)
  • *Working & semantic memory** (affected less so and middle of disease)
  • Procedural memory (not impaired until final stages)
62
Q

What is the basis of one of the treatments called cholinesterase inhibitors?

A
  • Degeneration of basal nucleus of the forebrain (nucleus of Meynert) and its cholinergic neurones

It does not address the cause but its supportive & helps delay some amnesic symptoms

  • Maximises residual cholinergic function
  • Results are marginal but delays progression of disease
63
Q

What are the 2 pathologies associated with AD?

A
  • Neurofibrillary Tangles
  • Amyloid Plaques
64
Q

What is working memory exactly?

A
  • Information of several types needs to be held in a short-term store at the same time
    (e. g. book title, colour of the cover, location on the shelf)
  • Information can be either be new sensory information or information retrieved from long-term storage which is ready to access

(ability tto hold onto information for a short period of time & lose memory when needed - does not need to be consoldiated)

65
Q

Describe the connections between the medial temporal areas & cortical association areas.

Involved in working memory

A
66
Q

Where does prefrontal cortex get information from to do with working memory?

A
  • Temporal Lobe inputs via dorsomedial thalamus
67
Q

Which part of the brain is very important in working memory?

A
  • Prefrontal Cortex
68
Q

What occurs if there is a lesion in prefrontal cortex?

Which test is there a deficit in?

A
  • Deficits in working memory for problem solving
  • Wisconsin card-sorting test
69
Q

Where are neurons active during a delayed response test?

A
  • Prefrontal Cortex
70
Q

What is the wisconsin card sorting test?

A
  • Asked to sort cards out in terms of a certain rule (e.g. numbers or suites or pictures)
  • Asked to keep doing it
  • They eventually forget what the rule was
71
Q

When are prefrontal cortex cells active during ?

A
  • Delay period in delayed-response task

(asked to do a task but cannot execute straight away –> need to wait for a momeny –> thus neurone activity is high whilst handing on & waiting –> then prefrontal activity drops as soon as action can be executed)

72
Q

What does pre-frontal cortex code for in terms of memory?

A

Pre-frontal cortex –> codes for short-term information that you temporarily hold onto (i.e. working memory)

73
Q

Where is memory found in the brain?

A
  • No single place in the brain for ‘memory formation & storage’
  • Different forms of memory mediated in different brain areas
74
Q

Where is memory distributed within a brain area?

A
  • Distributed everywhere within these brain memory areas (more involved in memory)
75
Q

How can we describe the properties of short & long-term memory?

A
  • Short-term memory –> FRAGILE
  • Long-term memory –> ROBUST

Long-term memory depends on a form of structural change (consolidated in a stable form –> takes time & repitition & sleep)

Short-term memory is maintained by electrical activity and is therefore very fragile

76
Q

What are declarative memories critically dependent on?

A
  • Medial Temporal Lobe
  • Nuclei in the Diencephalon (thalamic nuclei)
77
Q

What are procedural memories with a strong motor component dependent on?

(e.g. riding a bicycle)

A
  • Cerebellum