Memory Flashcards

1
Q

What is Atkinson and Shiffrin’s multistore model of memory

A

consists of modality-specific sensory stores, a short-term store of very limited capacity and a long-term store of essentially unlimited capacity capable of holding information over time

in this model, attention moves information from sensory stores to Short term memory and rehearsal then moves it to long term store

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2
Q

What are the 2 key sensory stores in the multi-store model of memory

A

iconic store
echoic store

these are brief sensory stores for visual and auditory information respectively

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3
Q

Describe of Sperling’s experiments in the 1960s

what were the results

what does this suggest about the iconic store

A

presented an array of numbers in a grid

Typically, participants could only report 4 or 5 of the letters correctly, but in a “partial report” condition, were able to report most of the letters from the requested line if the delay between removal of the array and presentation of the prompt was ~1 s or less.

suggests that information in iconic storage decays in less than a second

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4
Q

How did Treisman show the existence of an echoic store

A

presented participants with an auditory message to one ear and asked them to repeat the message back aloud while ignoring a second message being presented to the other ear.

If the second, ignored, message was actually identical to the first but started at a different time, participants only noticed they were the same if they started within 2 seconds of each other.

suggests the persistence of unattended information in the echoic store is ~2 s, otherwise information decays

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5
Q

How did Miller (1956) investigate the capacity (or “span”) of short-term memory

A

by asking subjects to recall digit strings. Typically, participants could recall strings correctly up to a length of 7 ± 2 digits. This result held for other stimuli like letters or words

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6
Q

What did Miller conclude was the capacity for short term memory

A

could hold 7 integrated chunks of info

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7
Q

How can information be retained in short term memory

A

by rehearsing it

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8
Q

How did Peterson and Peterson study short term memory forgetting

what did they find

A

by asking participants to remember a stimulus for a few seconds while counting backwards in threes.

The ability to remember the stimulus diminished rapidly, suggesting that information decays from short-term memory within a matter of seconds

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9
Q

How did Waugh and Norman (1965) show short-term memory forgetting is due to interference from exposure to additional information, rather than the passage of time.

A

manipulated the speed with which digits that were to be remembered were presented to participants and found that digit recall was (more or less) unaffected

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10
Q

Give some criticisms of the Multistore Model of memory

A

falsely suggests processing in the short term is required for encoding into long term memory

assumes short term and long term stores are unitary, operating in a single, uniform way

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11
Q

According to the multistore model, processing in the short-term store is required for encoding into
long-term memory. How do we know this is not true?

A

patient KF, with defective short-term memory (digit span) but preserved long-term learning and recall, provides evidence against this claim

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12
Q

Another assumption of the multistore model is that the short-term and
long-term stores are unitary, operating in a single, uniform way. How do we know this is wrong

A

patient KF had worse short term memory for auditory letters and digits than for visual stimuli, suggesting that there may be distinct short-term memory stores for different kinds of material

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13
Q

Which model, proposed by Baddeley and Hitch (1974), aimed to improve on the multistore model of memory

A

working memory model

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14
Q

Describe the working memory model

A

comprised 3 primary components:
an auditory-verbal phonological loop for short-term storage of speech-based information;

a visuo-spatial sketchpad for short-term storage of spatial and visual information;

a modality-free central executive, responsible for selecting and initiating cognitive processing routines

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15
Q

What is the phonological similarity effect

A

Baddeley (1966) found that serial recall of a list of phonologically similar words (such as FEE, HE, KNEE, etc.) was significantly worse than from a list of phonologically dissimilar words (such as BAY, HOE, IT, etc.).

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16
Q

What does the phonological similarity effect suggest

A

that speech-based representations are used in storing the words, and that recall requires discrimination between memory traces, which is more difficult for similar phonological representations.

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17
Q

Describe the word length effect (Baddeley et al., 1975)

A

recall of a list of long words (such as OPPORTUNITY, ALUMINIUM, etc.) is typically worse than recall of a list of short words (such as WIT, SUM, etc.).

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18
Q

How did Baddeley confirm that the word length effect depends on the phonological loop

A

by asking participants to silently mouth digits (articulatory suppression) during presentation and recall of words. This manipulation eliminated the word-length effect, suggesting that phonological storage capacity is determined by rate of rehearsal.

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19
Q

What is the articulatory control process proposed by Baddeley

A

he drew a distinction between a phonological store, concerned with speech perception, and an articulatory control process linked to speech production that gives access to the phonological store

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20
Q

What can the phonological similarity and word length effect be attributed to

A

e phonological similarity effect can be attributed to confusions between similar representations in the phonological store,

the word-length effect can be attributed to the time taken to rehearse longer words via the articulatory control process.

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21
Q

What is the visuospatial sketchpad used for

A

the temporary storage and manipulation of spatial and visual information, including visual imagery.

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22
Q

How did Baddeley discover the visuospatial sketchpad

A

asked participants to encode material using either rote verbal learning or an imagery-based strategy.

When this task was combined with pursuit rotor tracking (tracking a moving light), performance using the imagery-based strategy was disrupted, whereas performance using the verbal strategy was unaffected. (Pursuit rotor tracking involves visual perception as well as spatial localization)

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23
Q

In Baddeley’s experiment to assess visuospatial sketchpad, he used pursuit rotor tracking, which uses visual perception and spatial localisation. What further experiment was done to assess whether both of these factors are important?

A

repeated the previous experiment, contrasting specifically visual (making brightness judgements) and specifically spatial (pointing at a moving pendulum while blindfolded, guided by an auditory tone) concurrent tasks.

Learning using the imagery-based strategy was most clearly disrupted by the spatial concurrent task.

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24
Q

How did Logie argue the visuospatial working memory could be divided

A

into 2 components:
visual cache
inner scribe

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25
Q

What is the visual cache

A

passively stores information about visual form and colour and is subject to decay and interference by new visual information.

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26
Q

What does the inner scribe do

A

processes spatial information and allows active rehearsal of information in the visual cache

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27
Q

How does neuropsychological data support the division of the visuospatial sketchpad

A

eg patient NL, who had preserved perceptual skills but could not describe details of a scene from memory

patient LH, who performed better on spatial processing tasks than on visual imagery tasks

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28
Q

If you are given a list of words to remember, and then immediately asked to recall them, what pattern is seen in your recall?

A

you will usually exhibit a serial position curve, with much better recall of the first few items in the list (primacy effect) and the last few items (recency effect)

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29
Q

What did Atkinson and Shiffrin attribute the recency effect to

is this a correct assumption?

A

the last few items still being present in the short-term store from the end of list presentation

yes - Glanzer & Cunitz (1966) showed that the recency effect could be eliminated if participants counted backwards prior to recall, supporting the link
with short-term memory.

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30
Q

What did Atkinson and Shiffrin attribute the primacy effect to

why

A

long-term memory, as counting backwards had no effect, whereas manipulating word familiarity, presentation rate, age of participant etc. affects primacy but not recency (Glanzer, 1972)

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31
Q

What damage did Patient HM suffer

why is he important for short/long term memory studies

A

medial temporal lobe damage

had impaired long-term memory but normal digit span

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32
Q

Give a patient who contrasts HM

A

patient KF, suffered parieto-occipital lobe damage and had intact long-term memory but very poor digit span

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33
Q

Which 2 patients demonstrate the difference between short and long term memory

A

patient KF, suffered parieto-occipital lobe damage and had intact long-term memory but very poor digit span

patient HM, who suffered medial temporal damage and had impaired long-term memory but normal digit span

Results from functional neuroimaging data have typically been consistent with the view that different brain areas may support short-term and long-term memory.

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34
Q

Where is short term memory found in the brain

A

inferior frontal and parietal cortex

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35
Q

What was the first rigorous experimental investigation of human long term memory

A

conducted by Ebbinghaus (1885), who taught himself lists of nonsense syllables and repeated them until he could recite them correctly twice. He measured the time to learn the lists, and then the time saved in relearning them after various delays.
He found that retention decreased with a longer retention interval, but that the rate of forgetting slowed down after the first hour or so.

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36
Q

What is the limit of long term memory capacity

A

theoretically unlimited

but only 10^15 neurons in brain and rate of acquisition is limited by our lifespan:
if a human studies the maximum of 100 stimuli per min over 70 years = theoretical capacity limitation of ~3 billion stimuli.

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37
Q

How does forgetting from long term memory change over time

A

very rapid over the first hour or so after acquisition, then reduces approximately logarithmically.

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38
Q

What causes long term memory forgetting

A

primarily to interference from other experienced events

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39
Q

What are the 2 main forms of interference which cause long term memory forgetting

A

proactive interference - when previous learning interferes with later
learning,

retroactive interference - when later learning interferes with previous learning.

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40
Q

Give Underwood’s example of proactive interference leading to long term memory forgetting

A

found that the more nonsense syllable lists a participant had
previously learned, the more forgetting of new syllables the participant exhibited after 24 hours

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41
Q

How can retroactive interference be demonstrated

A

in the way that eyewitness memory for an event can be interfered with by post-event questioning

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42
Q

How is long term memory divided?

A

explicit:

  • episodic memory
  • semantic memory

implicit:
- perceptual representation system

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43
Q

What is the difference between explicit and implicit memory

A

explicit memory typically requires conscious recollection of a previous experience, whereas implicit memory is usually facilitated in the absence of conscious recollection

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44
Q

if a participant is
asked to study a list of words: CHAIR, APPLE, ZEBRA, etc. how could you test for
a) implicit memory
b) explicit memory

A

a)might include fragment completion (“complete these words with the first word that comes to mind: A-PL-, B-E-D”); word stem completion (“complete these words with the first word that comes to mind: AP—, BR—”); or degraded word naming

b) cued recall (“recall all the animals in the list”); or free recall
(“recall all the words from the list”).

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45
Q

How do different levels of processing affect encoding for explicit and implicit memory

how was this tested

A

deeper levels of
processing improved explicit memory but had little effect on
implicit memory.

Words (e.g., BRAIN) were encoded using one of the following tasks: Does the word contain the letter R? Does the word rhyme with drain? Is the word part of the nervous system?

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46
Q

Evidence from which patients demonstrates that deeper levels of
processing improved explicit memory but had little effect on
implicit memory?

A

patients with amnesia as a result of damage to medial temporal lobe.

eg, on pursuit rotor or Gollin figures tasks, performance of amnesiacs improves over trials, despite the patients not being able to recall having done the test before

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47
Q

Give an example of a patient who exhibits impaired implicit memory but not explicit memory

A

patient, MS, whose lesion affected occipital cortex, performed as well as controls at explicit memory, but was severely impaired on the implicit memory task

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48
Q

Which lesion impairs explicit but not implicit memory

A

medial temporal lobe

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49
Q

Define episodic and semantic memory

A

Episodic memory is considered to be memory of specific events or episodes occurring in a particular time and place (e.g., remembering what you had for breakfast this morning).

Semantic memory, by contrast, is general knowledge about objects, people, facts, concepts and the meanings of words, without awareness of where or when the information was learned (e.g., knowing that breakfast is a meal that you eat in the morning).

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50
Q

True or false

semantic memory can be culturally shared

A

true

Episodic memory is specific to each person, whereas semantic memory can be culturally shared.

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51
Q

What type of memory is referred to as ‘mental time travel’

A

episodic memory

involves thinking back to a specific moment in one’s personal past and consciously “re-living” a prior episode as it was previously experienced.

52
Q

Manipulating which factors in a memory experiment affects either episodic or semantic memory more than the other? (2)

A

different levels of processing at encoding improved episodic memory, but had no effect on semantic memory.

Providing stronger evidence, Jacoby (1983) reported a double dissociation, whereby reading a word out of context at encoding improved participants’ semantic memory, whereas generating the word themselves improved their subsequent episodic memory

53
Q

Are there patients that support the separation of episodic and semantic memory

A

patient HM, who had extensive medial temporal lobe damage, showed a severe impairment on episodic memory tasks, but was able
to name pictures of everyday objects, define concepts, etc

children with selective hippocampal damage acquired early in life all showed very impaired episodic memory, but performed well on tests assessing semantic memory (e.g., vocabulary, etc.).

54
Q

How do different forms of dementia show double dissociation between episodic and semantic memory

A

Patients with early Alzheimer’s Disease have medial temporal lobe atrophy, whereas patients with early Semantic Dementia have atrophy that is most apparent in lateral temporal lobe areas.

Simons et al. (2002) asked patients to perform a semantic task and later tested their episodic memory for the same drawings.

A double dissociation was observed between impaired episodic and preserved semantic memory in Alzheimer’s Disease, and impaired semantic and preserved episodic memory in Semantic Dementia.

55
Q

What are the 2 major forms of amnesia

A

retrograde and anterograde

56
Q

what is retrograde amnesia

A

the forgetting of events occurring prior to trauma (e.g. closed head injury or electroconvulsive shock therapy (ECT)). Often the gradient of forgetting diminishes with more remote memories and ‘shrinks’ or recovers with time

57
Q

what is anterograde amnesia

A

the inability to retain in a permanent form new material, i.e. an inability to learn

58
Q

give 5 causes of amnesia

A

anoxia,
ischemia,
encephalitis, alcoholism and associated dietary insufficiency (Korsakoff’s syndrome)
neurosurgery, i.e. to relieve epilepsy

59
Q

Alzheimer’s damage to which parts of the brain causes the prominent early amnesia component

A

especially the hippocampus and entorhinal cortex (within parahippocampal gyrus) of the temporal lobe.

60
Q

What was removed in patient HM

what did this result in

A

received bilateral resection of his temporal lobes (including hippocampus, amygdala and overlying temporal cortex) to relieve epilepsy

a profound, polymodal anterograde amnesia for verbal and non-verbal material

61
Q

Give 4 features which characterised patient HM’s amnesia

A

(i) severe recognition memory deficit as shown by performance on matching to sample

(ii) milder retrograde amnesia,
(iii) intact digit and spatial span and short term memory
(iv) preserved IQ.

62
Q

Patient HM received bilateral resection of his temporal lobes. What would have happened if it had been unilateral?

A

Unilateral lesions limited to right(R) or left(L) generally produce nonverbal or verbal memory deficits, respectively

63
Q

What happened to patient NA

what is this similar to

A

developed anterograde amnesia after a lesion of the mediodorsal nucleus of the thalamus.

Korsakoff’s which also is damage to diencephalic structures

64
Q

What is damaged in Korsakoff’s

A

diencephalic structures, including medial thalamus, fornix and mammillary bodies, structures of Papez’ circuit

65
Q

Give one way Korsakoff’s differs from patient HM

A

Korsakoff’s has a greater degree of retrograde amnesia

66
Q

What kind of memory loss does damage to the temporal-parietal lobe junction lead to

A

a selective deficit in immediate memory, as shown by deficient memory span - conduction aphasics

67
Q

Do conduction aphasics have problems with short or long term memory

A

impairments in short term memory but can consolidate knowledge into long term memory.

68
Q

Where is short term memory in different modalities found

A

Short term memory in other modalities, such as in vision (rather than verbal) may be a function of unimodal association areas related to the particular modality in question, i.e. posterior parietal in the case of spatial span?

69
Q

What can some forms of agnosia, aphasia and apraxia be regarded as

A

s losses of highly specific long term, semantic memories, generally resulting from damage to specific regions of association cortex.

70
Q

Give 2 examples of agnosias

A

movement agnosia in which a subject cannot ‘see’ movement and prosopagnosia, in which a subject cannot recognize faces

71
Q

What are the 2 main types of visual agnosia

A

associative agnosia,

apperceptive agnosia

72
Q

What happens in associative agnosia

A

a patient cannot recognize objects, name them or use objects appropriately but can identify objects by selecting the correct drawing and can draw the object accurately.

73
Q

What happens in apperceptive agnosia

A

patient can name an object if the appropriate
perceptual cues are present but cannot draw the object. They are also impaired at ‘naming’ the object if presented in an unusual view. Object recognition deficits can be category specific (eg could recognize inanimate objects but not living objects)

74
Q

Give examples of how patient HM and Korsakoff’s patients have working procedural memory

What is this a contrast to

A

HM and other anterograde amnesics show remarkable sparing of certain forms of memory, e.g. can learn to draw in a mirror even though no recollection of daily sessions of testing
In addition, NA, Korsakoff’s patients and ECT patients all learn the perceptual skill of mirror reading as rapidly as controls but are impaired at remembering what words they read.

By contrast, patients with Huntington’s disease are impaired at developing this skill but perform better on word recognition

75
Q

What did Squire suggest about the pattern of memory loss in anterograde memory loss

A

shows a distinction between knowledge for facts (declarative) and knowledge gained through performance (procedural)

He suggests that the two forms of learning are mediated by distinct neural systems, declarative having evolved more recently and depending upon structures that are damaged in different forms of anterograde amnesia ie. temporal lobe and diencephalon

76
Q

Where are the neural systems for explicit and implicit memory

A

explicit/ declarative: temporal lobe and diencephalon

procedural/ implicit; basal ganglia and cerebellum

77
Q

What is a DNMS task

A

Delayed Non matching - to - sample task
a test of recognition memory in monkeys

eg
required monkeys to remember having seen a junk object (sample) over longer and longer delays (ranging from a few seconds to 10 minutes).
At the choice stage, the monkey was confronted with the sample junk object and a novel object and was required to choose the novel object, thus indicating that he remembered which of the objects was familiar.

78
Q

What memory deficits did Mishkin demonstrate in monkeys with large lesions in the medial temporal lobe

how was this demonstrated

A

similar to those of human amnesiacs, i.e. impaired recognition memory but intact skill learning

could not do well in DNMS tasks but improved over time at the life saver motor skill task

79
Q

How was it demonstrated that there is mild retrograde amnesia with lesions to the hippocampus

A

Monkeys trained on concurrent object discriminations 2:4:8:12:16 weeks pre-surgery.
Impairment only on object discriminations post-surgery that were learned 2-8 weeks pre-surgery.

80
Q

What part of the brain specifically is important for recognition memory

A

rhinal cortex -

impairments in recognition memory are associated with damage
to rhinal cortex (perirhinal and entorhinal) within the medial temporal lobe.

81
Q

What are projections from the inferotemporal cortex into the rhinal cortex important for

A

visual recognition memory

82
Q

What larger system is the rhinal cortex thought to be part of

A

a larger system within the temporal lobes important for storing knowledge about objects that may be analogous to a semantic knowledge or specialized knowledge system in humans

83
Q

What type of memory is affected by amygdala damage

A

affective/ emotional/ motivational memory

84
Q

How would a person with amygdala damage present (in terms of memory)

A

no longer show emotional responses to fearful or pleasurable stimuli.

However, subjects may still recognize a particular stimulus and remember previous interactions with it but just have no emotional memory of it.

85
Q

Where is the amygdala found

A

temporal lobe of each hemisphere forms one continuous sheet of cortex. The most medial section is the hippocampus and dentate gyrus, which are primitive cortices (3 layers - allocortex)

86
Q

What type of cortex is the hippocampus

A

allocortex as it has 3 layers instead of 6 (in the neocortex)

87
Q

What lies between the hippocampus/ dentate gyrus and temporal neocortex

what type of cortex is this

A

the subiculum and parahippocampal cortex (PH), also primitive cortex

Some of PH cortex is transitional, 4-5 layered cortex.

88
Q

How does the hippocampus get its shape during development

A

nvaginates into the lateral ventricle forming a characteristic ridge, Ammon’s horn

89
Q

How is the hippocampus proper divided

A

into 3 longitudinal areas, CA1, CA2 and CA3 (comprising Ammon’s horn) consisting of pyramidal (output) cells and the neighbouring dentate gyrus consisting of granule (input)
cells.

90
Q

What composes the hippocampal formation

A

the hippocampus along with the dentate gyrus and subiculum,

91
Q

What are the 3 major classes of afferent connections from the hippocampal formation

A

All major cortical association areas

Subcortical structures

Non-specific arousal systems

92
Q

Where do the cortical association areas project to in the PH gyrus

which areas is this

A

entorhinal cortex

all of them including unimodal association areas as well as higher order polymodal processing areas such as inferior parietal lobule and prefrontal cortex

93
Q

Where does the cortex send afferents to

A

the dendrites of the dentate granule cells (the perforant pathway)

94
Q

what is the perforant pathway

why is it called this

A

a connection between the entorhinal pathway and all parts of the hippocampal formation

these fibres perforate the hippocampal fissure in reaching their destination

95
Q

Name 3 of the subcortical structures which have afferents to the hippocampal formation

A

septum
anterior thalamus
amygdala

96
Q

Name 3 non-specific arousal systems

A

cholinergic,

serotonergic and noradrenergic pathways.

97
Q

Which cells does the perforant pathway connect the entorhinal cortex with (2 examples)

A

dendrites of the dentate granule cells and also with the apical dendrites of the CA3 pyramidal cells

98
Q

What is the neural route through the hippocampus

A

perforant pathway -> dentate granule cells (+other places)

  • > mossy fibres to CA3 pyramidal cells
  • > Schaffer collaterals to CA1 pyramidal cells
  • > subiculum
99
Q

What are the 2 main efferent pathways from the hippocampus

A
  1. Projections from the subiculum and entorhinal cortex to neocortex
  2. fimbria-fornix
100
Q

Where does the fimbria-fornix project

A

from CA3 and subiculum to structures such as the hypothalamus, mamillary bodies, anterior thalamus and nucleus accumbens

101
Q

What is Papez’s circuit after leaving the hippocampus

A

m CA3 and subiculum through the fimbria-fornix to structures such as the hypothalamus, mamillary bodies,
anterior thalamus and nucleus accumbens
Projections via mamillary bodies to anterior thalamus and thence onto cingulate cortex, which, in turn, project back to entorhinal cortex and back to hippocampal formation

102
Q

What was wrong with patient RB

what did this result in

A

CA1 degeneration in the hippocampus

episodic memory deficits

103
Q

What is the Morris water maze and what is it used to test

A

rats are trained to escape from a pool of water by swimming to a submerged platform in opaque water.

started from different positions around the edge of the pool on different trials and gradually learns to swim directly to the submerged platform on the basis of knowledge about the position of the platform with respect to landmarks around the maze

tests spatial memory

104
Q

What have experiments with the Morris water maze taught us about spatial memory

A

the hippocampus is important for spatial memory

Hippocampal lesions impair learning of the task and even when it is eventually acquired, subsequent retention tests (in which the platform is removed, and the amount of time the rat spends searching for the platform in the correct quadrant is measured – transfer test), show that the lesioned rat has poor memory for the location of the platform

105
Q

What happens if a rat is trained at the Morris water maze then has a hippocampal lesion?

what does this suggest about the role of the hippocamus

A

there is a much weaker deficit on a subsequent retention test post lesion.
Thus, the hippocampus would appear to be more important in the laying down of the memory trace rather than in its retrieval.

106
Q

While we have not performed the Morris water maze task on humans to test the role of the hippocampus in humans, how have we tested its roles

A

Human hippocampus is activated during navigation and London taxi drivers show altered hippocampal volume!

107
Q

What do we think the hippocampus is important for in humans

A

coding the context or ‘episode’ (what, where and when) in which various memories take place

thus responsible for binding together disparate aspects of a memory and distilling them into a coherent
memory trace

108
Q

What is a key point to remember about the internal organisation of the hippocampal formation

A

there appear to be a number of stages where interactions can occur between different sets of inputs in a matrix-like manner

109
Q

Give an example of a matrix being formed in the hippocampus

A

in the dentate gyrus, where the perforant path (rows of matrix) synapse with dendrites of the dentate gyrus (columns of matrix).

110
Q

What is important about the matrix between the dendrites of the dentate gyrus and perforant pathway

A

These synapses are modifiable and their connectivity is increased if an activated afferent in the perforant pathway synapses
onto an already strongly activated post-synaptic neuron (i.e. granule cell) with different input patterns on the perforant pathway tending to activate a different pattern of output neurons.

enhanced by mutual inhibition of output neurons

111
Q

What is the competitive mechanism of inhibition found in the matrices of the hippocampus

A

inhibitory interneurons at each stage not only receive input from the previous stage (feedforward inhibition) but also from their own output neurons

112
Q

what is the typical sequence of events that takes place in the matrices of the hippocampus

A

first, in response
to a stimulus, strengthening of synapses occurs between active afferent axons and an already strongly activated post-synaptic cell. The effect of this modification is that next time the same stimulus is presented, the neuron responds more (because of the strengthening), more inhibition also occurs between pathways, with the result of even stronger modifications

113
Q

Why is the hippocampus considered an unsupervised learning system

A

unlike the cerebellum there is no teacher, i.e. a signal (like that of the climbing fibre) which can unconditionally set, or correct, according to an error, the output firing of each neuron.

114
Q

we know that certain episodes that have a significant emotional impact can be remembered more easily than non-emotional episodes. What does this suggest about learning in the hippocampus?

A

some general state may influence the level (or rate) of learning that occurs in the hippocampus such as that provided by the non-specific arousal pathways (ACh, NA, 5-HT) that innervate this structure

115
Q

How has it been proposed generally that the hippocampus supervises or guides the long-term storage of memories.

A

the back projections of the hippocampus to the neocortex

116
Q

What did Bliss show about LTP in the hippocampal formation

A

that in the dentate gyrus increases occurred in the amplitude of electrically evoked responses following brief trains of tetanic (high frequency) stimulation. Subsequently it’s been shown in the cell fields of the hippocampus proper

117
Q

Give an example of an experimental set up where you can show LTP in the hippocampal formation

A

Simulating electrodes are placed into Schaffer collaterals of CA3 and recording electrodes are placed into neurons of CA1

After a brief burst of tetanic stimulation, a marked and long-lasting (up to many days) enhancement of firing, in the CA1 neuron, to low frequency stimulation can be observed, that is pathway

118
Q

There are several properties of LTP that may make it a

useful synaptic ‘model’ for learning and memory. Give 5

A

1) . It is rapidly induced
2) . It is long-lasting
3) . It is synapse specific
4) . It can be associative in nature
5. It is seen in other structures including the neocortex.

119
Q

Why is the associative nature of LTP important for its implication in learning

A

like behavioural conditioning (i.e. if a weak input (cf. CS)
is paired with a strong one (cf. US), both sets of
synapses subsequently show LTP.) This does not occur
in CA3, where the LTP is non-associative only

120
Q

Is long term depression seen in the hippocampus

A

yes in response to high frequency stimulation, LTD is also seen in many neural structures including the hippocampus and of course the
cerebellum

121
Q

What is the NT in the hippocampal pathways

A

The perforant, mossy fibre and schaffer collateral pathways use the
excitatory amino-acid glutamate

122
Q

what are the 3 distinct types of glutamate receptor

what are the different roles?

A

quisqualate
kainate
n-methyl-D-aspartate (NMDA)

kainate and quisqualate receptors mediate normal fast transmission, while specific activation of the NMDA receptor by specific agonists has no effect (but may be implicated in LTP)

123
Q

Why do we think glutamate NMDA receptors are implicated in LTP in the hippocampus

A

specific NMDA antagonist, AP5, can block LTP development in the CA3-CA1 pathway

124
Q

Are all types of LTP the same

A

no
there are many different forms of LTP that are dependent upon different kinds of activity and with different underlying mechanisms; not all of which are dependent upon the NMDA receptor and not all of which are associative and dependent upon postsynaptic activity.

125
Q

How was it demonstrated that NMDA receptors are involved in spatial learning

A

When D-L AP5 is infused into the ventricles close to the hippocampus, over a long time and at a slow rate using an osmotic mini-pump, it impairs the learning of the same water maze task, described earlier, that is normally impaired following lesions of the hippocampus

126
Q

What does damage to the hippocampus do to memory

A

impairs ‘scene’ memory i.e. the hippocampus probably encodes the context or episode in which a particular memory occurs.

This is in agreement with the clinical literature in which a stroke patient RB, with damage localised to the CA1 field of the hippocampus, exhibited a marked anterograde amnesia but no retrograde amnesia.

127
Q

What would happen in a scenario where a subject has been burnt on a gas oven and immediately before or after suffers hippocampal damage

how is this different if they suffer damage to the adjacent amygdala but sparing the hippocampus?

what if the temporal cortex is damaged intead

A

next time they see that type of oven they will feel ‘apprehensive’ (emotional) about it but not know why i.e. they cannot remember the specific episode of being burnt by the oven

may remember the specific episode, but the sight of the oven will not evoke any emotional response.

this person, with impaired semantic knowledge, may not recognise it subsequently as an oven and not be able to say what it is used for