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
What is the visual cache
passively stores information about visual form and colour and is subject to decay and interference by new visual information.
26
What does the inner scribe do
processes spatial information and allows active rehearsal of information in the visual cache
27
How does neuropsychological data support the division of the visuospatial sketchpad
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
28
If you are given a list of words to remember, and then immediately asked to recall them, what pattern is seen in your recall?
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)
29
What did Atkinson and Shiffrin attribute the recency effect to is this a correct assumption?
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.
30
What did Atkinson and Shiffrin attribute the primacy effect to why
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)
31
What damage did Patient HM suffer why is he important for short/long term memory studies
medial temporal lobe damage had impaired long-term memory but normal digit span
32
Give a patient who contrasts HM
patient KF, suffered parieto-occipital lobe damage and had intact long-term memory but very poor digit span
33
Which 2 patients demonstrate the difference between short and long term memory
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.
34
Where is short term memory found in the brain
inferior frontal and parietal cortex
35
What was the first rigorous experimental investigation of human long term memory
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.
36
What is the limit of long term memory capacity
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.
37
How does forgetting from long term memory change over time
very rapid over the first hour or so after acquisition, then reduces approximately logarithmically.
38
What causes long term memory forgetting
primarily to interference from other experienced events
39
What are the 2 main forms of interference which cause long term memory forgetting
proactive interference - when previous learning interferes with later learning, retroactive interference - when later learning interferes with previous learning.
40
Give Underwood's example of proactive interference leading to long term memory forgetting
found that the more nonsense syllable lists a participant had previously learned, the more forgetting of new syllables the participant exhibited after 24 hours
41
How can retroactive interference be demonstrated
in the way that eyewitness memory for an event can be interfered with by post-event questioning
42
How is long term memory divided?
explicit: - episodic memory - semantic memory implicit: - perceptual representation system
43
What is the difference between explicit and implicit memory
explicit memory typically requires conscious recollection of a previous experience, whereas implicit memory is usually facilitated in the absence of conscious recollection
44
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)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”).
45
How do different levels of processing affect encoding for explicit and implicit memory how was this tested
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?
46
Evidence from which patients demonstrates that deeper levels of processing improved explicit memory but had little effect on implicit memory?
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
47
Give an example of a patient who exhibits impaired implicit memory but not explicit memory
patient, MS, whose lesion affected occipital cortex, performed as well as controls at explicit memory, but was severely impaired on the implicit memory task
48
Which lesion impairs explicit but not implicit memory
medial temporal lobe
49
Define episodic and semantic memory
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).
50
True or false | semantic memory can be culturally shared
true | Episodic memory is specific to each person, whereas semantic memory can be culturally shared.
51
What type of memory is referred to as 'mental time travel'
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
Manipulating which factors in a memory experiment affects either episodic or semantic memory more than the other? (2)
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
Are there patients that support the separation of episodic and semantic memory
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
How do different forms of dementia show double dissociation between episodic and semantic memory
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
What are the 2 major forms of amnesia
retrograde and anterograde
56
what is retrograde amnesia
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
what is anterograde amnesia
the inability to retain in a permanent form new material, i.e. an inability to learn
58
give 5 causes of amnesia
anoxia, ischemia, encephalitis, alcoholism and associated dietary insufficiency (Korsakoff's syndrome) neurosurgery, i.e. to relieve epilepsy
59
Alzheimer's damage to which parts of the brain causes the prominent early amnesia component
especially the hippocampus and entorhinal cortex (within parahippocampal gyrus) of the temporal lobe.
60
What was removed in patient HM what did this result in
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
Give 4 features which characterised patient HM's amnesia
(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
Patient HM received bilateral resection of his temporal lobes. What would have happened if it had been unilateral?
Unilateral lesions limited to right(R) or left(L) generally produce nonverbal or verbal memory deficits, respectively
63
What happened to patient NA what is this similar to
developed anterograde amnesia after a lesion of the mediodorsal nucleus of the thalamus. Korsakoff's which also is damage to diencephalic structures
64
What is damaged in Korsakoff's
diencephalic structures, including medial thalamus, fornix and mammillary bodies, structures of Papez' circuit
65
Give one way Korsakoff's differs from patient HM
Korsakoff's has a greater degree of retrograde amnesia
66
What kind of memory loss does damage to the temporal-parietal lobe junction lead to
a selective deficit in immediate memory, as shown by deficient memory span - conduction aphasics
67
Do conduction aphasics have problems with short or long term memory
impairments in short term memory but can consolidate knowledge into long term memory.
68
Where is short term memory in different modalities found
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
What can some forms of agnosia, aphasia and apraxia be regarded as
s losses of highly specific long term, semantic memories, generally resulting from damage to specific regions of association cortex.
70
Give 2 examples of agnosias
movement agnosia in which a subject cannot ‘see’ movement and prosopagnosia, in which a subject cannot recognize faces
71
What are the 2 main types of visual agnosia
associative agnosia, apperceptive agnosia
72
What happens in associative agnosia
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
What happens in apperceptive agnosia
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
Give examples of how patient HM and Korsakoff's patients have working procedural memory What is this a contrast to
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
What did Squire suggest about the pattern of memory loss in anterograde memory loss
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
Where are the neural systems for explicit and implicit memory
explicit/ declarative: temporal lobe and diencephalon procedural/ implicit; basal ganglia and cerebellum
77
What is a DNMS task
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
What memory deficits did Mishkin demonstrate in monkeys with large lesions in the medial temporal lobe how was this demonstrated
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
How was it demonstrated that there is mild retrograde amnesia with lesions to the hippocampus
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
What part of the brain specifically is important for recognition memory
rhinal cortex - impairments in recognition memory are associated with damage to rhinal cortex (perirhinal and entorhinal) within the medial temporal lobe.
81
What are projections from the inferotemporal cortex into the rhinal cortex important for
visual recognition memory
82
What larger system is the rhinal cortex thought to be part of
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
What type of memory is affected by amygdala damage
affective/ emotional/ motivational memory
84
How would a person with amygdala damage present (in terms of memory)
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
Where is the amygdala found
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
What type of cortex is the hippocampus
allocortex as it has 3 layers instead of 6 (in the neocortex)
87
What lies between the hippocampus/ dentate gyrus and temporal neocortex what type of cortex is this
the subiculum and parahippocampal cortex (PH), also primitive cortex Some of PH cortex is transitional, 4-5 layered cortex.
88
How does the hippocampus get its shape during development
nvaginates into the lateral ventricle forming a characteristic ridge, Ammon’s horn
89
How is the hippocampus proper divided
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
What composes the hippocampal formation
the hippocampus along with the dentate gyrus and subiculum,
91
What are the 3 major classes of afferent connections from the hippocampal formation
All major cortical association areas Subcortical structures Non-specific arousal systems
92
Where do the cortical association areas project to in the PH gyrus which areas is this
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
Where does the cortex send afferents to
the dendrites of the dentate granule cells (the perforant pathway)
94
what is the perforant pathway why is it called this
a connection between the entorhinal pathway and all parts of the hippocampal formation these fibres perforate the hippocampal fissure in reaching their destination
95
Name 3 of the subcortical structures which have afferents to the hippocampal formation
septum anterior thalamus amygdala
96
Name 3 non-specific arousal systems
cholinergic, | serotonergic and noradrenergic pathways.
97
Which cells does the perforant pathway connect the entorhinal cortex with (2 examples)
dendrites of the dentate granule cells and also with the apical dendrites of the CA3 pyramidal cells
98
What is the neural route through the hippocampus
perforant pathway -> dentate granule cells (+other places) - >mossy fibres to CA3 pyramidal cells - > Schaffer collaterals to CA1 pyramidal cells - > subiculum
99
What are the 2 main efferent pathways from the hippocampus
1. Projections from the subiculum and entorhinal cortex to neocortex 2. fimbria-fornix
100
Where does the fimbria-fornix project
from CA3 and subiculum to structures such as the hypothalamus, mamillary bodies, anterior thalamus and nucleus accumbens
101
What is Papez's circuit after leaving the hippocampus
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
What was wrong with patient RB what did this result in
CA1 degeneration in the hippocampus episodic memory deficits
103
What is the Morris water maze and what is it used to test
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
What have experiments with the Morris water maze taught us about spatial memory
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
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
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
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
Human hippocampus is activated during navigation and London taxi drivers show altered hippocampal volume!
107
What do we think the hippocampus is important for in humans
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
What is a key point to remember about the internal organisation of the hippocampal formation
there appear to be a number of stages where interactions can occur between different sets of inputs in a matrix-like manner
109
Give an example of a matrix being formed in the hippocampus
in the dentate gyrus, where the perforant path (rows of matrix) synapse with dendrites of the dentate gyrus (columns of matrix).
110
What is important about the matrix between the dendrites of the dentate gyrus and perforant pathway
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
What is the competitive mechanism of inhibition found in the matrices of the hippocampus
inhibitory interneurons at each stage not only receive input from the previous stage (feedforward inhibition) but also from their own output neurons
112
what is the typical sequence of events that takes place in the matrices of the hippocampus
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
Why is the hippocampus considered an unsupervised learning system
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
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?
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
How has it been proposed generally that the hippocampus supervises or guides the long-term storage of memories.
the back projections of the hippocampus to the neocortex
116
What did Bliss show about LTP in the hippocampal formation
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
Give an example of an experimental set up where you can show LTP in the hippocampal formation
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
There are several properties of LTP that may make it a | useful synaptic 'model' for learning and memory. Give 5
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
Why is the associative nature of LTP important for its implication in learning
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
Is long term depression seen in the hippocampus
yes in response to high frequency stimulation, LTD is also seen in many neural structures including the hippocampus and of course the cerebellum
121
What is the NT in the hippocampal pathways
The perforant, mossy fibre and schaffer collateral pathways use the excitatory amino-acid glutamate
122
what are the 3 distinct types of glutamate receptor what are the different roles?
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
Why do we think glutamate NMDA receptors are implicated in LTP in the hippocampus
specific NMDA antagonist, AP5, can block LTP development in the CA3-CA1 pathway
124
Are all types of LTP the same
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
How was it demonstrated that NMDA receptors are involved in spatial learning
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
What does damage to the hippocampus do to memory
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.
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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
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