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Psychology > Neurobiology of Memory > Flashcards

Neurobiology of Memory Flashcards

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1
Q

What is amnesia?

A

Pathological loss of memory

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2
Q

What are the types of amnesia?

A
  1. Retrograde amnesia: Loss of memory of events occurring before the amnesia-inducing damage took place.
  2. Anterograde amnesia: The inability to create memory concerning events occurring after the amnesia-inducing damage took place.
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3
Q

What are the causes of amnesia?

A
  1. Anoxia
  2. Ischaemia
  3. Encephalitis
  4. Alcoholism
  5. Dietary insufficiency
  6. Neurosurgery
  7. Neurodegeneration (e.g. Alzheimer’s)
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4
Q

What was removed in HM’s surgery?

A
  1. Hippocampus
  2. Amygdala
  3. Multimodal association areas of temporal lobe
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5
Q

What are the symptoms of medial temporal lobe amnesia?

A
  1. Severe anterograde: No longer form new LTMs
  2. Slight retrograde: Preserved memory of most events before his surgery, but deteriorated memory for events a few years before
  3. Preserved IQ
  4. Preserved working memory
  5. Declarative amnesia: Only explicit memory system affected, not implicit.
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6
Q

What are the symptoms of select unilateral medial temporal lobe damage?

A
  1. Left hippocampal damage causes verbal memory deficits
  2. Right hippocampal damage causes non-verbal memory deficits
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7
Q

What is Korsakoff’s syndrome?

A

Korsakoff’s syndrome is a specific type of amnesia experienced by long-term alcoholics.

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8
Q

What are the symptoms of Korsakoff’s syndrome?

A
  1. Anterograde amnesia
  2. Retrograde amnesia
  3. Declarative amnesia
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9
Q

What is the cause of Korsakoff’s syndrome?

A

Damage to diencephalic structures as a result of thiamine deficiency

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10
Q

What structures are specfically damaged in Korsakoff’s syndrome?

A

Components of Papez’s circuit:

  1. Medial thalamus
  2. Fornix
  3. Mammillary bodies
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11
Q

What are components of Papez’s circuit?

A
  • Fornix
  • Thalamus
  • Mammillary bodies
  • Amygdala
  • Hippocampus
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12
Q

What are the symptoms presented by patients with damage to the posterior cortex (temoral-parietal junction)?

A
  1. Impaired digit span
  2. Conduction aphasia
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13
Q

How is short-term memory coded in the brain?

A

STM for different types of sensory information may be mediated by the multimodal association areas associated with the areas of the brain responsible for processing information of that type (e.g. visual information associated with the visual cortex etc.).

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14
Q

What are the types of special knowledge system (semantic) defects?

A
  1. Aphasia: Language disorder affecting the generation, content and understanding of speech, but not articulation.
  2. Apraxia: Inability to make skilled movements accurately.
  3. Agnosia: Patients are unable to interpret sensory information correctly despite no deficits in sensory transduction pathways.
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15
Q

Which areas of the brain are damaged in special knowledge system defects?

A

Association cortices

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16
Q

What are the types of agnosias?

A
  1. Visual agnosia: Inability to interpret visual information and recognise visual objects.
  2. Speech agnosia: Inability to comprehend speech despite in tact hearing and speech production.
17
Q

What are the types of visual agnosias?

A
  1. Associative agnosia: Patients are able to perceive an object, but are unable to recognise and assign meaning to it.
  2. Appreciative agnosia: Patients are unable to perceive an object as a whole, but are still able to recognise an object based on individual characteristics such as colour, size and texture.
18
Q

How can drawing task be used to distinguish between the types of visual agnosias?

A
  1. Associative agnosics are able to copy the drawing, but are unable to name the object that has been drawn.
  2. Appreciative agnosics are usually able to identify the objects in the drawing, but are unable to copy it.
19
Q

What type of memory is object recognition?

A

Semantic memory (equivalent to agnosias)

20
Q

Which part of the cortex is recognition memory associated with?

A

Rhinal cortex in the medial temporal lobe

21
Q

What evidence is there to suggest that recognition memory is mediated by the rhinal cortex?

A
  • Lesion studies in monkeys.
  • Lesion to the rhinal cortex causes deficit in recognition memory.
  • Specific excitotoxic lesion of hippocamus and amygdala only (rhinal cortex spared) causes no defect in recogntion memory.
22
Q

What is a possible overall mechanism for storage of LTM?

A
  • There is a rehearsal circuit involving the hippocampus, mammillary bodies, thalamus and cortex.
  • Information is passed through this circuit repeatedly as part of rehearsal before it is permanently stored into cortex.
23
Q

How does the circuit model for memory help to explain HM’s symptoms?

A
  • Most of the circuit is removed in HM, preventing rehearsal and consolidation of new memory, explaining his anterograde amnesia.
  • Memories from the distant past have already been consolidated and are independent of the rehearsal circuit, so he has no problems recalling these.
  • Newer memories were still being consolidated by circuit when it was damaged, so memories formed nearer surgery were distorted.
24
Q

What structures send afferents into the hippocampus?

A
  1. Cortical association areas (uni/polymodal association areas of the frontal, parietal and temporal lobes) → Parahippocampal gyrux (inc. entorhinal cortex) → Dentate gyrus
  2. Subcortical structures (septum, anterior thalamus, amygdala)
  3. Non-specific arousal systems
25
Q

What is the structure of the perforant pathway?

A
  1. Fibres from the entorhinal cortex synapse with granule cells of dentate gyrus and apical dendrites of CA3 pyramidal cells.
  2. Dentate granule cells synapse onto CA3 pyramidal cells via mossy fibres.
  3. CA3 pyramidal cells synapse onto CA1 pyramidal cells via Schaffer collaterals.
  4. CA1 pyramidal cells project into cells of the subiculum.
26
Q

What features of long-term potentiation make it a suitable model to mediate learning and memory in the hippocampus?

A
  1. Rapidly induced
  2. Long-lasting
  3. Synapse specific
  4. Occurs in other areas of cortex
  5. Can be observed in nature (e.g. conditioning)
27
Q

What evidence is there to suggest that LTP is involved in memory-forming mechanism of the hippocampus?

A

Infusion of NMDA receptor antagonist D-L AP5 close to the hippocampus of a rat impairs its performance in the Morris water maze in the same way that hippocampal lesion does.

Psychology (12 decks)

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