Memory and Amnesias Flashcards

1
Q

What is Declarative Memory?

There are two examples

What parts of the brain is this memory

A

Facts and Events (rich in detail)

These are explicit (conscious) memories

Hippocampus and limbic system

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2
Q

What is Procedural Memory

There are two examples

What parts of the brain is this memory

A

Implicit (unconscious) memory that consists of:

Priming, skills/habits, and conditioning

Basal ganglia, cerebellum, motor skills

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3
Q

What is the road to memory formation?

A

Sensory input-sensory memory-attention-short term (working) memory-encoding-long term memory

Encoding-retrieval-consolidation

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4
Q

What is Retrograde Amnesia and what is the normal presentation for it?

A

When you can’t remember things from your past-

Temporal Amnesia: When you can remember things from a long time ago, but not recently (temporal gradient)

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5
Q

What is Anterograde Amnesia?

A

When you can’t make new memories

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6
Q

What is infantile amnesia?

A

When early childhood events can’t be recalled

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7
Q

Transient Global Amnesia

A
  • Occurs typically in older men
  • When you can only remember recent events for a few minutes, but everything else is fine. Usually due to TIA, Basilar artery migraine, physical, or psychic stress
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8
Q

Dissociative Amnesia

A

When you witness something very emotional and have retrograde amnesia

“Reaction amnesia”-emotional content and frenzy

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9
Q

Wernicke Korsakoff’s Amnesia

What is another name for it

What 5 parts of the brain are damaged

A

Diencephalic Amnesia

Caused by alcohol abuse and thiamine deficiency and includes confabulation, confusion, and severe memory impairment

Fornix, Mamillary bodies, thalamus, colliculi, periventricular gray matter,

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10
Q

What are the differences between Diencephalic and Bilateral Mesial Temporal Amnesias

A
  1. W.K has remote memory deficit (memory from the distant past), poor insight
  2. Bilateral Mesial Temporal has rapid rate of forgetting, impaired consolidation

BOTH has intact procedural learning, anterograde and retrograde deficit, and impaired encoding

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11
Q

What is an Engram

A

An Engram is what accounts for the persistence of memory due to a hypothetical change in neural tissue

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12
Q

What is Synaptic Plasticity

How are connections between the neurons strengthened?

How do you learn?

A

Short term: Transient changes in synaptic function
(perhaps mediated through altered metabolism

Long term: More permanent alteration of cellular function (perhaps change of protein expression and/or change of cellular structure)

  • repeated co-firing
  • Multi-modal binding of engrams
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13
Q

Where are memory engrams located?

What is the pathway?

What is rehearsal?

What is consolidation?

What does the prefrontal neocortex show?

A

In the neocortex, which gets info from the primary somatosensory, primary auditory, and primary visual cortex-these together are called “Association areas”

Association areas to medial temporal lobes so they can be processed in the hippocampal formation. The thalamo-cortical loops keep the neuronal assemblies co-active (rehearsal) until they are “bound” in a more permanent way (consolidation)

Support attention and working memory during initial memory formation and also information about the context/source of the memory which helps to relate memories to the time and place in which the stored information was received.

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14
Q

What is the seat of declarative memory formation

Which parts?

A

hippocampus

Crus Cerebri to Perirhinal cortex (Lateral geniculate nucleus, Parahippocampal cortex, and dentate)

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15
Q

What is the hippocampal trisynaptic circuit

A

Three-layered region of cortex in the medial temporal lobe is where hippocampal formation is and it consists of dentate, hippocampus and subiculum

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16
Q

What is the extended memory system

A

Perirhinal and Parahippocampal regions provide cortical input to the entorhinal cortex which projects to the hippocampus

EH to Denate to CA3 to CA1 to Subiculum back to EH

17
Q

What is the pathway for long term potentiation

A

Glutamate is released and binds AMPA and NMDA receptors on post-synaptic membrane which opens AMPA channels for Na entry. The EPSP’s summed to elicit depolarization. At the same time the NMDA receptor channels open and remove Mg2+

The Ca2+ through NMDA activates 2nd messenger pathways that activate PKA’s, mRNA modeling of NEW AMPA and release retrograde messengers that stimulate lasting increase in pre-synaptic glutamate release

18
Q

What is the early effect

and the late effect of AMPA?

A

early: increase AMPA conductance
early: increase in the number of receptors
late: increase in the number of synapses and synaptic boutons

19
Q

Is the difference between LTP and LTD?

A

Ca2+ concentration

LTD activates phosphatases