Memory And Learning Flashcards

1
Q

Learning

A

The process of acquiring new and relatively enduring information, behavior patterns, or abilities, characterized by modifications of behavior as a result of practice study, or experience.

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2
Q

Memory

A

The ability to retain info, based on the mental process of learning or encoding, retention across some interval of time, and retrieval or reactivation of the memory. The specific info that is stored in the brain.

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3
Q

Patient HM

A

A patient who, because of damage to the medial temporal lobe structures, was unable to encode new declarative memories. Could still encode implicit memories.

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4
Q

Retrograde amnesia

A

Difficultly in retrieving memories formed before the onset of amnesia

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5
Q

Anterograde amnesia

A

The inability to form new memories beginning with the onset of a disorder

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6
Q

Confabulations

A

Make up answer in place of memory bc don’t remember and say that it is always true. Korsakoff’s patients did.

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7
Q

Patient NA

A

Damage to diencephalon (thalamus and hypothalamus). No declarative memory and anterograde amnesia.

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8
Q

Patient KC

A

Motorcycle accident-extensive cortical damage. Lack of new declarative memory, can acquire new semantic memories, remembers semantic memories. Loss of episodic memories.

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9
Q

Encoding

A

A stage of memory formation which the info entering sensory channel is passed into short term memory

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10
Q

Consolidation

A

A stage of memory formation in which info in short term memory or intermediate term memory is transferred to long term memory. Requires hippocampus to do.

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11
Q

Consolidation pathway

A

Hippocampus sends info to cortex in area where first recognized. Use granule cells feed into system

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12
Q

Retrieval

A

A process in memory during which a speed memory is used by an organism

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13
Q

Fusiform gyrus

A

Recognizes faces

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14
Q

Declarative memory

A

Semantic (knowledge), and episodic (biographical).

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15
Q

Non-declarative memory

A

Skills, priming (give info the alter behavior later), and conditioning

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16
Q

Classical conditioning

A

US to trigemical nucleus, to cranial nucleus, to nictating memory(UR). When conditioned, cerebellum activated by signal, elicits response.

17
Q

Learning changes

A

Amount of NT released, interneurons release from presyn cell, formation of new synapses (increase dendritic spines).

18
Q

Enriched environments

A

Large environment, high intersection, lots of toys. Thicker, heavier cortex. Increase cholinergic cells/synapses and dendrites.

19
Q

Habituation

A

Decrease response as a result of experience. Think stimulus isn’t important. Ex: slug

20
Q

Sensitization

A

Opposite of habituation, every time stim presented, get more intense response. Nonassociative learning.

21
Q

Dishabituation

A

The restoration of response amplitude following habituation

22
Q

Reconsolidation

A

The return of a memory trace to stable long-term storage after it has been temporarily made volatile during the process of recall.

23
Q

Hebbian synapse

A

A synapse that is strengthened when it successfully drives the postsynaptic cell.

24
Q

Cell assembly

A

A large group of cells that tend to be active at the same time bc they have been activated simultaneously or in close succession in the past. Can change as a result of experience

25
Q

Long-term potentiation (LTP)

A

A stable and enduring increase in the effectiveness of synapses following repeated strong stim

26
Q

LTP pathway

A

EC (temporal cortex), to DG (dentate gyrus), to CA3, to CA1 (perforont pathway) in hippocampus.

27
Q

NMDA receptor

A

A GLU receptor in also binds the GLU agonist NMDA and that is both ligand-gated (Mg) and voltage-sensitive. (Ca).

28
Q

AMPA receptor

A

A GLU receptor that also binds the GLU agonist AMPA. Depolarizes cell, kicks off Mg of NMDA receptor, allows GLU to bind which allows Ca to come in.

29
Q

Protein kinases

A

Enzymes that add phosphate Groups to proteins. Activated by Ca entering cell.

30
Q

CREB

A

Transcription factor. Affects expression of genes, alters protein production in cell. Signals retrograde NT to release more GLU from presyn cell.

31
Q

CaMKII

A

Activates latent AMPA receptors to go to the surface and become active which increases NT produced.