Learning And Memory Flashcards

1
Q

What is learning?

A

Acquisition of new info

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2
Q

What is memory?

A

Retention of new info

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3
Q

What are the types of memory?

A

Procedural (implicit, non-declarative, reflexive)

Declarative (explicit)

Working (recall)

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4
Q

How is memory classified in terms of time?

A

Short term

Long term

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5
Q

What is procedural memory for?

Example?

A

‣ Skills and habits used so much they are automatic, motor sequences is memorized
‣ I.e bike riding

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6
Q

What are the anatomical substrates involved with procedural memory?

Function of each?

A
  • Cerebellum: motor skills

* Nucleus Accumbens: non-motor

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7
Q

What is declarative memory for?

Example?

A

‣ Conscious recognition/recollection of learned facts and experiences

I.e. the fact you learned for test; events/facts stored in memory

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8
Q

What is declarative memory subdivided into?

A

Episodic

Semantic

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9
Q

What is episodic memory?

A

Memory of events

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10
Q

What is semantic memory?

A

Memory of words, language, and rules

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11
Q

How long does short term memory last?

A

Seconds to hours

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12
Q

What is working memory?

Example?

A

Recall a fact/memory for use

‣ I.e. recall a fact for use in test question (very much like short term- actually a subset)

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13
Q

What does the production of memory and learning require?

A

Induction of neuronal and synaptic plasticity

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14
Q

What is plasticity?

Mechanism?

A

Alterations in CNS based on use

Change to Synaptic function
Change to Physical structure of neuron

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15
Q

What changes to synaptic function could be made for plasticity?

A

Post-tetanic potentiation

Long term potentiation (LTP)

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16
Q

What changes to the physical structure of neurons could occur as a result of plasticity?

A
  • Gain/loss synapses
    * Structure changes in dendrites
    * Sturcutral changes in soma of neuron
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17
Q

What is post-titanic potentiation?

What is its effects?

A

High level of stimulation that allows more ca to enter terminal than could be dealt with

More vesicle to fuse
Greater NTR release
Greater probability of AP in Post syn cell

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18
Q

What can stimulate Post-tetanic potentiation?

A

Brief high frequency discharge of pre synaptic neuron

= increased NTR for ~60 sec
= increased probability of AP in post syn.

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19
Q

What is long term potentiation?

A

Series of changes in pre- and post synaptic neurons of a synpase which leads to

increased response at NMDA receptors to released NTR that can last for hours

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20
Q

What changes are associated with Increased CREB’s gene transcription?

A

Long term potentiation

Neuronal plasticity

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21
Q

What does increased CREB do in terms of neuronal plasticity?

A

Changes synapse structure permanently
&
creates new synapses via protein synthesis

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22
Q

What proteins does CREB produce for neuronal plasticity changes?

A

NT synthetic enzymes

NT receptors

Proteins for growth/synapse formation

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23
Q

What could blocking protein synthesis lead to in term of learning and memory?

A

Bc neuronal plasticity relies on protein synthesis

Blocking it can block learning and formation of new memories

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24
Q

What is the basic pathway for creating Declarative memories?

A

Encoding —> storage —> consolidation —> retrieval —> recall ar WOrking memory

25
Q

What is the process of encoding?

A

Attending to new info (focus, attention) and linking it to previous memories and emotions

26
Q

What is storage in the process of creating declarative memories?

A

Retainment of info over time using short and long term

27
Q

What are the anatomical substrates used for storage in short term memory?

A

Hippocampus

Parahippocampal cortex

Prefrontal cortex

Nucleus of basalis of Meynert

Amygdala
Neocortex

28
Q

What does the Nucleus Basalis of Meynert do in terms of storage in short term memory?

A

Provides the interconnection to the neocortex and amygdala via ACh projections

29
Q

What is a target of Alzheimer’s disease?

A

Nucleus Basalis of Meynert

30
Q

In order to store info, what plasticity change do we need to occur?

A

Long term potentiation

31
Q

What is consolidation?

A

Process of making memory permanent

Aka moving it from short term to long term memory

32
Q

What are the anatomical substrates required for Consolidation?

A

Hippocampus
Temporal lobes
Papez circuit

33
Q

What is the papez circuit?

A
Cingulate cortex
—> hippocampus
—> hypothalamus/mammillary bodies
—> anterior thalamus
—> cingulate cortex
34
Q

What is the process for consolidation?

A

Memory is repeatedly send thru the Papez circuit, inducing long term potentiation and neuronal plasticity

35
Q

Where are long term memories stored?

A

In area of cortex related to MODALITY of the individual components

i.e. visual info of a memory stored in visual cortex

36
Q

What is Retrieval in the process of creating declarative memories?

A

Recall or use memory

Bringing fragment into Working memory

37
Q

When are memories modified or lost?

A

During retrieval (when you try and bring it into working memory)

38
Q

What anatomical substrates are required for recall/retrieval of memories?

A

Neocortex
Parahippocampal regions
Hippocampus

39
Q

What is the process of Recalling memories/

A

Memroy components from “storage area” back to parahippocampal regions

—> hippocampus, memory reconstructed here
—> thru parahippocampus (to keep trace)
—> cortex
—> working memory

40
Q

Where is an entire memory reconstructed?

A

In hippocampus

41
Q

What is the importance of the Parahippocampus?

A

Important in prolonging life of cortical trace of memory

42
Q

What uses the retrieved memories?

A

Working memory

43
Q

What is the 3 component model used by Working Memory?

A

Central executive
Phonological loop
Visuospatial loop

44
Q

What is the function of the central executive of working memory?

Anatomical substrates?

A

Directs/uses memory

Prefrontal cortex

45
Q

What is the function of the phonological loop of working memory?

Anatomical substrates?

A

Provides/interprets auditory info associated w/ memory

Broca’s and Wernicke’s area

46
Q

What is the function of the Visuospatial loop of working memory?

Anatomical substrates?

A

Provides/interprets visual info associated with memory

Occipital cortex (+others)

47
Q

What is spatial memory?

A

Detailed memory of space that serves as scaffold for RECONSTRUCTION of entire memory (hippocampus)

48
Q

Where is spatial memory stored?

Using what?

A

In hippocampus using special pyramidal cells in CA1 called “Place Cells”

49
Q

What are Place Cells?

A

◦ Neurons that are active only at specific places and especially active if you got a reward at that place

Final mediator of spatial memory

50
Q

When do place cells fire?

A

‣ Fire when in specific place or recalling a specific place

Especially active if you received a reward at that place

51
Q

What do Place Cells receive inputs fro?

A

Grid cells
Head direction cells
Border neurons

Etc.

52
Q

What is the function of head direction cells?

A

Give input to place cells about which direction your head was pointing to, to see/explore area

53
Q

When will border neurons fire and send info to Place Cells?

A

• Fire when near a border (wall, etc..)

54
Q

What is the function of Grid Cells?

A

◦ Creates a mpa of place you are in
‣ Grid map
‣ Triangular or hexagonal grid

Sends input to Place Cells

55
Q

Where are Grid Cells located?

A

In entorhinal cortex of hippocampus

56
Q

When are Grid Cells active?

A

When exploring an area

have to be in area for them to be active

57
Q

What is an important component of encoding/

A

Emotion

58
Q

What is the physiology for consolidation?

A

LTP as starting pt.,

continued activation (Papez circuit),

creation of new synapses in assoc. regions of brain (visual, auditory, etc.)

59
Q

What is the signal transduction pathways for Long Term potentiation?

A

EAA —> non NMDA, Na enters, DEPOLARIZATION

Mg released from NMDA r.
EAA—> NMDA, Ca and Na enters

Ca —> Calmodulin —>Incr. Adenylyl cyclase/cAMP —> AMPA r. Phosphorylation —> allows for INCREASE in Na Influx in response to EAA ==> bigger post synaptic response

Ca —> Calcineurin —> Activates NOS —> NO to diffuse back to presynaptic cell —> increase cGMP —> Increase NTR release