Learning and Memory Flashcards

1
Q

what are some things that help you remember?

A

retrieval cues
context

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2
Q

why might we forget things?

A

long time ago
other memories have formed

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3
Q

how is the limbic system involved with memory?

A

has the Thalamus, Hippocampus, Mammillary bodies of hippocampus, Amygdala, Hypothalamus, and Olfactory bulb

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4
Q

what is memory?

A

the capacity to encode, store, and retrieve information

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5
Q

what are the three memory systems?

A

sensory memory –> short term memory –> long term memory

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6
Q

taxonomy of memory (different flavors of memory)?

A

short term

long term
- declarative (explicit)
- semantic (facts)
- episodic (events)
- non-declarative (implicit)
- procedural (motor skills and habits)
- priming
- classical conditioning (two stimulus = elicited response)
- reflexes

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7
Q

sensory memory

A

Information in through senses (visual, auditory, etc.) translates stimulus into things the brain can understand

Occipital lobe (visual, auditory, etc. cortex)
Unattended information is lost.

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8
Q

short term memory

A

unrehearsed information is lost
Holds the information in the mind
Maintenance rehearsal

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9
Q

long term memory

A

Some information may be lost over time

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10
Q

what kinds of memories does non-declarative memory (long-term) include

A

reflexive and motor memory
Reflexes
Procedural (skill learning and motor movement)
Stimulus-response learning
classical conditioning
Priming

associated with cortical learning, cerebellum, basal ganglia

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11
Q

declarative memory (long-term)

A

semantic memory - facts

Episodic memory - events

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12
Q

what is semantic memory and what part of the brain is it associated with

A

Factual: “I know”
Not necessarily tagged with a context

associated with lateral temporal lobe, anterior cortical area
- semantic dementia

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13
Q

what does episodic memory include? what parts of the brain is it associated with?

A

Events
Tagged with spatial and temporal context; Specific in time and place

Autobiographical: “I remember”

associated with hippocampus and medial temporal lobe circuit
- amnesia
- Alzheimer’s disease

Particularly vulnerable to age (and other hippocampal diseases); first to go
Ex: HM hippocampi were removed resulting in severe memory loss (amnesia)
Medial temporal lobe amnesia

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14
Q

what would an amnesic brain look like

A

medial temporal lobe (middle part of hippocampus) is black in the brain scan so it means there is cortical thinning (less tissue) - degenerating or missing)

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15
Q

what would a semantic dementia brain look like

A

tiny TEMPORAL LOBE, cortical thinning
not specific to medial temporal lobe (hippocampus is usually intact)

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16
Q

semantic dementia (picture naming, immediate/delayed drawing)

A

Progressive neurodegenerative disorder (gets worse over time)
Loss of semantic memory
very difficult for patients to name specific items
- Can talk but cant get to the right word ( that… thingy)

Video example: she could name most of the things on the table but switched around names of scissors and pen. Procedural, motor memory was still there

picture naming: Can name the overarching category like “animal” and can name things that are more solidified in the memory bc of more repetition (ex: dog), but cant get other less common things like bear as “animal” or frog as “little thing”
- Stronger representations of a higher level category but less so in lower level categories

immediate and delayed drawing: shown a drawing of an animal then have to draw from memory. will generalize what it looks like (ex: animals have 4 legs, so they draw a duck with 4 legs as well) and less likely to remember more unique features (ex: a camel’s hump or a rhino’s horn)

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17
Q

Representation of knowledge in semantic memory

A
  • Association network hub
  • Semantic information widely distributed in neocortical association networks
  • Connected to semantic “hub” in anterior temporal cortex (represents concepts)
  • Not linked to a specific time and place
  • Gradually acquired and updated
  • If you activate one node, it could activate other things and features
18
Q

Medial temporal lobe amnesia (anterograde vs graded retrograde)

A

Anterograde amnesia (in the future):
Inability to form memories after brain damage
Have difficulty remembering what happened right before the trauma
Anterograde cant encode memories after trauma

Graded retrograde amnesia:
Loss of memories formed before brain damage
Retrograde dip could be because the recent memories were not rehearsed

19
Q

Neurocircuitry of episodic memory

A

Neocortical association areas send projections to medial temporal lobe
Widespread cortical projections and are funneled down into medial temporal lobe then to parahippocampal region then to hippocampus (talks to different areas in the brain). Great for episodic memory bc you have to link aspects together (ex: name and location)

20
Q

how does the hippocampus help with memory

A

Hippocampus is the apex of processing hierarchy
- forms associations between pieces of information stored in neocortex where it is sent to perirhinal cortex to get to ventral cortex

Partial cue will trigger hippocampus (serves as an indexing function of things that are associated with each other)

dorsal stream helps determine “where”
ventral helps determine “what”

21
Q

dorsal stream vs ventral streams do what

A

dorsal - where
sent to parahippocampal cortex in medial temporal lobe. enters rhinal cortex then hippocampus

ventral “what”
- item information from temporal cortex visual stream
Perihinal cortex gets info from entorhinal
Gets input from ventral visual stream (the ‘what’)
Represent individual perceptual stimuli
Neurons do not show strong spatial coding bc it doesnt care where
Cells respond to specific stimuli when re-appearing in recognition test

22
Q

Delayed-Match-to-Sample Task (when it comes to ventral stream in episodic memory)

A
  • Increased neural activity during retention interval for faces later correctly remembered
  • Hold object information in mind over 30s delay
  • Even when object not visually present in the environment
23
Q

What is perirhinal and what happens if it is lesioned

A

perirhinal helps differentiate things
uses ventral (the what) visual stream
when lesioned = can’t recognize complex objects/faces

Visual perception discrimination is impaired
Damage to perirhinal cortex results in object recognition memory deficits
* Lesions in primate perirhinal cortex impairs DMS performance (Gaffan & Murray, 1992)
* Impaired visual discrimination of complex objects and faces (Barense et al., 2007)

24
Q

parahippocampal cortex

A

uses dorsal stream to determine the where
helps with orientation and deciding environmental context

Process spatial context
responds to “scenes” or “3D spatial layouts”
Orientation / Reorientation in space (changes depending on orientation within a room for example)

If lesioned
Impair learning spatial configuration of objects
Identity of memory for objects is not impaired

Preferentially respond to scenes rather than objects
Parahippocampal “place” area (PPA)
* Lesions to postrhinal cortex (PPA homologue) result in context recognition impairments
* No preference for exploring incongruent contexts (can’t discriminate between congruent & incongruent contexts)

25
Q

Entorhinal Cortex (grid, path, place, and time cells)

A

Transition zone between hippocampus and temporal neocortex (perirhinal cortex & parahippocampal cortex)

Grid cells
Neural map of spatial environment
Regular firing of neurons in different environmental locations
Brain’s “coordinate system”

Path cells
Code direction (encode for clockwise /counterclockwise movement)
Evidence from single unit recordings in humans
Was not coding when it was counterclockwise
Entorhinal cortex encodes properties of current context (location or direction), feeds forward to hippocampus

Place cells
Fire when in a specific location in the environment
Seem to have a receptive field for specific places in space
Act as a cognitive representation of a specific location in space
Cognitive scaffolding; using space as a cue
London taxi drivers had an increased size of hippocampus bc of spatial expertise

Time cells
Activity in hippocampus can replay in the same way when resting
Tag experiences with temporal information (temporal cues)
* Hippocampus critical for remembering the order of events in experiences
* Hippocampal activity can ‘replay’ sequential events in memory

26
Q

Cognitive map theory of hippocampal function

A

MTL contains spatial maps that can be co-opted for memory
Hippocampus preferentially processes spatial relationships in environment
Cognitive map: mental representation of spatial representation of environment

27
Q

Relational Theory of Hippocampal Function

A

is important for storing relational information
Hippocampus critical for storing relations between elements of experience
* Object, space, time
* Forms associations between pieces of information stored in neocortex
* Associations critical for episodic memory

integrates what, where, and when info
neurons respond to combos of experiences elements

28
Q

Morris Water Maze

A

Animal must find a specific location of a hidden platform
Learn association with external visual cues
Animals with hippocampal lesions have difficulty finding platform

when intact animals learn to find the platform in the morris water maze, cells in hippocampus divide and generate new neurons

29
Q

MTL Dysfunction in Alzheimer’s Disease

A

Episodic memory is the first to go in neurodegenerative diseases
Decrease in volume in hippocampus volume (Hippocampal atrophy = pathological criteria for Alzheimer’s)

White matter connectivity to the hippocampus and parahippocampus is lessened as well

30
Q

Replay of cortical spiking sequences during human memory retrieval

A

Patterns that are seen when reactivating memory is the same as what occurred when it was being encoded

Replay of activity and memory connection

Hippocampus → MTL → cortex → memory retrieval (behavior)

31
Q

How do MTL circuits support episodic memory?

A

Bidirectional → Outputs leaving hippocampus and communicating with cortex

32
Q

Aplysia as a model system

A

Has big neurons that can be seen with naked eye; simple circuits
Behavior: simple gill-withdrawal reflex
Touch siphon → withdrawal gill
Habituation is a decreased response to repeated stimulations

Changes at synapse
1. Reduced neurotransmitter release = change strength of synapse
2. Reduced number of synapses = long-term habituation

Repeated stimulation → alters synaptic transmission between siphon synaptic transmission between siphon sensory neuron and gill motor neuron

Touching siphon activates sensory neurons which → activates motor neuron causing → gill contract

  • Sensory neurons release less glutamate onto motor neurons
  • Reduce epsp which means reduced gill contraction
33
Q

Synaptic plasticity (physiological and structural changes)

A

Physiological changes include increased/decreased neurotransmitter release and/or a greater effect due to changes in neurotransmitter-receptor interactions.

Structural changes include increasing/decreasing # synaptic
contacts, formation of new synapses, elimination of synapses

34
Q

synaptic plasticity in mammals

A

Stimulate presynaptic cell (CA3) and record postsynaptic response (CA1)
High frequency burst of stimulation (called a tetanus) will cause you to see a longer lasting increase in epsp amplitude
Synapse is stronger/more effective = more effective (potentiation)

35
Q

Long term potentiation (LPT)

A

lasting potentiation of synaptic transmission following repeated strong stimulation
Pairing presynaptic and postsynaptic activity also causes LTP

36
Q

what leads to LTP

A

CA3 stimulated AND CA1 neuron’s membrane potential is briefly depolarized (by applying current pulses through the recording electrode)
→ persistent increase in the EPSPs in CA3 (LTP)
Depolarization of CA1 + CA3 stimulation leads to LTP
Cellular cascade leads to changes in synaptic strength

37
Q

what leads to LTP

A

CA3 stimulated AND CA1 neuron’s membrane potential is briefly depolarized (by applying current pulses through the recording electrode)
→ persistent increase in the EPSPs in CA3 (LTP)
Depolarization of CA1 + CA3 stimulation leads to LTP
Cellular cascade leads to changes in synaptic strength

38
Q

how is LTP state dependent

A

Degree of depolarization in post-
synaptic cell determines whether LTP
occurs

39
Q

Molecular Mechanisms Underlying Synaptic Plasticity

A

AMPA and NMDA receptors (ionotropic glutamate receptor)
AMPA
Na+ passes through

and NMDA receptors
Ca2+ and Na+ pass through
When glutamate binds, the channel does not open. Mg blocks the ion channel so Ca2+ and Na+ do not pass through

NMDA cant be activated bc of Magnesium plug
If there is a strong or prolonged stimulus, more glutamate is released, ampa receptors are activated/opened longer
Depolarizes neuron

40
Q

NMDA receptor is a coincidence detector. what does that mean

A

it has to detect the depolarization coming from post synaptic neuron and the presence of glutamate

If both happen, the Mg plug will be removed and leads to calcium influx which activates cellular cascade. This activated protein kinases (enzymes that add phosphate groups to protein molecules).
Gated by voltage (depolarization via AMPA receptors) and ligand (glutamate)

41
Q

how does CAMKII affecs AMPA receptors in early/late phase

A

Early phase
Ampa receptors added to postsynaptic membrane
Increases conductance of Na+ and K+ ions in membrane bound AMPA receptors

Late phase
Can release growth factor to create more synapses
Activated CREB transcription factor which changes gene expression for variety of proteins → long-lasting effects
Trigger release of retrograde messengers (affect presynaptic)
Is travels back across synapse and alters presynaptic neuron function (enhanced NT release) to make a positive feedback loop