Learning and Memory Flashcards
what are some things that help you remember?
retrieval cues
context
why might we forget things?
long time ago
other memories have formed
how is the limbic system involved with memory?
has the Thalamus, Hippocampus, Mammillary bodies of hippocampus, Amygdala, Hypothalamus, and Olfactory bulb
what is memory?
the capacity to encode, store, and retrieve information
what are the three memory systems?
sensory memory –> short term memory –> long term memory
taxonomy of memory (different flavors of memory)?
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
sensory memory
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.
short term memory
unrehearsed information is lost
Holds the information in the mind
Maintenance rehearsal
long term memory
Some information may be lost over time
what kinds of memories does non-declarative memory (long-term) include
reflexive and motor memory
Reflexes
Procedural (skill learning and motor movement)
Stimulus-response learning
classical conditioning
Priming
associated with cortical learning, cerebellum, basal ganglia
declarative memory (long-term)
semantic memory - facts
Episodic memory - events
what is semantic memory and what part of the brain is it associated with
Factual: “I know”
Not necessarily tagged with a context
associated with lateral temporal lobe, anterior cortical area
- semantic dementia
what does episodic memory include? what parts of the brain is it associated with?
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
what would an amnesic brain look like
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)
what would a semantic dementia brain look like
tiny TEMPORAL LOBE, cortical thinning
not specific to medial temporal lobe (hippocampus is usually intact)
semantic dementia (picture naming, immediate/delayed drawing)
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)
Representation of knowledge in semantic memory
- 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
Medial temporal lobe amnesia (anterograde vs graded retrograde)
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
Neurocircuitry of episodic memory
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)
how does the hippocampus help with memory
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”
dorsal stream vs ventral streams do what
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
Delayed-Match-to-Sample Task (when it comes to ventral stream in episodic memory)
- 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
What is perirhinal and what happens if it is lesioned
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)
parahippocampal cortex
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)
Entorhinal Cortex (grid, path, place, and time cells)
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
Cognitive map theory of hippocampal function
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
Relational Theory of Hippocampal Function
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
Morris Water Maze
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
MTL Dysfunction in Alzheimer’s Disease
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
Replay of cortical spiking sequences during human memory retrieval
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)
How do MTL circuits support episodic memory?
Bidirectional → Outputs leaving hippocampus and communicating with cortex
Aplysia as a model system
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
Synaptic plasticity (physiological and structural changes)
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
synaptic plasticity in mammals
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)
Long term potentiation (LPT)
lasting potentiation of synaptic transmission following repeated strong stimulation
Pairing presynaptic and postsynaptic activity also causes LTP
what leads to LTP
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
what leads to LTP
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
how is LTP state dependent
Degree of depolarization in post-
synaptic cell determines whether LTP
occurs
Molecular Mechanisms Underlying Synaptic Plasticity
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
NMDA receptor is a coincidence detector. what does that mean
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)
how does CAMKII affecs AMPA receptors in early/late phase
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
