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Systems Neuroscience > Memory > Flashcards

Memory Flashcards

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1
Q

Learning

A

Process of acquiring new understanding, knowledge, behaviours, skills, values, attitudes and preferences

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2
Q

Memory

A

Faculty of the mind by which data or information is encoded stored and retrieved when needed. It is the retention of info over time for the purpose of influencing future action

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3
Q

Reasons to research memory

A

Neurodegen diseases - dementia
Improve human memory
Get rid of unwanted memories (PTSD)
Basic mechanisms
Technology to improve memory
Ageing and enhancing lifespan of memory

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4
Q

What systems can be used to study memory

A

Humans - brain imagining (london taxi drivers), average memory span
Mice - behaviour, invasive brain studies
Invertebrates - aplecia (snail), sensitisation, gene expession, calcium signalling
Computer simulations

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5
Q

Distinctions of memory types

A

Memory vs habit
Explicit vs implicit
Knowing that vs knowing how
Memory without record vs memory with record
Declarative vs procedural

Biological info
Structure to function

Explicit - hippocampal
Implicit - striatum

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6
Q

Neocortex

A

Context and perceptual learning

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7
Q

Amygdala

A

Emotional responses (PTSD)

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8
Q

Medial temporal lobe

A

Declarative memory
Patient HM - medial temporal lobe removed to cure epilepsy, could not form new memories
Frontal lobe also needed for acquisition and refinement of new memories

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9
Q

Task: predict weather based on 14 card combos

A

Cards and whether guess
AD - damage in hippocampus so cannot make associative memories
Parkinson’s - damage in striatum cannot make procedural memories

Control - gets better
AD - got better at it
Parkinson’s - didn’t not get better

Training episode eg room, person etc
AD very low memory
Parkinson’s good

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10
Q

Virtual reality study with flag collection

A

Strategies
spatial and landmarks so hippocampal activation

Non soatial eg habit like the striatal activation, caudate nucleus

So different types of memory

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11
Q

What strategy is VPM Essen using to memorise pi digits

A

Declarative - visual, cake at entrance of his house
So probably Hippocampal

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12
Q

Ethical considerations in memory research

A

Emotional memories - psychological harm
Animal experiments - regulations
Invasiveness - so imagining studies
Informed Consent , right to withdraw (Helsinki convention)
Clinical trials - no unwanted effects
Up to individual not higher authorities (eg memory deletion)

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13
Q

Anterograde

A

No new memories

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14
Q

Retrograde

A

Lose old memories

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15
Q

Engram cells

A

Memory trace
The neuronal substrate responsible for storing and recalling memories, not yet a memory but provides physical conditions for memory to emerge
Memory emerges when appropriate retrieval cues reactive engram

Activated by learning experience
Physically or chemically changed by learning experience
Deactivated by subsequent presentation of the stimuli present at the learning experience

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16
Q

Multiple levels of analysis to understand memory storage

A

Network of brain regions
Population of nucleus
Cells (spines needed)
Synapse (NTs)
Nucleus (gene expression and histones)

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17
Q

Morris water maze

A

Test learning and memory in rodents
Finds platform and learns where it is and go straight there each time after learning

Prost training prove test
Control stay in the region of platform after removal
Hippocampus lesion, doesn’t remember so spend same amount of time in each quadrant
Same with subuculum lesion and when both lesions

NMDA receptor blockade
Blocks memory (so need NMDA for memory)

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18
Q

Molecular mechanisms of memory
Neuronal plasticity

A

Long term potentiation of synaptic response

Change of synaptic connections
Post synaptic response
Change in post synaptic spine number

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19
Q

Studies in invertebrate systems

A

Aplysia
Sensitises to poke (learns to ignore)
AP decreases
No longer reacts

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20
Q

Synaptic plasticity: neural circuits can change following stimulation

A

Synapses in the hippocampus whose efficient is influenced by activity which may have occurred several hours previously
In rabbit in denate area
These procedures are invasive

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21
Q

Long term potentiation: a cellular and molecular model of learning and memory

A

In mouse (invasive)
Extract mouse brain and extract hippocampus, Cut transverse hippocampus slices and place into recording chamber and place electrodes to record post synaptic activity
Response mediated by glutamate

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22
Q

How does synaptic plasticity occur

A

AMPA and NMDA receptors
Low Neurotransmitter release only AMPA receptors open as NMDA usually blocked by magnesium ions
Increased glu AMPA and NMDA open due to AP and so magnesium moves

NMDA also permeable to calcium so intracellular calcium requirement

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23
Q

Hebbian plasticity

A

Cells fired together are wired together
need for associative firing for plasticity

Hebbian learning: Presynaptic activity is well timed with postsynaptic depol leading to postsynaptif ca2+ increase (importance of NMDA receptors)

High frequency stimulation = LTP so increase synaptic function
Low frequency firing = LTD so decrease synaptic function

Postsynaptic cell - LTP causing high calcium influx so more AMPA receptors in post synaptic membrane
LTD weak calcium increase and can only activate some phosphotases which change phosphorylation of post synaptic receptors sometimes leading to internalisation

Low frequency LTP 1 every 10 seconds to make it spike and achieve LTP with greater postsynaptic activity
Vs same condition but lower post synaptic activity causing LTD

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24
Q

Intrinsic properties of neurons and their make up of voltage dependent channels influence their integration of signals and plasticity

A

Adult neurones vs newly generated neurones
Dentate gyrus (makes new neurons here)
Demonstrated immature neurones are relatively weak TBS were able to undergo plasticity more than mature neurones
Needed for new learning and memory

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25
Spike timed dependent plasticity
Low frequency stimulation constantly If firing doesn’t correlated with time of post synaptic response then doesn’t cause AP so depression Demonstrates in cortical neurones of rats (EPS constant response but EPS and APs result in increased response) TIMING MATTERS AP before EPSP = LTD
26
Critical window for induction of synaptic potentiation and depression
LTP - EPSP followed by spike of AP LTD - EPSP after spike of AP
27
Theta burst stimulation
Rapid burst of 4/5 spikes that are separated by 10 ms Activity of hippocampal neurones in vivo when animal exploring a new environment Cause LTP
28
Postsynaptic sppines importance in memory
Memory storage May be locus storage of the brain (theory)
29
Hebbian idea of plasticity
Axon A near enough to excite cell B of repeatedly/ consistently takes part in firing it, some growth or metabolic change takes place in one or both cells such that As efficiency as one the cells firing B is increased
30
Glutamate signalling in synapse
Recording of hippocampal slice Stable baseline induce LTP and LTD Basal conditions, glu bind to AMPAR AND NMDAR but NMDAR blocked due to low stimulation Strong, glu bind AMPAR and NMDAR mg leaves and so ca2+ and na+ enters cell
31
How to measure plasticity
Extracellular stimulation and recording for post synaptic response Extracellular stimulation and patchbclamp recording Dual path clamp/ paired recordings Voltage and current
32
Induction protocols that induce plasticity
High/low frequency Low frequency stim couple with weak/string postsynaptic depol Spike timing dependent plasticity Theta burst stimulation (100 Hz with 5Hz frequency) 0.1 Hz once every 10 seconds 1Hz once per second 100Hz 100 times per second
33
What is happening in postsynaptic spines during plasticity?
Glutamate and depol Block NMDAR no LTP So ca2+ and NMDAR needed for plasticity
34
What is downstream of ca2+ signalling
CAMKII activation - molecular switch for memory In hippocampus- 1-2% of total protein by mass, ~10% of protein in post synaptic density (PSD), acutely activated by auto phosphorylation
35
CAMKII
Association and regulatory domains Regulatory domain binds CaM, separation of domains and so exposure and activation of threonine (T286) CAMKII becomes independent and keep self phosphorylated Molecular switch for memory
36
Changes in post synaptic AMPA receptor number and conductance are associated with LTP/LTD
CAMKII leads to insertion of new AMPAR in the membrane through trafficking mechanisms Rab11a protein important for trafficking of receptors to membrane due to LTP LTD - lower inpulses we have through synapses still require calcium, activates calcineurin and PP1 (phosphotase) which removes AMPAR from membrane (internalisation)
37
Structure of AMPRA and NMDA receptors
Detrimers (4 subunits) N terminal domain is outside cell C terminal inside cell (post transcriptional modifications) AMPAR - post translation modification important to determine synaptic inclusion (eg phosphorylation of serine 831 seen after LTP and interacts with trafficking mechanism)
38
Hypothetical timescale of CaMKII signalling in dendritic spines
Ca2+ in via NMDAR CA2+ CaM binding T286 phosphorylation CaMKII activity (CaNKII and NMDA containing subunits gluN2B- maybe more plastic) Actin polymerisation And AMPAR insertion
39
CaMKII: central molecular organiser of synaptic plasticity, learning and memory
Inactive spine to begin with sewn through blue flouresence End - spine frown and active CaMKII activity (keeps growing due to auto phosphorylation) and CaMKII-CaM (stays same ish) association separated relatively quickly
40
Immature spine
Plastic Lots of glua2b in receptors Some synapses start with only NMDA receptors (strong input causes insertion of AMPAR)
41
Mature spine
Store own history in its proteomic composition and it’s shape
42
Does associative plasticity actually occurs in vivo after learning? Does it mediate learning?
Electrophysiological observation of LTP in vivo Inhibitory avoidance - dark side has footshock, stays in light despite wanting dark so learnt something CA1 electrodes - trained has increased post synaptic function in the ca1 neurones LTP increase isn’t that high and varies on intensity and electrodes Serine 831 is phosphorylated after LTP in trained mice It shows associative plasticity Shows correlation so doesn’t really showing it mediates learning - manipulations are quite global so unknown if it’s really due to the LTP and AMPAR
43
Ways to delete an engram
Non targeted ablation Targeted ablation Neuron specific ablation Engram neurone specific ablation
44
Deleting engram experiment
Contextual fear learning Activation of neurones in dentate gyrus, cortex and lateral amygdala Tag neurons CREB viral vector to make neurones more likely to be part of engram. Same vector allowed toxin mediated destruction Mice with ablated neurones could still acquire fear learning but worse memory Ablating similar number of random neurones did not disrupt memory
45
Capturing then reactivating an engram
Cfos expressed when learning Causes expression of tTA which activates TRE (promoter) Channel redopsin 2 will be expressed too So can label neuron that has undergone learning make it fire by activating with light On DOX - sequesters tTA so do not express channel redopsin Off DOX - channel redopsin expressed Baseline, context a (gear learning), context b (light and freezing despite not having fear learning in that context)
46
Optogenetic stimulation of circuits
Express exogenous a protein in the brain Ion channels incorporated Shine laser results in activation (channel redopsin is sensitive to blue)
47
Modulation of plasticity in L and M
Behavioural states influence memory formation (brain states) Neuromodulators (ACh), monoamine and catecholamines Excitatory/Inhibitory balance Synapse Glial (tropic, release of neuro modulators)
48
Field activity
Regular steel electrode Impaired spatial learning and suppression of sharp wave ripples by cholinergic activation of at the goal location Spike amplitude clustering Separate activity of individual neurones Sleeping animal - can reply the route it took backwards
49
Two stage model of memory formation
ACH for exploration and initial encoding of memory trace brain state 500ms DA for reward and novelty enhance SWRs during immobility and for reactivation of memories. Brain state 50ms Volume transmission
50
Main producer of ACh in the brain
Medial septum (MS)
51
Main producer of dopamine in the brain
Ventral tegmental area (VTA) and Loccus coeruleus (LA) Areas activated by vagus nerve
52
Rat in novel cage evokes DA release in accumbens
Increase DA levels Hippocampal VTA loop - controls the entry of info into long term memory 2 input experiment Baseline and activated neurones Block of dopamine receptors blocks late phase LTP Memory - inhibitor, rats explore more because couldn’t make the memory as well
53
Cholinergic activation
Promotes theta/gamma oscillation Suppresses ripple oscillation Regulation of cholinergic tone allows switching between attentive and offline memory Disrupted cholinergic activity impairs memory Eg AD loss of ACh signalling
54
Impaired spatial learning and suppression of sharp wave ripples by cholinergic activation at the goal location
Impairs DA part of two stage learning Fewer sharp wave ripples
55
Synaptic tagging and protein synthesis dependent plasticity
Code place when something important happens A lot of protein synthesis happens at spine
56
Strong stimulus before weak can make weak strong
2 input study Weak stimulus at stimulus 2 - LTP iffy Strong stimulation to s1 and then weak to s2 gives good LTP Cell active, increased CREB levels and excitability, input if recently fired synapse becomes stronger of new stimulus
57
Synaptic tagging
Presynaptic AP Synaptic tag and E-LTP Increased CREB levels Synapse specific potentiation and LLTP Increased CREB levels Memory a and b positive neurone
58
Systems consolidation of memory
Interinal cortex maps position in general space without landmarks Hippocampus is putting landmarks on Other cortical areas also include info eg prefrontal cortex (have I been here before?)
59
Context learning
Hippocampus - electrodes Dendogram - how correlated is the firing of a particular neurone depending on what the animal has to do Object, valence, position, context encoded in that order
60
Prefrontal cortex
Helps hippocampus have control of what it retrieves and what it doesn’t Hippocampus maps Prefrontal cortex guides what info gets retrieved by interacting with dorsal hippocampus
61
Oscillation in the brain
Context exploration - hippocampus leads Object sampling - PFC leads, hippocampus follows Anatomical mapping Brain Waves - theta waves (field), spikes (individual cells) Spike before theta oscillation like animal is anticipating (ACh)
62
Organisation and control
Prefrontal cortex supports cognitive control of memory by developing representations that employ current contextual cues to select context appropriate memory representations and suppressing context inappropriate memories Eg PTSD
63
Conclusions on memory
Distinct types of memory eg hippocampus and associative memory Associative plasticity requires NMDA receptor signalling, ca2+ increase and CAMKII

Systems Neuroscience (5 decks)

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