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Neural Circuits > Learning and Memory > Flashcards

Learning and Memory Flashcards

1
Q

What is the engram?

A

physical embodiment of a memory

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2
Q

What is Procedural memory?

A

Skills and unconscious movement (e.g. playing the piano, typing on a keyboard)

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3
Q

What is Declarative memory?

A

Available to the conscious mind, can be encoded in symbols and language

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4
Q

What is Explicit Memory?

A

memory that can be consciously recalled such as a memory like an event

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5
Q

What is Implicit memory?

A

memory that cannot be consciously recalled e.g. riding a bike

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6
Q

What systems are used to study the foundations of memory and why?

A
  • ‘Simple systems’ such as Aplysia Snail
  • Primates etc are too complex
  • Worms only contain around 300 neurons with v. specific functions
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7
Q

What are the advantages of simple systems?

A
  • Smaller, larger neurons
  • Simpler circuit complexity
  • Temperature dependence, dont react much to temp changes
  • Mapping tools (genetic manipulation is easier)
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8
Q

What memories do simple systems possess?

A

Habituation and Sensitisation

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9
Q

What is habituation? (incl. example)

A

Repetitive stimulus where the neurons respond less and less if there’s no negative association with it

For example:
- Gill withdrawal reflex in snails, touch or water jet causes gill withdrawal
After repeated jets, the gill stops withdrawing and the reflex reduces

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10
Q

What is sensitisation?

A

Repeated exposure to a stimulus results in an increased response to that stimulus over time

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11
Q

How does the gill withdrawal reflex occur in snails?

A
  • Motor neuron L7 synapses with gill muscle causing contraction
  • This motor neuron sees synaptic input from a sensory neuron, firing and then firing to gill muscle causing contraction
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12
Q

How does habituation effect the gill withdrawal reflex?

A
  • Presynaptic input remains the same (i.e. recognition of the sensory stimulus)
  • Habituation effects DOWNSTREAM of the PRESYNAPTIC NEURON
  • Level of habituation is in between the presynaptic and post synaptic body
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13
Q

What is the cellular basis of habituation?

A
  • RRP is the readily releasable pool of neurotransmitters at the active zone
  • With repeated exposed to a stimulus, there is a decrease in release of neurotransmitters RRP in response to each stimulus due to no time for vesicles to replenish the RRP store
  • So overstimulation = less response
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14
Q

How does sensitisation occur in snails in regards to the gill withdrawal reflex?

A
  • Increased gill withdrawal reflex evoked by tail pinch or shock
  • Third neuron in the system: L29 sensory neuron
  • L29 responds to electric shock and projects to the sensory neuron
    So
    L29 sensory neuron –> sensory neuron –> motor neuron
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15
Q

What is the molecular basis for sensitisation in the snail in terms of the gill withdrawal reflex?

A
  • L29 releases serotonin upon activation
  • Serotonin binds to receptors on sensory neuron
  • Activates G protein –> adenylate cyclase –> increased cAMP –> Protein Kinase A activation
  • Increased PKA activity phosphorylates and inactivates K+ channels
  • Longer depolarisation –> more vesicular release –> increased activation of motor neurons and larger contraction of gill muscle

SEROTONIN-ERGIC FEEDBACK

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16
Q

What are the conditions for associative learning?

A

both stimuli have to be paired at the same time to see a response (conditional stimulus (e.g. sound of bell ) and unconditioned stimulus (e.g. the food) )

17
Q

What is the molecular mechanism for associative learning?

A
  • When stimuli are paired the L29 neuron is activated - L29 releases serotonin
  • Serotonin receptor cascade (cyclic AMP, PKA etc.)
  • There are Ca2+ channels on the sensory neuron post synaptic membrane when the membrane is polarised
  • Cascade increases Ca2+ levels sending +ve feedback to adenylate cyclase
  • Larger influx of cAMP –> larger response

SO.. CA2+ INFLUX INCREASES RESPONSE

18
Q

Why are the mechanisms of sensitisation and conditioning complex?

A
  1. Involves complex models and pathways
  2. Multiple intracellular signalling pathways
  3. Require Pre and postsynaptic neurons
  4. Long term involves the nucleus signalling, triggering gene expression so the sensitization and conditioning responses last
19
Q

What is the Hebbian Synapse?

A
  • Fundamental concept in neural plasticity
  • To store information you need several neurons to fire at the same time ( associative learning), if there is coordinated activity of a presynaptic terminal and a post synaptic neuron then there is strengthening in the synaptic connections between them
20
Q

Where was the idea of the Hebbian synapse found?

A

In the hippocampus

21
Q

What are some indication examples that the hippocampus is involved in learning information?

A
  • Alzheimers (memory loss) hits the hippocampus early
  • Taxi driver hippocampus in london is larger as hippocampus stores a lot of spatial memory
22
Q

What is the structure of the hippocampus?

A

3 layers:
1. Dentate gyrus
2. CA3 neurons (aka mossy fibres)
3. CA1 neurons

Several synapses:
1. Dentate gyrus to CA3
2. CA3 to CA1***(the one we are interested in)
3. Output via fornix and subiculum

23
Q

How can the CA3 to CA1 synapse be stimulated?

A

Using electrodes and a high frequency stimulus to measure the amplitude of the EPSP
(CA1 is post synaptic)

24
Q

What is Long Term Potentiation?

A

The phenomenon that there is increased amplitude of the EPSP after frequent depolarisation

25
Q

How does LTP show input specificity?

A
  • CA1 has multiple inputs that can all be stimulated but not have the same EPSP
  • High freq. stimulation in just one of the input shows LTP in synapses that receive the highest freq. stimulation and not the others
26
Q

How does LTP show cooperativity?

A
  • EPSP amplitude increases when pre and post synaptic neurons are stimulated and depolarised at the same time
  • Pre and post synaptic are depolarised by different stimuli but together generate a bigger EPSP response
  • One pathway can be quite weak but if they converge on the same target and fire together the response will be strong
27
Q

What are the 3 types of glutamate receptors?

A
  1. AMPA: Important for depolarisation of the neuron, ionotropic so it opens when it binds glutamate and is non-selective.
  2. Kainate: Metabotropic causes metabolic reactions with G proteins
  3. NMDA: Receptor is a channel but its not non-selective, its fairly selective for Ca2+
    For NMDA to be open it has to bind a glutamate, the Ca2+ going inside the cell doesnt depolarise the cell much but it triggers certain reactions
    NMDA also binds Mg2+, when it does its blocked even if a glutamate binds

***Synapse between CA3 and CA1 is glutamatergic

28
Q

How does LTP occur?

A
  • Activation of NMDA receptor: glutamate binds, depolarisation, Mg2+ block removed, influx of Ca2+
  • Cascade of intracellular events that increase synaptic strength such as increasing number of AMPA receptors on post synaptic membrane
  • Ca2+ influx also leads to activation of protien kinases such as calmodulin kinase II and PKA
29
Q

How does calmodulin kinase II play a role in increasing the amplitude of the post synaptic EPSP?

A
  • The kinase has a regulatory unit and a catalytic unit, catalytic unit phosphorylates other proteins
  • The active site is hidden by the regulatory subunit, when it binds calmodulin and Ca2+ there is a change which exposes the active site
  • Phosphorylates itself to keep in active state and then phosphorylates AMPA to increase responses
30
Q

What is AMPAfication?

A

LTP causing increase in number of AMPA receptors due to vesicles fusing with the post synaptic membrane

31
Q

What is Late phase LTP?

A

Long term changes of the synapse -requires protein synthesis
- Takes longer as signal needs to go into nucleus, trigger gene expression so the protein can go back and alter the synapse

32
Q

How does Late phase LTP occur?

A
  • CRE (cyclic AMP response element) is a promoter region for TFs on genes
  • CREB1 is a TF that becomes phosphorylated due to LTP (PKA mechanisms and CKII) and binds to CRE
  • CREB2 is inhibitory and normally blocks this unless CREB1 is activated
  • CREB1 activates transcription of target genes, these proteins then return to the synapse and alter it for Late phase LTP
33
Q

What are nootropics?

A

Drugs to enhance memory - also increase LTP

34
Q

What is the Cerebellum LTD Circuitry?

A

Inputs = +ve mossy and climbing fibres

Outputs Dentate Nucleus = Purkinje fibres which receive input from granule cells (parallel fibres) and climbing fibres

There are also inhibitory interneurons such as MLIs

35
Q

How do purkinje fibres relate to LTD?

A
  • Paired granule cell/parallel fibres and climbing fibres input to a single purkinje cell evokes LTD
  • CF input indicates a motor error and weakens the parallel fibres: purkinje cell synapse
36
Q

What are the cerebellar LTD mechanisms?

A
  • NO NMDA RECEPTORS
  • Metabotropic and AMPA and Ca2+ activated channels involved
  • Needs co-incident activation of both intracellular signalling pathways
  • PKC phosphorylates AMPA GluR2 subunit and reduces currents by endocytosis
37
Q

How does Hippocampal LTD occur?

A
  • LTD occurs at the CA3- CA1 synapse with LFS- Ca2+ dependent
  • Can reverse a previous LTP
    LOW LEVELS OF NMDA RECEPTOR ACTIVATION
38
Q

What are the hippocampal LTD mechanisms?

A
  • Phosphatase/kinase balance
  • Small increases in Ca2+ from NMDA trigger more phosphatase (calcineurin) action and reduce AMPA efficacy by dephosphorylating
  • If there are more kinases, AMPA efficacy increases and there is LTP

Neural Circuits (9 decks)

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