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Neural Circuits > Memory > Flashcards

Memory Flashcards

1
Q

What does 1) learning 2) memory 3) recall 4) engram mean?

A

1) Changes of how neurons respond to an input and adjust their output.

2) storage of learned information

3) Specific neurons fire leading to recall of perception or behaviour.

4) physical embodiment of a memory (What constitutes memory, such as coordinated activity of neurons which cause recallection of memory)

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2
Q

What is a) Procedural memory b) Declarative memory?

A

a) Skills and association largely unavailable to the conscious mind
>E.g. juggling or riding a bike

b) Available to the conscious mind, can be encoded in symbols and language. (explicit memory that can be written down or spoken)

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3
Q

What is a) Explicit memory b) Implicit memory?

A

a) Explicit – memory that can be consciously recalled (e.g. recalling riding a shiny new bike on the Christmas day when you were 5)

b) Implicit – memory that cannot consciously recalled (e.g. learning to ride a bike process).

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4
Q

What are the 3 different types of implicit memory?

A
  1. Procedural memory
    >Similar to Procedural memory (unconscious skill)
  2. Classical conditioning
    >Where animals can associate specific stimuli with a positive or negative reward and act accordingly.
  3. Priming
    >When one stimulus influences the response to subsequent stimuli
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5
Q

What are 2 simple forms of memory?

A
  1. Habituation
    >Form of memory where the amplitude of response reduces if the same stimulus is repeated many times
  2. Sensitisation
    >Leads to increasing amplitude of response, a weaker response will become bigger and bigger when repeating a stimulus many times
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6
Q

What is an example of habituation on Alpysia?

A

After continuous repeating activation of the gill withdrawal reflex, the reflex decreases in response (gill stops withdrawing from touch)

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7
Q

When touching the gill of an Alpysia, what happens to the gill and why?

A

After stimulation, the gill will withdraw due to the gill withdrawal reflex.

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8
Q

What are 2 organs that Aplysia use the gill withdrawal reflex to protect?

A

Siphon and Gill

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9
Q

What is a simple overview of the gill withdrawal reflex circuit?

A

Stimulation of siphon skin -> sensory neuron activates -> releases glutamate to motor neuron -> Gill muscle contract

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10
Q

What neurons are found in the a) Siphon b) Gill and what connections do they form?

A

a) Sensory neurons in Siphon
b) Motor neurons in Gill

> Form glutaminergic connections.

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11
Q

Where does habituation in the gill withdrawal reflex occur?

A

habituation occurs at the synapse between the presynaptic and postsynaptic neuron.

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12
Q

What is the cellular basic of habituation?

A

Depletion of the readily releasable pool (RRP), meaning reduced neurotransmitters released as quickly, causing a reduced amplitude.

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13
Q

What type of neuron is L29 and what is its effect on surrounding proteins?

A

L29 neuron is serotoninergic, serotonin activates G-protein which activates adenylyl cyclase, uses ATP to produce cAMP which activates protein kinase A, which phosphorylates proteins which changes conformation leading to change in function.

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14
Q

What is the molecular basis of sensitization?

A

Protein kinase A phosphorylates and inactivates K+ channels, leading to longer depolarization. Meaning more vesicular release to the postsynaptic membrane of the sensory neuron leading to an increased muscle contraction due to greater depolarisation of motor neuron.

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15
Q

What is a simple overview of a) Habituation b) Sensitisation and what are they an example of?

A

a) Habituation: depletion of the synaptic vesicle pool

b) Sensitisation: serotonin-ergic feedback from other sensory neuron, leads to more release of synaptic vesicles from sensory neuron leading to greater motor depolarisation.

> These are the 2 simplest forms of learning.

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16
Q

What is Pavlovian-like learning?

A

The association of a conditioned stimulus (e.g. bell, dog wouldn’t salivate to this without being conditioned) with an unconditioned stimulus (e.g. food, the dog already salivates in response to this), the two stimuli have to occur at the same time to cause the conditioning of a stimulus to another.

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17
Q

How does an Aplysia react to a weak siphon touch (unconditioned) paired with a strong shock (conditioned)?

A

Pair these stimuli and the gill withdrawal reflex is stronger and lasts for a long time (Pavlovian-like associative learning example)

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18
Q

How is the Pavlovian-like associative learning by Aplysia (weak touch paired with shock) different to sensitization?

A

Different from sensitization as that doesn’t require stimuli to be paired to trigger a stronger response.

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19
Q

Describe the simple model of Pavlovian-like associative learning during the gill withdrawal reflex

A

> Shock (conditioned) activates L29 and Touch (unconditioned) activates Sensory neuron.

> When L29 and sensory are activated together, when L29 releases neurotransmitter the sensory neuron is already depolarised by itself, this causes Ca2+ influx into the sensory neuron post synapse, this potentiates activity of adenylyl cyclase causing much more activity of cAMP so much more neurotransmitter is released from sensory to motor neuron.

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20
Q

Where does the L29 neuron synapse to in the gill withdrawal circuit?

A

Synapses to the postsynaptic side of sensory neuron, so is near to the synapse from sensory neuron to motor neuron.

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21
Q

What are the 3 main kinases used in learning and what secondary messengers are they activated by and what are they used for?

A

i. Kinase A: (Late stage LTP)
>Activated by cyclic AMP

ii. Kinase C: (LDP)
>Activated by diacylglycerol

iii. CamKinase II: (Early stage LTP)
>Activated by Ca

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22
Q

What is an example of a protein kinase which causes sensitization of vesicle release to last longer?

A
  1. MAP Kinase is a protein kinase that travels from cytoplasm into the nucleus

2.phosphorylates transcription factors in nucleus to trigger gene expression

  1. Proteins are then transported out and into the cytoplasm to establish a longer response due to change in gene expression, so the sensitization of vesicle release for example would last a lot longer.
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23
Q

What did Donald Hebb suggest about synapse strength?

A

“Coordinated activity of a presynaptic terminal and a postsynaptic neuron, strengthen the synaptic connections between them.” (If two neurons are active, this strengthens a synapse. )

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24
Q

What is an overview of LTP as a post-synaptic event in 5 steps?

A
  1. Increased frequency in stimulation of presynaptic neuron or neurons
  2. Glutamate released binds to AMPA receptors, influx of Na+ causes fast depolarisation of postsynaptic membrane.
  3. Depolarisation dissociates Magnesium block from NMDA channels, open on postsynaptic membrane

4.. Increasing Ca2+ conc in postsynaptic membrane

5.. Increased Ca2+ conc activates kinases (as Ca2+ binds with Calmodulin to activate kinase II) which phosphorylates proteins leading to increase in EPSP amplitude.

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25
Q

What are the 3 types of glutamate receptor and what do they allow transport of?

A
  1. NMDA receptor
    >Ca2+ ion channel, doesn’t depolarise cell much but leads to synaptic exocytosis of vesicles (does still cause some Na entry and some K+ efflux)
  2. Non-NMDA receptor (AMPA)
    >Ion channel for Na+ entry (influx) and K+ exit (efflux) causing depolarisation.
  3. mGlut Receptor
    >Metabotropic (GPCR)
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26
Q

Where has LTP and LDP been studied the most and why?

A

The Hippocampus, as it is involved in learning and memory.

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27
Q

What is observed during the LTP phenomenon?

A

Increased frequency in presynaptic stimulation also increases amplitude of postsynaptic EPSP, leading to higher and longer lasting activity in postsynaptic neurons.

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28
Q

What is meant by LTPs being triggered by co-operative activity?

A

Postsynaptic neurons receive input from many presynaptic neurons, if multiple presynaptic neurons receive increased frequency of stimulation there is an increased EPSP amplitude (action potentials fire more and last longer).

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29
Q

What is input specificity in terms of LTP and what does this show?

A

> Stimulating different presynaptic neurons triggers different amplitudes of EPSP. Also If one presynaptic neuron has increased input frequency the EPSP will increase (observe LTP), but after woulds if we stimulate another presynaptic neuron (for the same postsynaptic neuron) at a normal frequency the EPSP generated from these neurons will not be increased like the other

> Shows the mechanisms for LTP are in parts of the neurons that are not shared by both presynaptic neurons (either on presynaptic neuron or on side of postsynaptic neuron but close to the presynapse)

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30
Q

How does LTP help learning?

A

Helpful for associative learning, as if a neuron for a stimulus and a neuron for a behavioural response are frequently active together it will strengthen the shared synapse

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31
Q

What type of synapse is between a presynaptic neuron and a postsynaptic neuron for triggering LTP?

A

Glutaminergic (glutamate = excitatory neurotransmitter)

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32
Q

What is an idea to LTP occurring by pre-synaptic changes?

A

An increase number of neurotransmitter available for release

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33
Q

Does evidence suggest LTP is caused by a pre or post synaptic event?

A

postsynaptic event

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34
Q

Why is high frequency stimulation of pre-synapse necessary for LTP?

A

NMDA receptors require depolarisation of the postsynaptic membrane as well as glutamate release from the presynaptic membrane to open. This is as glutamate can bind to AMPA receptors which allow influx of Na+ for fast depolarisation of postsynaptic membrane which causes dissociation of Mg2+ block of NMDA (as well as AMPA) receptors. So when glutamate also binds to NMDA Ca2+ can enter.

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35
Q

Why do NMDA receptors not open without high frequency pre-synaptic stimulation?

A

As without activation of AMPA channels (by AMPA), which depolarises the postsynaptic membrane, the magnesium block of NMDA does not allow Ca2+ flow even with glutamate bound

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36
Q

What would be the effect on LTP if there was just weak stimulation of presynaptic neurons?

A

Small amounts of glutamate release would just activate AMPA receptors (not NMDA receptors) leading to some depolarisation but not LTP (not increased EPSP amplitude) due to less Ca2+ influx and therefore less vesicle exocytosis.

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37
Q

What is the overall effect of LTP?

A

Enhanced communication between pre and post synaptic neurons, leading to more efficient neurotransmission at these synapses.

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38
Q

What is meant by increased EPSP amplitude (observation for LTP) and what is an example of how this is caused?

A

> The amplitude of an EPSP refers to the strength or size of the depolarization that occurs in response to the incoming excitatory signal. An increased amplitude of EPSP means that the depolarization generated by the incoming signal is larger than normal, and thus more likely to trigger an action potential in the receiving neuron.

> E.g. an increase in the amount of neurotransmitter released by the presynaptic neuron

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39
Q

How long does LTP usually last?

A

he persistence of LTP can last for weeks or even months, allowing for long-term changes in the brain that support memory and learning.

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40
Q

What are the 2 phases of LTP?

A

1) Early LTP (induction)
>Changes evoked by different mechanism to strengthen existing synapses short term (does not require protein synthesis)

2) Late LTP (expression)
>Protein synthesis to make long term changes to synapses, new synapses can be made.

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41
Q

What is the process of short term LTP in 5 steps

A
  1. NMDA receptor activation and unblocking by increased presynaptic stimulation (depolarisation by AMPA activation as well as glutamate binding)
  2. Increased influx of Ca2+
  3. Ca2+ binds with Calmodulin, this complex binds to Kinase II (CaMKII) causing conformational change exposing subunits for phosphorylation.
  4. Kinase II phosphorylates itself (autophosphorylation), stabilising the whole molecule in active conformation
    >So removal of Ca2+ doesn’t result in immediate hault in phosphorylation.
  5. Phosphorylation enhances AMPA currents due to AMPAfication (increase in AMPA receptors at postsynaptic site).
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42
Q

Why does removal of Ca2+ not cause immediate decrease in LTP?

A

As after Ca2+ induces Kinase II autophosphorylation of itself, it is stabilised in an active conformation (so doesn’t need Ca2+ for a while)

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43
Q

How does AMPAification occur at postsynaptic neurons stimulated by LTP?

A

Vesicles containing AMPA receptors are released onto the postsynaptic membrane upon stimulation of LTP.

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44
Q

How does the long phase of LTP work in 5 steps?

A
  1. cAMP activates Kinase A
  2. Kinase A enters nucleus and phosphorylates proteins in nucleus
  3. CREs is bound by CREB-2, but when Kinase A phosphorylates this, CREB-2 is replaced by CREB-1 which activates the promotor region
  4. Genes such as BDNF or immediate early genes (e.g. C4) have increased transcription
  5. These genes lead to increased number of receptors on the postsynaptic, leading to increase in EPSP amplitude.
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45
Q

What is CREs and CREB?

A

> CREs = a type of DNA called cAMP response element

> CRIB = CRE binding protein e.g. CRIB1 or CRIB2

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46
Q

How long does the long phase take during LTP development and why?

A

Takes effect » 1 hour after initiation (as involves gene expression)

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47
Q

What would be found bound to CREs in a cell that has not undergone the long phase of LTP development?

A

CREB-2 (gets replaced by CREB-1 after Kinase A phosphorylation).

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48
Q

What is experimental evidence on mice which shows that LTP is involved in memory?

A

> Repeatedly putting a mouse in water and it will learn where the hidden platform is to get out quicker

> Mice knockouts for genes for LTP, the mice do not remember where the platform is, showing the spatial memory has decreased without LTP activity.

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49
Q

During LTP experiments, why can’t we just knockout the protein kinase A

A

As kinase A is found in the body for many processes, so need to only knock it out in the cells we know are involved.

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50
Q

What protein kinase is involved in a) Short phase b) Long phase of LTP?

A

a) Kinase II (CamKII/ Calcium–calmodulin-dependent protein kinase II)

b) Kinase A

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51
Q

What is a distinguishable morphology of Purkinje cells?

A

Dense dendritic trees only facing upwards.

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52
Q

What is the simple circuit in the cerebellum?

A

Mossy fibres (or climbing fibre) input -> granule cells (parallel fibres are axons of granule cells) -> Purkinje cells output to deeper cerebellum nuclei

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53
Q

What are the 2 ways a climbing fibre can synapse to a Purkinje cell and what is the effect of this?

A
  1. A climbing fibre only synapses to one Purkinje cell, forms many synapses with one Purkinje cell
    >So if climbing fibre is activated, leads to massive depolarisation with Purkinje cell (if has many synapse)
  2. Or climbing fibre can form one synapse with many Purkinje cells
    >Activation of climbing cell will depolarise many Purkinje cells slightly
54
Q

What is the Albus Marr model of LDP in the cerebellum?

A

> Paired PF (parallel) and CF (climbing) input to a single Purkinje cell (P) evokes LTD.

> CF input indicates a motor error and weakens the PF : P synapse

55
Q

What channels are used for LTD in the cerebellum?

A

Metabotropic Glu-R, AMPA receptors, and voltage-activated Ca2+ channels.

56
Q

What are the 2 receptors found at the synapse between a) Climbing fibre to Purkinje cell b) Parallel fibre to Purkinje cell?

A

a) Voltage gated Ca2+ channels, and AMPA receptors

b) Metabotropic glutamate receptor (mGlu-R), and AMPA receptors

57
Q

What is the difference in morphology of climbing fibres and parallel fibres (from granule cells)?

A

> Climbing fibres coil around Purkinje cells, “climbing them” with a synapse between.

> Parallel fibres form a synapse which is parallel to the Purkinje cell.

58
Q

What occurs in Purkinje cells of the cerebellum if just parallel fibres are activated?

A

At parallel fibre to Purkinje synapse causes glutamate to activate metabotropic glutamate receptors, the G-protein activates DAG which activates some protein kinase A. But without Ca2+ influx at the Climbing fibre: Purkinje synapse means kinase A is not potentiated so cannot dephosphorylate AMPA receptors as much meaning LTD doesn’t occur.

59
Q

How does long term depression occur in Purkinje fibres of the cerebellum?

A
  1. Co-incidence activation of Climbing fibres and Parallel fibres
  2. At parallel fibre to Purkinje synapse causes glutamate to activate metabotropic glutamate receptors, the G-protein activates DAG which activates some protein kinase C.
  3. At climbing fibre to Purkinje synapse causes glutamate to activate AMPA receptors, influx of Na+ depolarises the Purkinje cell opening voltage gated Ca2+ channels which further potentiate protein kinase C.
  4. Protein kinase A phosphorylates AMPA receptors at different sites than during LTP, leading to endocytosis (removal) of AMPA receptors from the Parallel fibre: Purkinje synapse.
  5. Less Na+ can enter from parallel fibre activation, meaning a decrease in EPSP.
60
Q

In the hippocampus, what occurs in the CA1 (postsynaptic neuron) if CA3 (presynaptic neuron) has high frequency stimulation?

A

The EPSP amplitude at CA1 increases (LTP).

61
Q

In the hippocampus, what occurs in the CA1 (postsynaptic neuron) if CA3 (presynaptic neuron) has low frequency stimulation?

A

THE EPSP amplitude at CA1 will decrease (LDP)

62
Q

> What is a similarity between LTP and LDP mechanisms but what is different about this mechanism too?

A

> Both are reliant on Ca2+ influx, so require NMDA activation

> But LTD is caused when NMDA is only activated a bit, while LTP is caused when NMDA is activated in a lot

63
Q

Can LTD effect LTP and why would this happen?

A

Yes LTD can reverse LTP (if presynaptic neuron decreases frequency of stimulation, then LTD reverses LTP/ EPSP decreases in amplitude)

64
Q

What enzyme is needed for LDP development in a) Cerebellum b) Hippocampus?

A

a) Protein kinase C

b) Phosphatases

65
Q

How does LDP occur in the hippocampus?

A
  1. Decreased presynaptic stimulation frequency
  2. Decreased glutamate binding to NMDA receptors and therefore less Ca2+ influx into postsynaptic membrane
  3. Is still a Ca2+ influx, but less than enough to activate protein kinases for LTP, instead a lower amount of Ca2+ activates Phosphatases.
  4. Phosphatases dephosphorylate AMPA receptors which decreases efficacy, decreasing depolarisation and therefore lowering EPSP amplitude (LPD)
66
Q

How are LTP and LDP managed by Ca2+?

A
  1. Large influx of Ca2+ activates more protein kinases, increasing AMPA-R efficacy triggering LTP
  2. Less influx of Ca2+ activates more phosphatase enzymes which decrease AMPA-R efficacy, triggering LDP.

> So balance of phosphatase and kinase balances whether a synapse undergoes LTP and LTD.

67
Q

Describe Classical conditioning involving the example of Pavalov.

A

> If a unconditioned stimulus (e.g. food for a dog) coincides or precedes a conditioned stimulus (e.g. a bell ringing), the unconditioned stimulus becomes associated with the conditioned stimulus meaning the conditioned stimulus now causes the same response that the unconditioned stimulus would

> e.g. food causes dog to salivate, if ringing a bell as well as food is present causes dog to salivate, association formed and now when the bell rings on its own it causes the dog to salivate

68
Q

What are the cells called which are present in the mushroom body of Drosophila?

A

Kenyon cells

69
Q

What is a simple circuit for the Olfactory system in Drosophila?

A

Odour -> Olfactory receptor neurons -> Projection neurons -> Lateral horn (for innate) or Mushroom body/ Kenyon cells (for learned).

70
Q

What makes Kenyon cells very selective to specific odours?

A

Each Kenyon cell receives inputs from many olfactory receptor neurons (all responding to a certain odour) and due to Kenyon cell’s high spiking threshold, each Kenyon cell needs multiple projection neurons to fire at the same time to trigger a response.

71
Q

What is the mechanism which inputs reward and punishment onto Kenyon cells?

A

Dopaminergic neurons respond to reward or punishment, these modify the output between Kenyon cells to output neurons which leads to a behaviour.

72
Q

Where is olfactory memory stored in Drosophila?

A

Kenyon cells (in mushroom body the area for learned olfactory behaviours).

73
Q

What system allows us to artificially express arbitrary transgenes in specific cells in Drosophila?

A

GAL4/UAS system

74
Q

What are the mechanisms of the GAL4/UAS system and what is it used for?

A

> GAL4 is a transcription factor found in yeast, when in genome of flies it binds to UAS (upstream patterning sequence) of DNA to initiate transcription of downstream genes

> Could create many different UAS lines for transcription of different proteins (can make any protein we want)

75
Q

What is a transgene?

A

A gene which is artificially introduced into the genome of another organism.

76
Q

How do you express a protein in just one neuron in the brain?

A

Using the Split-GAL4 system

77
Q

What is the process of the Split-GAL4 System?

A

> GAL4 is made up of 2 domains (binding domain- BD and Activation domain- AD). only cells with promotor regions of DNA which allow DB and AD to overlap will express the GAL4 complex. Transcription factors are recruited to initiate gene transcription of a wanted transgene.

78
Q

What is the Split-GAL4 system useful for?

A

For expressing specific transgenes in specific neurons.

79
Q

What is the role of the Mushroom body in Drosophila?

A

Associative memory

80
Q

What does “MBONs” stand for?

A

Mushroom body output neurons

81
Q

What does “DANs” stand for?

A

Dopaminergic neurons

82
Q

What is the structure of Kenyon cell axon compartmentalisation in the mushroom body of Drosophila?

A

Kenyon cell axons are subdivided into compartments innervated by mushroom body output neurons (MBONs) and dopaminergic neurons (DANs). The compartments of MBONs and DANs match, meaning DANs release dopamine to the same Kenyon cell axon compartment as specific MBONs (so at the compartment where MBONs receive input from Kenyon cells, DANs input onto the synapse).

83
Q

How do you test for the effect of Mushroom body output neurons (MBONs) activity on approach or avoidance behaviour on flies?

A
  1. Express an activator (e.g. crimson, red activated ion channel) in MBONs using split GAL4 system.
  2. Shine red light on one half of area.
  3. If crimson was expressed in specific neurons, the flies approached the red light, as it would activate MBONs.
  4. Other neurons when activated with red lights causes avoidance behaviour.
84
Q

How do Kenyon cells trigger learned behaviour?

A

By activating avoid and approach output neurons in a biased way

85
Q

What is a method to show how Dopaminergic neuron (DANs) can retain aversive or appetitive memory when activated ontogenetically (artificially)?

A
  1. Using split-GAL4 to label specific DANs and crimson to activate these specific DANs in red light.
  2. Put flies in arena and present with odour while pairing with flashing red lights activating particular DANs
  3. Pair odour A with red lights and B with nothing
  4. Activating DANs with crimson while showing odour A causes the fly to avoid Odour A while they will go to odour B. (Shows this DAN is a punishment encoding neurons that create avoidance memory when active)
86
Q

How do dopaminergic neurons (DANs) interact with mushroom body output neurons (MBONs) in Drosophila?

A
  1. The reward DANs are lined up with avoidance MBONs
    >So when a fly avoids an odour which has been paired with a an electric shock, it gets rewarded with dopamine
  2. The punishment DANs are lined up with approach MBONs.
    >So when a fly associates an odour with a shock, the approach MBONs are “punished” so the fly no longer approaches that odour as it is associated with a painful shock.
87
Q

Describe how learning occurs in the mushroom body of flies by weakening of synapses?

A

If a shock is paired with an odour, punishment DANs release dopamine on to the Kenyon cell and MBON synapse causing LDP. Next time smelling this odour, the avoid Kenyon cell - MBON synapse is still strong while the approach EPSP is much lower due to LDP. The fly will not approach the odour.

88
Q

What is the effect of putting the unconditioned stimulus before the conditioned stimulus, discuss this using an example of odour and shocks on flies?

A

> Unconditioned stimulus first and then conditioned stimulus after, causes the opposite reaction to if the conditioned stimulus is first.

> E.g. Do shock then odour, the flies learn to approach the odour as the odour predicts a release from pain.

89
Q

What is found in flies if a) odour is before punishment b) punishment is before odour?

A

a) When odour is before punishment they learn to avoid odour

b) When punishment comes before the odori they learn to approach odour.

90
Q

What is the difference in outcome if 1. reward is before odour 2. odour is before reward?

A
  1. If reward (dopamine) is before odour (Kenyon cell activity) the response is much bigger (synaptic potentiation) (as reward and that odour are linked)
  2. If odour and reward are done at the same time (Kenyon cell and dopamine activation at same time) or dopamine is slightly after Kenyon cell activation (reward slightly after odour) causes synaptic depression. (as odour ends the reward)
91
Q

What is a) Conditioned approach b) Conditioned avoidance?

A

a) Conditioned approach= odour then reward

b) Conditioned avoidance= reward then odour (as odori predicts reward is going away)

92
Q

What are the 2 dopamine receptors in drosophila Kenyon cells?

A

In fly Kenyon cells DopR1 and DopR2 are the key dopaminergic receptors (2 different GPCRs which signal through different G-protein pathways)

93
Q

What are the molecular mechanisms of 1) DopR1 2) DopR2 in Drosophila Kenyon cells?

A

1) DopR1
>Gs activates adenylyl cyclase (rutabaga) -> increase cAMP activating Protein kinase A causing LTP (aquesition)

2) DopR2
>Gq activates PLC, which makes IP3, which makes the IP3 receptor release Ca2+ from the endoplasmic reticulum causing LTD (forgetting)

94
Q

What are 2 optical indicators used for testing signalling pathways in the mushroom body of Drosophila?

A
  1. EPAC: sensor for cAMP
  2. ER-GCaMP – measure calcium in the endoplasmic reticulum
95
Q

How are a) EPAC b) ER-GCaMP used to measure dopaminergic receptor activity in the mushroom body of Drosophila?

A

a) EPAC detects if DopR1 pathway is active due to cAMP production

b) ER-GCaMP detects if DopR2 pathway is active due to Ca2+ conc in ER

96
Q

When are a) EPAC b) ER-GCaMP dopaminergic receptors active?

A

a) cAMP is temporally symmetrical
>cAMP response occurs when odour and dopamine are present at the same time no matter the order (forward learning)

b) ER Ca2+ release is temporally asymmetrical
>Only occurs when dopamine comes before Kenyon cell activation by odour (reverse learning)

97
Q

What is the molecular que which detects the order of odour and dopamine (reward)?

A

ER Ca2+ release

98
Q

How does dopamine activate the DopR1 and DopR2 pathways during a) reverse learning (reward then odour/ unconditioned then conditioned) b) forward learning (odour then reward/ conditioned then unconditioned)

A

a) If dopamine comes first (unconditioned first), activates both of them but DopR2 outweighs DopR1 pathway. Reverse learning (synaptic depression) as food (reward) before bell/food (conditioned) leads to DopR2 activation causing LTD (ER Ca2+ release causing Kinase C) and forgetting.

b) If odour comes before reward (conditioned then unconditioned), only DopR1 pathway is active triggering forward learning (synaptic potentiation) as cAMP production activates Kinase A for LTP leading to acquisition of association

a) Forward learning=
>Odour activates DopR1
>Gs -> adenylyl cyclase -> cAMP -> Kinase A -> LDP of wrong MBON
>Fly approaches odour as avoid MBON has been depressed by reward DAN due to fly entering odour (conditioned) to get reward (unconditioned)

b) Reverse learning
>Reward first (unconditioned) leads to dopamine activating DopR2 first.
>Gg -> IP3 -> binds to IP3 before DopR1 cAMP binds -> release of ER Ca2+ -> LTP of the learnt pathway.
>If fly has learnt that going to an odour rewards them (forward learning) the synapse is depressed, so if the reward is now given before the odour (unconditioned then conditioned) then the approach MBON is potentiated by DANs so they don’t approach as it no longer associated with getting a reward.

99
Q

What is a) reverse learning b) forward learning

A

a) Reward then odour

b) Odour then reward

100
Q

Why does the DopR2 pathway (ER Ca2+) not activate if the odour is present before the reward?

A
101
Q

How to tell if Kenyon cell activation by odour is before dopamine release by reward?

A

> Just see if the IP3 came before Ca2+:

  1. If its IP3 then Ca2+ ER calcium channel opens (DopR2 activation) - forgetting
  2. If its Ca2+ then IP3 ER calcium channel doesn’t open (Just DopR1 activation) -aquesition
102
Q

Explain the molecular mechanisms of 1) forward learning b) reverse learning

A

1) Odour then reward (Forward learning)
>If Odour is first, no IP3 will bound (activation of DopR1) to IP3 receptors so Ca2+ will bind to IP3 receptor sooner and lock the receptor in conformation so IP3 cannot bind anymore so ER Ca2+ channels don’t open.
>Kenyon activation before dopamine receptor

2) Reward then odour (Reverse learning)
>If IP3 binds before Ca2+ (activation of DopR2 as well as DopR1), allows IP3 receptor to enter conformation where both IP3 and Ca2+ (arrives later with DopR1 activation) can bind allowing ER Ca2+ channels to open.
>Dopamine receptor activation before Kenyon

103
Q

How do you know if Kenyon cell activation comes before dopamine receptor activation and vice versa?

A

> Kenyon cell activation before would cause just Ca2+ to be present at IP3 receptors so no ER Ca2+ is released. (aquesittion)

> If dopamine receptor activation is before would cause IP3 to bind first and then Ca2+ to IP3 receptor, allows Ca2+ release from ER (forgetting)

104
Q

What is the function of the techniques: a) GAL4/UAS system b) Optogenetics c) Encoded Ca2+ indicator imaging?

A
  1. GAL4/UAS system
    >Express proteins in neurons
  2. Optogenetics
    >Tell us the function of very specific neurons
  3. Imaging neural activity using genetically encoded calcium indicators
    >Used for DopR2 pathway imaging.
105
Q

How does training teach using examples of odour, punishment and reward?

A

> Training reduces the “wrong” behaviour

  1. Odour + punishment = reduces approach
  2. Odour + reward = reduces avoidance
106
Q

What it is the similar structures in the cerebellum compared to in the mushroom body: a) Projection neurons b) Kenyon cells c) Kenyon cell synapse to MBONs modified by dopaminergic neurons d) dopaminergic neurons

A

a) Mossy fibres (like projection neurons) synapse onto lots more granule cells

b) Granule cells (like Kenyon Cells) all converge onto Purkinje cells

c) Synapse between Granule cells and Purkinje cells is modified by climbing fibres (like Kenyon cells synapsing to MBONs modified by dopaminergic neurons)

d) Climbing fibres convey error signal (like dopaminergic neurons)

107
Q

What is a cerebellar-like structure in electric fish like Gnathonemus petersii?

A

Electro-sensory lobe

108
Q

What is the role of electro-sensory lobe in electric fish like Gnathonemus petersii?

A

This circuit allows the fish to learn to ignore electric signals generated by its own electric organ (i.e., “wrong” signals) so they can detect the electrical signal from the prey they want to chase.

109
Q

What are the 3 levels of David Marr’s mode of analysis?

A
  1. Computational problem.
    >What problem are you trying to solve?
  2. Algorithm.
    >What abstract method(s) of processing information could you use to solve this problem?
  3. Physical implementation.
    >How can you implement the algorithm to solve the problem, on actual physical hardware, like a biological brain or electronic computer?
110
Q

In the Drift-diffusion model, how is it proposed that a decision is made?

A

Individuals integrate noisy and sometimes conflicting pieces of information over time until they reach a decision threshold.

111
Q

What is the purpose of the Drift-diffusion model in decision making?

A

Model for understanding how animals integrate noisy sensory information and reach a decision from this.

112
Q

What is a Gaussian distribution?

A

Normal distribution (like a bell shape in the middle of the graph).

113
Q

When is reaction time in a) non-Gaussian distribution b) Gaussian distribution?

A

a) Distribution has skewed right side when reaction time is plotted on the x-axis

b) Distribution is normal (in the middle) when the reciprocal of reaction time (RT/1) is plotted on the x-axis.

114
Q

What is Latency in terms of reaction time?

A

How long it takes to react to motion dots and flick gaze (reaction time)

115
Q

What is the formula for reaction time?

A

t = 1/r

Reaction time (t) = decision bound threshold (A) also written as 1 / rate of evidence accumulation (r )

116
Q

What is the rate of information accumulation dictated by?

A

Efficiency of neurons and how good the evidence is in favour of the decision

117
Q

What does the drift-diffusion model assume?

A

The drift-diffusion model assumes that individuals have a decision-making threshold

118
Q

What is the underlying variable that varies the distribution of a reaction time graph?

A

Rate if evidence accumulation (r in the formula)

119
Q

Do flies in a chamber containing a bad odour and a) a very low concentration of that bad odour b) a slightly lower concentration of that bad odour react quickly or slowly?

A

a) Fly leaves to low conc odour quickly

b) Fly hesitates to leave, takes longer to decide which odour to be in

120
Q

What is the effect of giving a mouse less time to react to information in decision making?

A

The accuracy drops off if the mouse gets less time to accumulate information.

121
Q

How does the drift-diffusion model show why being forced to make a decision early leads to less accurate decision making?

A

Premature decision leads to evidence accumulation traces that would’ve reached
decision threshold to not have reached it, as not enough sensory input evidence has built up to reach the correct decision.

122
Q

Why would the decision threshold (decision bound) be moved?

A

Can move decision threshold dependent on the urgency of the decision

123
Q

What is the effect of lowering the decision threshold?

A

To prioritise speed over accuracy of the decision made.

124
Q

Is it possible to move decision bounds (thresholds) during a task and why?

A

Yes, decision bounds might get lower over the course of decision making as the need to decide becomes more “urgent” (Are willing to accept less confidence in your decision over more time)

125
Q

How is the drift-diffusion model implemented by neurons?

A

Key neurons may either ramp up spike rate or the sub-threshold membrane potential, the greatness of this is effected by the strength of the stimuli (e.g. more noisy evidence causes less ramp up of spike rate).

126
Q

What is the example of evidence accumulators in the monkey visual cortex and how do we know this?

A

lateral intraparietal area (LIP) reaches threshold 90 seconds before generating the saccades (decision made), showing they accumulate evidence to make the decision for eye movement.

127
Q

In fruit flies what is the relevant accumulator instead of spike rate in key neurons like Kenyon cells?

A

The relevant accumulator is not spike rate but is the subthreshold membrane depolarisation of a key neuron.

128
Q

What neuron retains the memory of a specific odour with a reward or punishment?

A

The evidence of whether they’re smelling the same odour or a different odour is accumulated as the membrane potential of the specific Kenyon cell.

129
Q

Why do flies with mutated FoxP transcription factors take longer to make a decision?

A

> As non-functional FoxP leads to less K+ channel downregulation, so neurons like Kenyon cells have excess leaky K+ channels meaning the cell loses excess K+ making the membrane potential more negative.

> It will take longer for evidence stimuli to depolarise the the evidence accumulators before reaching the decision threshold.

130
Q

What 2 aspects of decision making does the drift-diffusion model explain?

A
  1. The frequency distribution of reaction times
    >Plotting reciprocal of reaction time gives off Gaussian distribution
  2. Speed-accuracy trade-off
    >By moving decision threshold up or down

Neural Circuits (5 decks)

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