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Brain And Behaviour > Cerebellar LTD > Flashcards

Cerebellar LTD Flashcards

1
Q

What does LTD in the cerebellum allow for?

A

Co ordinated motor learning

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2
Q

What does LTD provide a mechanism for?

A

In appropriate motor signals, relayed to the cerebellum via parallel fibres are selectivity weakened through their close temporal association with climbing fibres

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3
Q

What does climbing fibre activation of PC at the same time as PF allow for?

A

It essentially ‘confirms’ that the input to the PC from the PF is inappropriate for execution of that motor sequence. This wil weaken the PF->PC connection and means on subsequent execution of the same motor plan that PC will not fire. Only the correct PC cells which alllow correct movement will fire.

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4
Q

What cells induce the complex spike?

A

Climbing fibres

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5
Q

What cells induce the simple spike?

A

Parallel fibres

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6
Q

The simple spike consists of current from two receptors. What are they?

A

AMPAR mediates current followed by mGluR mediate current

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7
Q

Layers of cerebellar cortex?

A

Molecular layer
Purkinje cell layer
Granule cell layer
White matter

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8
Q

Where do climbing fibres orginate and terminate?

A

The inferior olive and terminates on PC. 1 PC will receive inputs from only 1 CF. but 1 CF can terminate on multiple PC

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9
Q

What do cells from the inferior olive convey?

A

Error signals from sensory feedback of movement so fire when an unexpected even occurs. Propioceptive inputs and inputs from cerebral cortex

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10
Q

Where do mossy fibres come from?

A

Motor cortex and sensory afferents and contain the the information on the context of movement

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11
Q

Mossy fibres synapse onto…?

A

Granule cells

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12
Q

What do granule cells go?

A

Send axon into molecule layer and they bifurcate to form the parallel fibres. PF synapse on thousands of purkinje cells

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13
Q

What else does the mossy fibres and the CF synapse on?

A

The deep cerebellar nuclei (fastigial, dentate, interposed) provide positive inputs

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14
Q

What is the output to of PC’s?

A

Negative to deep cerebellar nuclei

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15
Q

What happens to the deep cerebellar nuclei on movement?

A 
Initial excitation (CF+MF)
Followed by inhibition (PC)
PC cell inhibition will not occur for long due to Pf autoinhibition via Golgi cells. Therefore, deep nuclei will be inhibited again. Pattern of excitation-inhibition-excitation produces a coded message which allows movement execution.
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16
Q

How does LTD modulate deep cerebellar nuclei output?

A

If PF->PC synapses is depressed due to LTD this cell will produce a decreased rate of firing thus reduced deep nuclei inhibition on subsequent movement. Thus input to deep nuclei will vary following synaptic modulation producing a move co-ordinate movement

17
Q

If the executed movement completely matched the motor plan what would happen to CF firing?

A

It would decrease

18
Q

Who proposed a theory on how the cerebellum worked?

A

David Marr - the purpose of the cerebellum is to learn motor skills

19
Q

How was David Marr wrong?

A

He thought learning occurred through potentiation of synapses not LTD

20
Q

What differences are observed in the complex and simple spikes following 1Hz stimulation of CF and PF for 5 minutes

A

Initially both produce their respective spikes.
After traine of stimulus = no change in CF mediated PC EPSP
EPSP in PC from PF shows a depression

21
Q

What receptors are responsible for the PF->PC simple spike

A

AMPAR (mainly GluR2+3)
mGluR. mGluR activation depends on the external of PF firing activity and glutamate release as mGluR’s are located on the periphery of the synapse. This is way later but of simple spike mGluR mediated

22
Q

What receptors are important for complex spike firing?

A

Complex spike is forms from large EPSP superimposed with large Ca2= current.
AMPA receptors and p/q type VGCC are present

23
Q

What does PF activation of mGluRs in PC cause?

A

Localised calcium spike

24
Q

Characteristics of PF firing?

A

Graded responce (more fire the larger to PC EPSP)
Fast transmission mediated by AMPA
Tetanic PF simulation actives mGluR

25
Q

What does CF activation of PC cause interms of calcium?

A

Global rise in calcium

26
Q

What are the characteristics of PC LTD?

A

Separate PF and CF activation is not suffocating to cause depression
Temporal association of both is needed and must occur within certain time frame (associative).
PF before CF causes an increase in localised calcium levels, when the CF then fires there will be an area of substantial calcium rise which is relatively localised to the area the pf stimulated

27
Q

How does the combined effect of increase in calcium from PF and CF activation of the same PC allow for learning?

A

It causes an association between the two which is relatively input specific (substantial rise in calcium localised to area the PF stimulated)

28
Q

What molecules are important in LTD

A

PKC
Protein tyrosine kinases (PTK)
Phospholipase A2 (PLA2)
Inositol 1,4,5 trisphosphate

29
Q

What causes eh substantial rise in calcium on combined CF and PF activity on PC?

A

Ip3 signalling from mGluR (PF) and rise from VGCC (CF) causing CICR

30
Q

In terms of molecular signalling how does LTD occur?

A

High PF activity will cause mGluR activation which signals via Gq > PLC > Ip3 and acts on Ip3 receptors on ER to release intracellular calcium stores. Simultaneously Ca2+ from VGCC from PC activation from CF cause CICR. Ca2+ activates PKC which phosphorylates AMPA and leads to internalisation and desentisation of receptor a PF-PC synapse

31
Q

What else may activate PKC other than Ca2+

A 
Diacylglycerol (DAG) from PLC
Arachodonic acid (mGluRs may activate phospholipase A2 signalling which forms AA) which leads to PKC activation
32
Q

Why might phosphorylation cause internalisation?

A

PKC is known to phosphorylate GluA2 at serine 880 (the S of the SVKI aminoacid sequence). This promotes binding from glutamate receptor interacting protein (GRIP) to protein interacting with c kinase 1 (PICK1) which causes receptor internalisation. Could be occurring here?

33
Q

What other molecule may play a role in LTD?

A

Nitric Oxide

34
Q

What is he evidence which supports the role of NO in LTD?

A

NOS/ sGC / PKG inhibitors can attenuate LTD is some but not all cases

35
Q

In terms of molecular pathways why does NO allow for LTD?

A

NO released from PF binds and activates sGC in PF (100-200 fold increase in activity). Forms cGMP which:

  1. Activates PKG which activates G substrate and inhibits protein phosphatase (thus AMPA is not dephosphorylated)
  2. Increases cycle ADP ribose which acts of ryanodine receptors to increase Ca2+ release. ca2+ actives PKC which phosphorylates AMPA

Both mechanism promote the phosphorylated state of AMPA

36
Q

NO is a voluble transmitter what does this mean for LTD?

A

NO may act on neighbouring spines to cause LTD here thus may = lack of input specificity

37
Q

What may be the function of NO acting at neighbouring synapses?

A

May be a safety mechanism that reinforces a desired effect by encoding information to spare synapses. OR If a group of PC have undergone LTP and one cell becomes depressed the volume transmitting effect of NO will cause LTD on may spines within the depressed cell. This will therefore decrease the firing output of this neurone to a great degree. Since surround PC are still potentiated this spread of LTD in this one cell will enhance the output contrast

Brain And Behaviour (12 decks)

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