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Molecular and Cellular Neuroscience > NO Signalling In The CNS > Flashcards

NO Signalling In The CNS Flashcards

1
Q

What are the different types of nitric oxide synthase (3 genes)

A

eNOS - endothelial involved in vascular tone
nNOS - within neurons
iNOS - involved in inflammation induced by cytokines

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2
Q

Characteristics of nNOS

A

Associated with NMDAR
needs calcium/ calmodulin to activate
Involved in synaptic plasticity

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3
Q

What NOS are regulated by calcium calmodulin

A

eNOS And nNOS

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4
Q

Characteristics of iNOS

A

Membrane bound
Make up to 1000 items more NO than eNOS
Involved in inflammation

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5
Q

What happens to LTP when you KO nNOS

A

It is attenuated

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6
Q

Different domains of nNOS

A

N terminal to C terminus

Oxygenase domain (contains arg, heme and BH4)
Reductase domain ( contains FAD and NADPH)

May/ may not have PDZ domain

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7
Q

What are the splice variants of nNOS and how do they differ?

A

Alpha, beta, gamma and mew

Have various domains due to varying length
E.g. Only alpha has a PDZ domain (located on N terminus)
Gamma is probably inactive due to partial oxygen domain

Have different subcellular locations as a result alpha at membrane
Beta cytoplasmic

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8
Q

Is NOS a monomer, dimer or trimmer

A

It is a HOMOdimer

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9
Q

Why is calcium calmodulin important?

A

It completes the electron transport chain from the reductase domain to the oxygenase domain also increase the rate of ETC

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10
Q

Equation for NO synthesis

A

Arginine + O2 -> citrulline + NO

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11
Q

Functions of NO

A

Stimulates guanylyl cyclise (soluble)
Nitrosylation of proteins
Free radical formation

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12
Q

Soluble guanylyl cyclase contains a heme group…why?

A

Allows NO to bind to regulatory domain

This causes conformational change which activates the catalytic domain to make cGMP (100-200 fold increase in activity)

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13
Q

What can block the function of nNOS?

A

L-NAME (competitive antagonist of arginine)

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14
Q

Name a NO donor which can be used experimentally to mimic the function of NO.

A 
Sodium nitroprusside (SNP)
Broken down in cells to release NO
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15
Q

What inhibits sGC?

A

ODQ

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16
Q

What stimulates sGC?

A

Bay 41-2272

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17
Q

Addition of heme experimentally does what to NO?

A

Decreases it as it will chelate the NO

18
Q

How can we increase the levels of cGMP?

A

Stimulate production via Bay 41-2272 OR

decrease degradation via inhibition of phosphodiesterase (sildenafil will inhibit PDE5)

19
Q

List the characteristics of a conventional neurotransmitter

A

Manufactured in cell
Packed as stored in vesicle
Releases of calcium dependant
Acts on receptors on post synaptic memebrane
Exocytosis
Inactivated by reuptake or enzyme activity

20
Q

Why is NO an unconventional NT?

A

Not packed into vesicles
Cannot be stored
Non released by exocytosis
Although calcium needed for synthesis has nothing to do with release
No specific inactivation system
Very short half life
Receptor is a soluble protein is cytoplasm

21
Q

What does the term ‘volume transmitter’ mean?

A

Can act as a neurotransmitter in a volume of tissue and not isolated to the post synaptic neuron

22
Q

As a volume transmitter what can NO do?

A

Retrogradely influence pre synaptic cell (pre synaptic LTP)
Act in neighbouring cells not within its the connectome
Cell trafficking
Gene expression
Nitosylation
Integrate neuronal activity over a limited diffusion space

23
Q

Is nNOS present in the auditory brainstem?

A

Yes (immunohistochemicak studies say so)

24
Q

What does a synaptic stimulus protocol of the calyx of held do to k+ Kv3 currents on the medial nucleus of the trapezoid body?

A

It decreases it

As Kv3 is HVA this only occurs at high mV’s

25
Q

What is the synaptic stimulus protocol

A

60s at 100HZ (50% duty cycle)

Approx 3000 stims per min

26
Q

What happens in an neurone following SSP of a unconnected neurone?

A

There is a similar decrease in Kv3 activity

Presumably there is a diffusable NT which modulates this unconnected neurone

27
Q

In the connected model of the calyx and MNTB what is the effect of SSP in the presence of 1400w?

A

No decrease in Kv3 mediated currents as 1400w inhibits nNOS therefore no NO

28
Q

What is the effect of adding DEA to an unconnected neurone?

A

A similar decrease in kv3 current is seen similar to that of an unconnected neurone following an SSP.
Since DEA is a NO donor SSP must have the effect of increasing NO in the unconnected cell

29
Q

Name a Kv3 blocker

A

Tetraethylammonium (TEA)

30
Q

What happens to Kv3 current on addition of TEA compared to addition of NO donor SNP?
Why is this important?

A

They both show a similar decrease in current.

As TEA at low concentrations is selective for Kv3 it shows that the NO is acting to block Kv3 channels

31
Q

What does 10Hz synaptic stimulation do over 1 hour?

A

Increases Kv current

32
Q

What happens to Kv current within 20 minutes of NO donor exposure

A

Kv3 current will decrease

33
Q

What will happen to Kv2 current after NO donor exposure of 1 hour

A

Kv2 current will increase k+ current to above control (similar pattern to synaptic stimulation for 1 hour)

34
Q

Is TEA is applied at 1 hour following NO donor stimulation what will have to the voltage current relationship

A

It will stay the same as current mediated by Kv2 which is not blocked by TEA
Is inhibited by r-stromatoxin-1 which blocks Kv2 channels

35
Q

Which kinase phosphorylation Kv3 channels

A

PKC

36
Q

What does Kv3 phosphorylation do to channel conductance?

A

Decreases conductance

Therefore blocking PKC will increase Kv3 current

37
Q

Over a period of time what happens to Kv currents

A

Kv3 decreases and Kv2 increases

38
Q

What happens to Kv3 phosphorylation over prolonged period of inactivation?

A

Becomes more phosphorylated and therefore decrease in activity

39
Q

What happens to phosphorylation of Kv2 over prolonged activation?

A

It increases
This causes and increase in activity
Increase in NO over long period = increase in PKG = phosphorylation of Kv2 = increased activity

40
Q

What is the advantage of Kv2 over Kv3?

A

Kv2 is able to fire at a sustained high frequency for a long period of time, Kv3 is not.
Therefore Kv2 takes over for k+ current for prolonged synaptic activity

41
Q

How does the switching of Kv3 to Kv2 related to hearing?

A

Hypothesis: moderate activity Kv3 = predominant as it is dephosphorylated

For prolonged periods of time (high frequency) NO activity is greater than phosphatase activity therefore phosphorylation predominates and Kv3 and Kv2 is phosphorylated which activates Kv2 and inhibits Kv3

Molecular and Cellular Neuroscience (11 decks)

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