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ICB - Neurobiology > Neurobiology 4 > Flashcards

Neurobiology 4 Flashcards

1
Q

Describe Loewi’s experiment that demonstrated chemical transmission.

A

The vagus nerve of an isolated frog’s heart was stimulated, the heart rate decreased.
If the fluid from this vagus nerve was transferred to another heart, its heart rate also decreased.

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2
Q

Which neurotransmitter did Loewi discover? (unknowingly - referred to as vagus substance originally)

A

Acetylcholine.

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3
Q

Name an electrical synapse.

A

A gap junction.

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4
Q

Give an example of a tissue that uses gap junctions.

A

Used by cells in the brain - hippocampal interneurons.

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5
Q

What is the disadvantages of gap junctions?

A

Bidirectional - cannot control the direction of ion flow - this can result in them diffusing away (decay of signal).
No regeneration of signal (but much faster).

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6
Q

Describe the proteins involved in gap junctions.

A

Connexons - form a hexameric complex to give a channel - the pores of the proteins connect.

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7
Q

What are the 3 main advantages of chemical transmission over gap junctions?

A

Slower, unidirectional transmission.
Integrative – can sum different responses from different neurons.
Amplifies and regenerates the signal.

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8
Q

Name the 5 steps of of chemical neurotransmission.

A
  1. Synthesis of the neurotransmitter in the presynaptic neuron
  2. Storage of the neurotransmitter and/or its precursor in the presynaptic nerve terminal in vesicles
  3. Release of the neurotransmitter into the synaptic cleft
  4. Binding and recognition of the neurotransmitter by target receptors
  5. Termination of the action of the released transmitter
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9
Q

What puts the neurotransmitters into vesicles?

A

A vesicular transporter that utilises ATP.

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10
Q

How many neurotransmitters can be stored in 1 vesicle?

A

Over 1000

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11
Q

What causes the vesicles to fuse with membrane?

A

Depolarisation causes Ca2+ influx which causes them to fuse and be released.

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12
Q

What are the two types of receptor NTs can bind to on the post synaptic cleft?

A

Ionotropic or mechanotropic receptors.

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13
Q

How is the signal terminated?

A

Glial cells in the CNS are astrocytes, these can take up neurotransmitter from the synaptic cleft and recycle it back to the neurons.
Or the NTs are degraded by an enzyme (Ach).

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14
Q

What are 3 things that can occur downstream of NT binding on post synaptic cleft?

A

Opening of ion channels.
The release of second messengers that modulates ion channels.
Activation of GTP-binding proteins coupled to ion channels.

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15
Q

What is the size of the synaptic cleft (typically)?

A

20nm

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16
Q

How long does synaptic transmission take?

A

~1ms

17
Q

What is the delay between Ca2+ influx and postsynaptic response?

A

~200us

18
Q

Where are vesicles generated and how are they transported to the synapse?

A

In the golgi and are transported along the axon by specialised kinesin motor proteins.

19
Q

Briefly describe how Katz proved NTs were stored in vesicles? (Quanta)

A

Isolated nerve cells and measured depolarisation of cell each time it was stimulated - found it occurred in packets of 0.4V (multiples of 0.4).

20
Q

How is a vesicle recycled if it fuses completely with the synaptic membrane?

A

Using clathrin-dependent exocytosis.

21
Q

What does ‘kiss and run’ recycling result in?

A

Formation of a fusion pore - this means that the whole vesicle doesn’t melt into the membrane but instead pulls back off as an intact vesicle.

22
Q

Why is there heavy dependence of local production of vesicles at synapse?

A

Vesicle production in the Golgi and transportation along the axon is too slow - only acts as a housekeeping control.

23
Q

Describe the function of synapsin.

A

Reversibly binds to vesicles - involved in keeping vesicles tethered in the reserve pool by binding them to each other and actin cytoskeleton.

24
Q

How is synapsin removed from vesicles to allow mobilisation?

A

Synapsin is phosphorylated by Ca2+/calmodulin dependent kinase.

25
Q

How do synaptic vesicles fuse with the presynaptic membrane?

A

SNARE proteins were shown to be necessary for vesicle fusion.

26
Q

What cells was SNARE interaction first discovered in?

A

Yeast cells.

27
Q

Where is syntaxin (SNARE) found?

A

Associated with the presynaptic membrane.

28
Q

Where is synaptobrevin found?

A

Associated with the vesicular membrane.

29
Q

What is the function of SNAP24?

A

Forms a 4 bundle helix with syntaxin and synaptobrevin to bring the vesicle into position.

30
Q

Describe the primed vesicle.

A

Once the 4 bundle helix has formed and the vesicle is ready to be released.

31
Q

Why is the primed vesicle formation an important process?

A

This allows for quicker release once the calcium has entered the presynaptic terminal.

32
Q

What is the function of Synaptotagmin ?

A

Binds calcium ions in a series of low affinity calcium binding sites - causing allosteric shape change, which causes the helix bundle to bring the vesicle closer to the membrane to allow fusion.

33
Q

Describe the function of complexin.

A

Protein bound to the 4-helix bundle, in the primed vesicle, possibly clamping the bundle together.

34
Q

What is the suggested combined function of synaptotoagmin and Complexin?

A

Suggested that synaptotagmin then causes a conformational change in complexin which causes it to dissociate, allowing the vesicle to be pulled towards the membrane.

35
Q

Is ATP required to assemble the complexes formed during the fusion process?

A

Yes - a high level.

36
Q

How were SNARE proteins studied?

A

Using toxins, mostly from bacteria, that cleave the SNARE proteins and kill the host

37
Q

Give an example of a toxin used to study SNAREs?

A

Botox

ICB - Neurobiology (8 decks)

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