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Topics in Medical Biosciences > Neuro > Flashcards

Neuro Flashcards

1
Q

Where is memory located?

A

In the hippocampus in the medial temporal lobe

- there are also other memory systems

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2
Q

How do neurotransmissions take place?

A
  • an electric impulse that travels down an axon
  • triggers the release of a neuro-transmitter at the synapse
  • binding of the neurotransmitter to a receptor in the dendritic membrane triggers the opening of ion channels
  • this provokes influx of Na+ ions
  • influx of Na+ ions creates an electric impulse that travels down the axon
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3
Q

What causes the action potential?

A
  • asymmetric distribution of ions in the membrane
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4
Q

What is the membrane potential seen in axons?

A

Higher conc of K+ inside the cell and Na+ outside the cell.

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5
Q

What does the sodium potassium pump do?

A

3 Na+ out and 2K + into the cell (active transport) causing a negative electrical gradient

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6
Q

What is the resting potential inside the axon?

A

-50-60mV

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7
Q

What is saltatory conduction?

A

Where axons are surrounded by myelin, the sodium channels are restricted to the nodes of Ranvier. The ionic currents jump from one node to the next, resulting in a higher conduction velocity (faster)

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8
Q

What synaptic proteins are in the vesicles in the pre-synaptic neurones?

A

Synaptotagmin: Calcium sensor that triggers the release of the neurotransmitter
Synaptobrevin: involved in the fusion of the vesicle to the plasma membrane
Proton Pump: constantly brings protons into the lumen of the vesicle
Vesicular transporters: move transmitters into vesicles

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9
Q

Which 3 proteins form the SNARE complex?

A

Synaptobrevin (vSNARE) binds Syntaxin (tSNARE) and SNAP-25, anchoring and tethering the vesicle to the plasma membrane

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10
Q

What does the SNARE complex do?

A

When the synaptic transmission reaches the axon, the SNARE complex pulls the vesicle apart so that they fuse. When they fuse, the vesicle releases neurotransmitter into cleft.

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11
Q

How do neurotoxins block synaptic transmission?

A

Cleave the SNARE complex so that it cannot fuse the vesicle to the plasma membrane.

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12
Q

What enables the SNARE complex to start the fusion to release the neurotransmitters?

A

Once the synaptic transmission reaches the axon, the voltage gated calcium channels release calcium. The synaptotagmin binds to the calcium which then enables/ signals the SNARE complex to fuse the membranes.

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13
Q

What does the active zone in the presynaptic neurone do?

A

Enables the calcium channels to be in the same place as where the vesicle will be docked. So individual synapses can be regulated locally.

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14
Q

What is the life cycle of a classical neurotransmitter?

A
  1. precursor in neuron
  2. vesicular transport to the pre-synaptic neurone
  3. release and binding to post-synaptic receptors
    - this regenerates action potential in the post synaptic cell
  4. Then cleared away
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15
Q

What are the different ways neurotransmitters can be cleared away from the post-synaptic cell?

A
  1. diffuse away
  2. membrane transporter can re-uptake it back into the pre-synaptic neurone
  3. can be taken into the mitochondria to be destroyed
  4. can be taken up by glial cells
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16
Q

What is the life cycle of a Serotonin?

A
  • Tryptophan in neuron produces Serotonin
  • Serotonin in packaged into vesicles by vesicular mono-amine transporters
  • Serotonin is released and binds to the post-synaptic receptors
  • Serotonin is taken up by SERT (membrane transporter) and goes back into the vesicles or metabolised by MAO in the mitochondria
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17
Q

How is Glutamate cleared away in the post-synaptic neuron?

A

Glia uptakes glutamate and turns it into glutamine. This goes back into the pre-synaptic neuron and is able to be metabolised back into glutamate and used again.

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18
Q

What is facilitation?

A
  • if you have a stimulus the probability of vesicle release will increase if you have a second stimulus happening within a very short time period
19
Q

What is synaptic depression?

A

The probability of a second same vesicular release diminishes over time

20
Q

What is synaptic depression resulting from?

A

vesicle depletion

  • if the vesicle pool inside the pre-synaptic neuron is large, then the probability of multiple vesicle releases are high and no depression seen
  • if vesicle pool is small, the probability of fusion and vesicle release is low, but if it happens, then there will be strong depression and the second stimulus releases half as many quanta / probability of release again is low
21
Q

How are the vesicles replenished in the pre-synaptic neuron?

A

Recycled using endocytosis of plasma membrane in the pre-synaptic neuron.

  • “kiss and run” can occur where the vesicle pulls back in quickly after the release of neurotransmitter
  • vesicle covered in clathrin, so clathrin mediated endocytosis can occur to pinch off parts of the membrane to create a vesicle.
22
Q

What are the two types of neurotransmiter receptors?

A

Ionotropic and Metabotropic

23
Q

What are the characteristics of the different structures of ionotropic receptors?

A

There are 3. One has 5 subunits, one has 4 and one has 3 subunits. Binding different neurotransmitters but they are all channels.

24
Q

What type of glutamate receptors is responsible for action potentials being created?

A

Ionotropic - AMPAR receptors

25
Q

What type of glutamate receptors is responsible for learning and memory?

A

Ionotropic - NMDAR receptors

26
Q

What happens in the NMDAR receptor during resting state?

A

The Arg binds to Mg2+ which blocks the channel, not allowing any cations to flow through.

27
Q

How can the Mg2+ be expelled from the NMDAR receptor?

A
  • by simultaneously having an action potential (depolarisation of the neuron) and glutamate bind to the receptor (coincidence detector)
28
Q

How can the coincidence detector occur?

A

Either there is a lot of inputs from one stimulus, and so the neuron is still depolarised when a glutamate binds, or there are multiple stimuli depolarising the neuron at the same/similar time

29
Q

What is the consequence of opening up the NMDAR receptor?

A
  • up-regulation of AMPAR receptors
  • enhances probability of firing AP in the post-synaptic neuron
  • contribute to long lasting changes
30
Q

What happens once G proteins have been activated through the metabotropic receptors during Learning?

A
  • g proteins will activate adenyl cyclase
  • generate cAMP
  • activates PKA
  • PKA phosphorylates multiple targets inc Ca channels
  • phosphorylation of the Ca channels increases the probability of them opening
  • leads to changes in membrane conductance
31
Q

What is the PLC pathway?

A
  • pathway that metabotropic receptors activate
  • g proteins activate phospholipase C
  • result in production of IP3 and DAG
  • IP3 activates Ca stores in the ER, increasing cytosolic Ca
  • DAG activates PKC, which phosphorylates substrates
  • inc Ca activates CaMKII also phosphorylates substrates (important in learning)
32
Q

How does cAMP and Ca2+ pathways and activation of CREB lead to memory?

A
  • activation of metabotropic receptors activates AC, producing cAMP which activates PKA
  • an increase in Ca2+ levels activates CaMKII, which phosphorylates AMPAR
  • PKA and caMKII phosphorylate CREB which activates gene expression causing long lasting changes at synapses
33
Q

How is PKA activated by cyclic AMP?

A

The normal resting state (inactive kinase) sees the catalytic subunit preventing binding of the auto-inhibitory substrate. The addition of cAMP reduces the affinity of the regulatory subunit to the catalytic subunit, therefore liberating the catalytic subunit as free and active and can phosphorylate

34
Q

What happens to PKA if cAMP levels are low?

A

Dissociation is reversible and so the the catalytic subunit will bind again to the inhibitory region.

35
Q

What happens to PKA if cAMP levels are too high?

A

Regulatory subunits are degraded through proteolysis and the catalytic subunit stays active

36
Q

How does calcium activate CaMKII?

A

auto-phosphorylation upon Ca binding. triggers domino effect until all 12 subunits are phosphorylated. CaMKII is then constitutively active and can increase response to glutamate, excitability and can phosphorylate CREB causing gene expression and protein synthesis.

37
Q

How do you turn CaMKII off?

A

Through phosphates’ - switching pathways off / things that have been phosphorylated.

38
Q

Why is activation of CREB important?

A
  • CREB is a transcription factor
  • causes gene expression and protein synthesis (which long term memory requires)
  • can promote new synapses and repair of neurons
39
Q

What is habituation?

A

Reduction in response to a stimulus that is delivered repeatedly

40
Q

What is sensitisation?

A

Enhancement of a response produced by a presentation of a strong stimulus

41
Q

What is associative learning?

A

Associating two things together
- classical conditioning
- Pavlov’s experiment
conditioned stimulus, unconditioned stimulus, unconditioned response, conditioned response.

42
Q

What is the mechanism of classical conditioning?

A
  1. the unconditioned stimulus will trigger the sensory and motor neuron
    - depolarisation will occur
  2. The conditioned response will also activate the sensory neuron
  3. Release glutamate
  4. As multiple depolarisations are occurring simultaneously to the glutamate binding, the NMDA receptor opens
  5. Activation of the PKA pathway, increasing the probability of neurotransmitter release
  6. increase in AMPAR receptors
    overall increase in sensitisation
43
Q

What are the four consequences of the actions of neurotransmitters?

A
  1. activation of ion channels (AP) lasts milli seconds
  2. activation of G protein coupled receptor
    - lasts minutes
  3. persistent transmitter activation of G protein coupled receptor - persistent synaptic action
  4. transmitter action of local protein synthesis through activation of CREBS and CaMKIII pathway - stabilises new synapses
44
Q

What cells are present in the hippocampus that aid with learning and memory?

A

Place cells and grid cells

- protein synthesis occurring and formation of new synapses that allow us to link place with time.

Topics in Medical Biosciences (12 decks)

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