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Physiology 2 > Neuro: Neurotransmitters Systems I: Glutamate > Flashcards

Neuro: Neurotransmitters Systems I: Glutamate Flashcards

1
Q

What is a neurotransmitter?

A

Chemical messengers that transmit signals from a neuron to a target cell across a synapse

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2
Q

What are the criteria for a molecule to be considered a neurotransmitter?

A
  • The molecule must be synthesised and stored in the presynaptic neuron.
  • The molecule must be released by the presynaptic axon terminal upon stimulation
  • The molecule must produce a response in the postsynaptic cell
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3
Q

Why must a neurotransmitter be synthesised and stored within the presynaptic neuron?

A

Because synaptic transmission is extremely fast so there must always be a pool of neurotransmitters ready to be released from pre-synaptic neuron

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4
Q

What is it that triggers the release of neurotransmitters from the pre-synaptic axon terminal?

A

An action potential

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5
Q

Briefly describe the different stages of an action potential within a neuron

A
  1. Cell is at rest so only Na+/K+ pump is open pumping 3 Na+ out and 2 K+ into cell
  2. Stimulus causes ligand-gated Na+ channels to open leading to influx of Na+ into cell causing depolarisation
  3. Depolarisation leads to threshold potential being reached leading to activation of voltage-gated Na+ channels
  4. Activation of voltage-gated Na+ channels leads to more Na+ influx leading to apex of action potential being reached
  5. Once apex of action potential reached voltage-gated Na+ channels become inactivated and voltage-gated K+ channels open leading to outflow of K+
  6. Outflow of K+ leads to hyperpolarisation which eventually leads to undershoot - membrane potential reaches below resting potential
  7. At this point voltage-gated K+ channels close and Na+/K+ pump returns membrane potential back to normal
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6
Q

Briefly describe how an action potential causes synaptic transmission

A
  1. Action potential arrives at synaptic terminal and causes ligand-gated Na+ channels to open
  2. This causes depolarisation to occur which activates voltage-gated Ca2+ channels leading to Ca2+ influx
  3. Ca2+ influx causes synaptic vesicle to fuse with pre-synaptic membrane
  4. This causes release of neurotransmitter into synaptic cleft via exocytosis
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7
Q

What neurotransmitter is the major excitatory nuerotransmitter in the CNS?

A

Glutamate

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8
Q

How is glutamate synthesised within the presynaptic nerve terminal?

A
  • Glutamine is converted into glutamate
  • This reaction is catalysed by the enzyme glutaminase
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9
Q

Once glutamate is synthesised within the pre-synaptic neurone how is it stored?

A
  • Glutamate is transported into the synaptic vesicles while H+ ions are transported out of the synaptic vesicles
  • This transport is facilitated by vesicular glutamate transporters (VGLUT)
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10
Q

What are the 2 types of glutamate receptor?

A
  • Ionotropic receptors (ligand-gated ion channels)
  • Metabotropic receptors (G protein-coupled receptors)
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11
Q

What are the different types of glutamate ionotropic receptor and what agonist activates each one of them?

A
  • AMPA receptors (activated by AMPA)
  • NMDA receptors (activated by NMDA)
  • Kainate receptors (activated by kainic acid)
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12
Q

What ion do each of the different glutamte ionotropic receptors cause the influx of?

A
  • Na+
  • NMDA can also cause influx of Ca2+
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13
Q

What ion do each of the different glutamte ionotropic receptors cause the efflux of?

A

K+

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14
Q

What are the 4 different AMPA receptor subunits?

A
  • GluA1
  • GluA2
  • GluA3
  • GluA4
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15
Q

What is the most common configuration of AMPA receptor subunits within an AMPA receptor?

A
  • Form tetramers
  • 2 GluA2 subunits and any combination of the other 3 subunits (GluA1, GluA3 and GluA4)
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16
Q

How many ligand binding sites are on the AMPA recptors and how many need to be occupied for the AMPA receptor to be activated?

A
  • 4 AMPA receptor binding sites
  • At least 2 need to be occupied to cause activation
17
Q

What does the presence of GluA2 subunits within the AMPA receptor mean for the flow of ions through the receptor?

A

Presence of GluA2 subunits mean that AMPA receptors are unable to allow Ca2+ influx

18
Q

What are 3 different NMDA receptor subunits?

A
  • GluN1
  • GluN2
  • GluN3
19
Q

What is the most common configuration of NMDA recptor subunits within the receptor?

A
  • Form tetramers
  • 2 GluN1 subunits and 2GluN2 or GluN3 subunits
20
Q

What does the presence of GluN3 subunits mean for the NMDA receptor?

A

Presence of GluN3 subunits causes NMDA receptor to not function

21
Q

Apart from glutamate what other ligands are capable of binding to the NMDA receptors?

A
  • Glycine
  • D-serine
22
Q

What NMDA subunit do each of the ligands capable of binding to the NMDA receptor bind to?

A
  • Glutamate binds to GluN2 subunit
  • Glycine and D-serine bind to GluN1 subunit
23
Q

What special property does the NMDA receptor that the other 2 glutamate ionotropic recptors don’t have?

A
  • NMDA receptors are voltage-gated as well as ligand-gated
  • This is why NMDA receptors can also cause influx of Ca2+
24
Q

Because NMDA is a voltage-gated channel it, like the rest of the voltage-gated channels, has to be inactivated during resting potential. What ion is able to inactivate the NMDA receptors?

25
Q

What is synaptic plasticity and how does glutamate play a role in this?

A
  • Synaptic plasticity is the ability of a synapse to strengthen or weaken
  • Repeated stimulation of AMPA and NMDA receptors by glutamate will cause the post-synaptic cell to acquire more AMPA receptors over time - this is called receptor trafficking
  • More AMPA receptors means more Na+ influx which eventually leads to activation of enzyme P-CamKII
  • This increases ionic conductance of these receptors to influx Na+ even more
  • This increase in synaptic plasticity over time is called long-term potentiation
26
Q

What are the different receptor subunits of the kainate receptors?

A
  • Gluk1
  • Gluk2
  • Gluk3
  • Gluk4
  • Gluk5
27
Q

What are the most common configurations of the Kainate receptor subunits within the receptor?

A
  • Form tetramers
  • GluK1-3 can form homomers or heteromers.
  • GluK4 & 5 can only form heteromers with GluK1-3 subunits
28
Q

What are the different types of glutamate metabotropic receptor?

A
  • Group 1
  • Group 2
  • Group 3
29
Q

What are some common characteristics of the glutamate metabotropic receptors?

A
  • G protein-coupled receptors
  • Venus fly trap domain for ligand binding
  • 7 transmembrane domain
  • Intracellular C-terminal domain which contains the G-protein
30
Q

What are the 8 sub-types of glutamate metabotropic receptor and what group do each of theses subtypes fall into?

A
  • Group 1: mGlu1 and mGlu5
  • Group 2: mGlu2 and mGlu3
  • Group 3: mGlu4, mGlu6, mGlu7 and mGlu8
31
Q

What are the common configurations of the glutamate metabotropic receptors?

A
  • Form dimers
  • Homodimers
  • Heterodimers (mGlu1 and mGlu5)
  • Can form heterodimers with 5-HT2A receptors (serotonin receptor)
32
Q

What G protein are each of the groups of glutamate metabotropic receptor coupled to?

A
  • Group 1 coupled to Gq
  • Group 2 and 3 coupled to Gi/o
33
Q

What effect do each of the groups of glutamate metabotropic receptors have on glutamate synaptic transmission?

A
  • Group 1 are post-synaptic and have a role in long-term potentiation
  • Group 2 and Group 3 are pre-synaptic and inhibit glutamate release
34
Q

What transporter is responsible for the re-uptake of glutamate?

A

Excitatory amino acid transporter (EAAT)

35
Q

What is excitotoxicity?

A

Pathological process by which excessive excitatory stimulation can lead to neuronal damage and death

36
Q

Explain how dysfunctional vesicular glutamate transporters (VGLUTs) can result in glutamate-mediated excitotoxicity

A
  • Dysfunctional VGLUTs mean that glutamate isn’t stored in pre-synaptic vesicles and just stays within cytosol of pre-synaptic neurone
  • High glutamate concentrations within pre-synaptic neurone causes excitatory amino acid transporters (EAATs) to reverse function and release glutamate into synaptic cleft
  • This causes activation of the AMPA receptors on post-synaptic neurone which will lead to influx of Na+ and depolarisation
  • Depolarisation causes activation of NMDA receptors leading to Na+/Ca2+ influx
  • High levels of Ca2+ leads to excitotoxicity
37
Q

What can excessive Ca2+ levels lead to?

A
  • Mitochondrial damage
  • Oxidative stress
  • Apoptosis - leads to cell death
38
Q

What conditions are linked with glutamate-mediated excitotoxicity?

A
  • Alzheimer’s disease
  • Stroke
  • Autism
39
Q

Name a drug that can be used to reduce glutamate-mediated excitotoxcity and explain how it does this

A
  • Memantine - low-affinity NMDA receptor antagonist
  • Blocks NMDA receptor which prevents excessive Ca2+ influx into post-synaptic neurone

Physiology 2 (29 decks)

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