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Molecular Pharmacology > iGluR 1 > Flashcards

iGluR 1 Flashcards

1
Q

What is the structure of iGluRs?

A

ATD (No effect if deleted)
LBD
TMD
CTD

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2
Q

What iGluRs is glutamate an agonist for?

A

AMPAR
KAR
GluN1

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3
Q

What iGluRs is glycine/D-serine an agonist for?

A

GluN1

GluN3

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4
Q

How can we determine the structure of iGluRs using X-ray crystallography?

A
  1. Sample crystalized
  2. Make an electron density map
  3. Make an atomic crystal structure model
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5
Q

What are the pros and cons of X-ray crystallography?

A

:) High resolution

:( Uses crystals

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6
Q

How can we determine the structure of iGluRs using cryo-electron microscopy?

A
  1. Sample is frozen in an electron microscope

2. Make 2D pics > 3D map > 3D model

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7
Q

What are the pros and cons of cryo-electron microscopy?

A

:) Can use single particles

:( Difficult to get high resolution

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8
Q

How did we work out that iGluRs are tetramers?

A
  1. Electrophoresis and sedimentation used to separate proteins from neurons
  2. Western blot analysis used to show AMPAR formed tetramers
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9
Q

What are the subunits in AMPAR, KAR and NMDAR tetramers?

A

AMPAR: GluA2 assembles with 1, 3 and 4
KAR: GluK 4 and 5 assembles with 1, 2 and 3
NAMDAR: 2 GluN1 with 2 GluN2 or with GluN2,3

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10
Q

What did they discover in 1950 and 1970 with regards to glutamate?

A

1950: injected into brain = convulsion
1970: injected into brain = depolarisations (thought they were ion channel)

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11
Q

What did they discover in 1970 and 1980 with regards to glycine?

A

1970: NMDAR + conditioned medium = depolarisation
1980: realised it was glycine

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12
Q

How did they discover that NMDA and glycine are co-agonists and when?

A

1988:
1. Extracted RNA from rat brains
2. Injected into frog oocytes
3. express for few days
4. measure electrophysiology of cells with NMDA and Gycine = large depol

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13
Q

What did they find in 1979 and how?

A
  1. Rat brain slices isolated and synaptic membranes washed
  2. Add kainate and glutamate serum = little radioactivity because they compete for same site
  3. Add kainate alone = lots of activity
  4. Add kainate and NMDA = lots of activity because they have different sites
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14
Q

What blocks NMDAR and when did they find this?

A
  • Magnesium

- 1980

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15
Q

Describe ion permeability in iGluRs

A
  • AMPAR: Na, K, Ca (least)
  • KAR: Na, K, Ca
  • NMDAR: Na, K, Ca (most)
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16
Q

Describe an experiment to test antagonists of non-NMDAR

A
  1. Stimulate synapses = depolarisation
  2. CNQX + YDDG antagonists given = no depolarisation.
  3. AP5 = depolarisation

Conclusions: CNQX and YDDG are non-NMDAR antagonists whilst AP5 isn’t

17
Q

Describe an experiment to test antagonists of NMDAR

A
  1. NMDAR given tetanus = high depol (LTP)
    BUT
  2. When AP5 is given followed by tetanus = normal levels of depolarisation

Therefore, AP5 must be a selective inhibitor of NMDAR not non NMDARs.

18
Q

How can we stop seizures (give an example)?

A
  • Block glutamate receptors

e. g. block AMPAR with CNQX

19
Q

Where are different AMARs found in the brain?

A 
GluA1 = not in entorhinal cortex 
GluA3 = in hypothalamus and amygdala 
GluA4 = olfactory bulb/cerebellum/auditory pathway
20
Q

What type of neurons are permeable/impermeable to Ca?

A

Interneurons - permeable

Principle neurons - impermeable

21
Q

Where in the brain are different NMDARs found?

A
  • GluNB (embryonic) and GluN2A (adulthood) in the hippocampus
  • GluN2C (adult) and GluN2B (embryonic) in cerebellum
22
Q

What is the iGluR channel conductance equation?

A

G = i/V

G = conductance (ability of channel to pass current) 
I = current 
V = voltage

NMDAR has higher conductance current vs AMPAR

23
Q

Describe microscopic currents

A
  • Caused by rapid transitioning of opening/closing channels
  • Detected using patch clamp technque
  • Difficult to record tho cos its so small
24
Q

Describe macroscopic currents

A
  • Caused by activation/deaction (when agonist binds/comes off = conform change)
  • Desensitisation = when agonist binds to closed channel but it is still stable
  • Resensitisation = channel stays shut but becomes unstable so agonist comes off
25
Q

DIDN’T INCLUDE:

A
  • CLONING

- MEASURING GENE EXPRESSION IN NEURONS

Molecular Pharmacology (5 decks)

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