Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Molecular and Cellular Neuroscience > Glutamate Receptors > Flashcards

Glutamate Receptors Flashcards

1
Q

NMDA stands for?

A

N-methyl-D-aspartate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name the 3 ionotropic glutamate receptors and what ions they are selective for

A

nmda (Na, K, Ca)
Ampa (Na, K, only those without GluR2 subunit allow Ca)
Kainate (Na, K)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

AMPA agonists include

A

AMPA

GLUTAMATE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

AMPA antagonist include

A

NBQX (competitive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NMDAR agonists include

A

NMDA
Glutamate
Glycine (cofactor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NMDA antagonists include

A

AP5 (competitive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How many subunits exist for AMPARs?

A

4 (GluR1-4)
Sometimes go by GluA
Splice variants exist which can mean they are either in a flip or flop variant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How many NMDAR subunits are there?

A

GluN1

GluN2 (A-D)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What NMDAR subunit dictates its properties?

A

Mainly GluN2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How many subunits come together to form an NMDAR?

A

4 - tetremer
2xGluN1 (bind glycine)
2xGluN2 (bind glutamate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Draw a AMPA/NMDAR subunit structure

A 
Extracellular N terminus
S1
TM1
TM2 (pore loop)
TM3
S2
TM4 
Intracellular C terminus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 3 domains of a ionotropic glutamate receptor subunit?

A

Amino N terminal domain
Ligand binding domain
Intracellular C terminal domain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of the N amino terminal domain?

A

Contributes to receptor assembly (not NMDAR)

NMDAR it is important for receptor modulation and desentisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the function of the ligand binding domain?

A

Formed by end of the N terminal domain and extracellular loop between TM3 and 4

Acts as a clamp shell to enclose ligand when bound
Full agonist cause clamp shell to close by 20 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

At -40mV what mediates glutamatergic currents? At what rate does it occur?

A

Fast outward inward current due to AMPARs.

At -40mV extracellular Mg2+ blocks the NMDAR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

At +40mV what channels mediate glutamatergic currents? Which direction is current?

A

Fast initial AMPAR
Slow NMDAR component (extracellular Mg2+ block is removed when depolarised)
Current is outwards as equilibrium potential is 0mV for both channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some unique features of NMDARs as compared to AMPARS.

A

Calcium permeability
Need coagonist to open
Voltage dependant
Blocked by phencyclidine- gives hallucinations

18
Q

Who proposed that AMPARS are tetramers?

A

Rosenmund et al 1998

19
Q

How did rosenmund et al discover AMPARs were tetramers?

A

Fast perfusion exchange from NBQX to ampa agonist
Observed how conductance increased in a stepwise manner

Closed - closed - small open - medium - large
Each step represented the dissociatation of antagonist and binding of agonist

20
Q

Why were there only 3 steps in Rosenmund et al (1998) study yet they concluded AMPA was a tetramer?

A

Transition time from closed to small opening different than from small to medium and medium to large

C -> S = two component wait time on graph
S->M and M->L = only one exponential transition time graph

21
Q

Why are AMPARS described at dimers or dimers?

A

2 GluA subunits must first interact at the level of the N terminal domain to then be able to interact with another dimer at the level of the S2 tranmemembrane domain to form tetramers

22
Q

What is the evidence of the existence of the ligand binding domain?

A

What is left from the Cleavage of the linker molecules which bind s1/s2 to the rest of the protein is still able to bind glutamate with high affinity

23
Q

How many glutamate are needed for full AMPA opening?

A

4 - each bind to 1 GluA subunit

24
Q

In NMDARs which subunit bind glutamate and which binds glycine?

A

GluN1 binds glycine (2 glycine cofactors needed)

GluN2 binds glutamate

25
Q

What can’t glutamate bind to GluN1?

A

It is prevented by hydrophobic environment by valine and tryptophan which favour glycine

26
Q

What is the difference between deactivation and desensitisation?

A

Both cause channel closure

Deactivation requires the ligand to be removed I.e. Clearance of neurotransmitter via uptake or enzymes

Desensitisation occurs when the ligand is still bound

27
Q

How does glutamate open ionotropic glutamate channels?

A

Conformational change which open pore via subunits being pulled apart

28
Q

How does desensitisation occur?

A

Desensitised state has a higher affinity for glutamate

Interdomain conformational change close channel pore as subunits are pulled together

29
Q

Where does alternative splicing occur in the GluA subunit?

A

Within the S2 region

30
Q

What states does alternative splicing cause?

A

A flip or flop state

Which changes sensitisation rate

31
Q

Which splice variant causes quick desensitisation?

A

FLOP

32
Q

Which splice variant causes a slow desensitisation?

A

FLIP

33
Q

NMDAR receptor kinetics is a result of….

A

Activation
Deactivation
Modulated by GluN2 subunit

34
Q

Work by what scientist discovered why some AMPARs are permeable to calcium?

A

Burnashev et al 1992

35
Q

what amino acid is encoded for in the gene of GluA2?

A

Glutamine (Q)

36
Q

mRNA modification changes this glutamine to what amino acid? Why is this important?

A

Arginine, which is positively charged

Therefore, since this change occurs in the pore loop region GluA2 subunits do not allow calcium influx

37
Q

Why are most AMPARs impermeable to calcium?

A

Most contain a GluA2 subunit

Not in the hippocampus and auditory neurons

38
Q

With NMDARs which aminoacid (at the same respective region to the Glua2 subunit) allows calcium permeability?

A

Asparagine which allows 3-4 times more calcium influx than calcium permeable AMPARS

39
Q

Where does CaMKII phosphorylate glutamate receptors? What does this achieve?

A

GluA1 subunit
Intracellular domain
S831
Increases AMPAR current

40
Q

Where does PKA phosphorylate glutamate receptors? What does this achieve?

A

GluA1 subunit
S845
Increases ampa current
Dephosphorylation here causes LTD via internalisation

41
Q

Where does PKC phosphorylate glutamate channels?

Why is this important?

A

GluA2 subunit
Serine 880
Promotes PICK1 binding over GRIP binding

Molecular and Cellular Neuroscience (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions