How does the topology and amino acid sequence vary between NMDAR and AMPA/Kainate receptors?

Where is the Q/R site and what does it determine?

What is the structure of the AMPA receptors? What are the constitutional subunits?

What is the endogenous agonist which binds to AMPAR and Kainate receptors?

What are the subunits which make up a kainate receptor? Which subunits can not form a functional receptor if they are the sole subunit?

What shape is the Amino terminal domain in an GluA2 tetramer? And the LBD?

What is the structure of the transmembrane domain similar to?

What type of synaptic transmission do AMPA receptors mediate?

Which ions pass through an AMPA receptor?

Why do GluA2 receptors have relatively low Ca2+ permeability?

What percentage of GluA2 receptors are edited to express the arginine (R) residue?

What are the molecules on the Q/R site? What effect do they have?

What type of current is seen in a GluA2Q/GluK2Q (neutral glutamine at Q/R site). What happens at positive membrane potentials up to 80mV?

What is the current like through GluA2R or GluK2R (R edited +charge at Q/R site)?
Why?

Name three endogenous AMPA agonists - which is the partial?

What is NBQX?

What does AMPA cause at at AMPARs?

What is perampanel?

What type of drug is Cyclothiazide? What does it do?

What are the differences in terms of current/desensitisation induced by Kainate and 5-fluorowillardine (or AMPA)?

Explain the structure of the ligand binding zone (S1S2) in terms of dimers.

Through which part of the dimer that makes up S1 and S2 is the majority of the dimer assembled?

What happens when glutamate binds in between D1 and D2?

How does desensitisation occur regarding the dimer?

Which is more potent: LY404187 or cyclothiazedine?

How do positive allosteric modulators (AMPAKINES) enhance the effect of agonists?

Where do ampakines bind? What effect does this have?

What affect do ampakines have on NMDARs?

What other effect does increased current through AMPARs have?

What are the potential therapeutic uses of ampakines? What is this based on?

Where is it thought that NAMs bind to AMPARs? How do they work?

What is a therapeutic use of perampanel?

Where are Kainate receptors expresses? (3)
(GluK1?)

What type of transmission are kainate receptors involved in in the hippocampus?

What ions are kainate receptors permeable to and what does this depend on?

Where are kainate receptors located in the hippocampus?

What does activation of the kainate receptors in the CA3 mossy fibres lead to? (2)

What effect does kainate have at kainate receptors?

What is Domoate? What effect does it have at AMPAR?

What are CNQX and ACET? How do they differ in terms of selectivity?

Where can Kainate be extracted from and what can it be used for?

What does lectin concanavalin A (con A) do? What is it?

How has it been shown in CA3 mossy fibres that KAR are responsible for LTP?

How might the KAR (Gluk1) be involved in glut release and why is this a positive feedback loop?

What might the Ca2+ induced release of glutamate via KAR underly?

What are the 3 potential therapeutic uses of Kainate receptor antagonists?

How might KAR antagonists work to prevent epilepsy?

How might KAR antagonists work in neuropathic pain?

How might KAR antagonists work to treat migraines?

What is sumatriptan? What does it treat?