Graphs of Kainate Receptor Paper II

Question 1

Answer 1

with 2081 (KA antagonist) f is not increased, however it is increased in the presence of AMPA antagonist 2206

2081 gives you a tiny burst b/c it is actually an agonist that induces desensitization

Question 2

Answer 2

KA receptor antagonist diminishes mIPSC f, not AMPA antagonsit

Question 3

Answer 3

Ability of KA to trigger mIPSCs did not correlate with somatic depolarization

Question 4

Answer 4

Ability of KA to trigger mIPSCs did not correlate with somatic depolarization

Question 5

eIPSC

Answer 5

IPSC evoked by extracellular stimulation

Question 6

Answer 6

glycine and GABA blockers each diminished the amplitude of IPSCs generated extracellularly, indicating that both NTs have their role

Question 7

Answer 7

when normalized to peak values, each has distinct decay kinetics

Question 8

Answer 8

shows you have to block both GABA and glycine

Question 9

Answer 9

Shows you frequency is similarly increased under each antagonist, though for some reason less so (6/8 rather than in all experiments) for the GABA blocker

amplitude doesn’t change, indicating that INDIVIDUAL mIPSCs were typically mediated by one or the other. This has previously been attributed to differential spacing of receptors, not release of NTs

Question 10

Answer 10

When we replaced extracellular Na+, KA no longer enhanced mIPSC frequency. Ca++ was still there, so, even if KA is Ca++ permeable, Ca++ can’t do it.

Without extracellular Na+, but with elevated extracellular K+, KA still enhanced mIPSC frequency, indicating its an ionotropic mechanism not absolutely dependent on sodium cations.