KA Paper 2

Question 1

Answer 1

We found that KA-triggered GABA/glycine release, but not spontaneous quantal release, was sensitive to changes in extracellular Ca++.

Question 2

Answer 2

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.

Question 3

Answer 3

Various blockers of voltage-gated Ca++ channels are tested. The L-type antagonist did not cause a significant difference from control, but this is expected because L-type channels are not prevalent at terminals.

Question 4

Answer 4

Various blockers of voltage-gated Ca++ channels are tested. The L-type antagonist did not cause a significant difference from control, but this is expected because L-type channels are not prevalent at terminals.

Question 5

Obviously, depolarization caused by KA receptor activation must be larger at axon terminals then was observed in the cell body. To explain this

Answer 5

input resistance is greater at the terminals and KA receptors may be more densely expressed.

Question 6

Answer 6

Biphasic modulation of eIPSC

We know KA enhances mIPSC f, so we expeted it might facilitate eIPSC

Low does KA had no effect, high dose only supression

therefor, we though facilitation might not happen in standard conditions, so we raised divalent cation concentrations, and indeed, facilitation was observed

Question 9

Argue against:

KA-induced depolarization of presynaptic terminals may cause voltage-gated Na+ and Ca+ channel inactivation

KA increases membrane conductance in axon terminals, causing electrical shunting that blocks the effect of an action potential

Answer 9

Neither GABA_B Receptor ligands (bac) nor alteration in Ca/Mg ratio would be expected to change ability of KA to cause voltage-gated channel inactivation or current shunting, yet those mechanisms produced supression, ergo supression does not com from inactivtion or shunting

Question 10

Answer 10

divide second hump#1 by first hump#1 or second hump#2 by first hump#2 to show supression via autoreceptor (as long as you also have Ca++ and KA receptor)

Question 11

what it means that altered [Ca++] did not alter supression

Answer 11

Reduced Ca++ prevents KA from causing vesicle release, and we know vesicles are not depleted. If its not vesicle depletion, preventing autoreceptor function is likely.