My question can be further teased apart.
Consider the heterogeneity of receptors present on neuronal cells.
When recording GABAergic events, for example, why does one choose to use CNQX versus kynurenic acid? If one is blocking EPSCs, how can one justify still allowing other glutaminergic activity?
Another example, if recording Glutaminergic events one blocks GABA events. How does one decide to use picrotoxin or something like bicuculline?
In carrying out experiments, I feel it's important to understand the 'why's' behind every step, so I am looking for why in these instances.
I apologize for any unintended ignorance.
Thanks everyone.
Kynurenic acid is cheap, and it blocks NMDA, KA and AMPA receptors. It is a favourite of old-school physiologists and people without much money. However, it is a pain to dissolve, and at 3 mM, god knows what else it does.
CNQX only blocks AMPA channels, so you need an NMDA antagonist too. It used to be only soluble in DMSO, so some people didn't like it. NBQX is more selective for AMPA receptors over NMDA receptors than CNQX, that is why some people like it, but then 95% of them use it with AP5 (to block NMDA receptors) so it seems a moot point. Though these days, the CNQX Na salt is available, and it's water soluble.
PTX, vs Bicuculline vs Gabazine. PTX blocks the pore, so blocks spontaneously opening subtypes, but is DMSO soluble. No good reason to use Bic any more as we know it blocks SK currents. Gabazine is pretty good, but there may be some element of subunit selectivity at low concentrations.
These questions go on and on... for any given receptors there are dozens of ligands. My advice is to pick one that is cheap, water soluble, and active in a ~1uM range, because things that work in the 1nM range are annoying to work with, and often are slow to take effect