3 hypothesis on why when surround-illuminated you are releasing less Glu and you are hyperpolarizing these cells that some how leads to depolarization of cone center presynaptic terminal membrane
1.) GABA hypothesis:
center + surround = less GABA released = less inhibition becomes horizontal cells become more hyperpolarized by surround cells
so if you give exogenous GABA, it blocks depolarization, abolishes the response
not just local when you do this so it can be changing input resistance of the whole membrane (explains suppression of HC feedback sys)
2.) EPHATIC HYPOTHESIS
adding charged cations is equivalent to depolarizing charge on the inside and might inibit cahnnel opening and reducing NT release
if this is correct you would expect finding a lot of open hemi-channels (1/2 gap junctions), not found in mammals
if you block these channels, you can suppress horizontal feedback (but you don’t know if it’s affecting just local synaptic region, could effect other VG-channels)
use blocker and you don’t see block of these gap junctions
if you get rid of these channels (lacks connexin), you can reduce but not eliminate CS LH
if you knock it they can go to a different compensatory change
can contribute but not the only mechanism
3.) pH hypothesis
release protons, artifically acidify/alkanize cleft you can account for horizontal feedback, has an effect
block-it clamps pH, changes in proton release can’t change pH and block feedback
show-it, have fish express reporter of pH (GFP) you get changes in pH in predicted region
timing of pH and magnitude changes at the right time, CS illumination and place
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