Edge enhancement in the retina is thought to be mediated by classical
center-surround antagonism, first encountered as the interactions betw
een horizontal cells and cones. But in the salamander retina these int
eractions do little to enhance edges. Instead, a robust dynamic intera
ction between amacrine and bipolar cells appears to be responsible for
a sharp edge enhancement. To demonstrate this we recorded extracellul
arly from a single ganglion cell and moved a flashed square, 300 mu m
on a side, over a 1.5 x 1.0 mm(2) grid at 25-mu m increments. Playing
back all of these recordings simultaneously simulated the pattern of r
esponses that would have been measured from an array of ganglion cells
. The emerging pattern of ganglion cell activity first faithfully repr
esented the flashed square, but after similar to 60 ms the center of t
he representation collapsed, leaving a representation of only the edge
s. We inferred that the feedback synapse from amacrine to bipolar cell
s at gamma-aminobutyric acid-C (GABA(C)) receptors mediated this effec
t: bicuculline and strychnine were ineffective in altering the respons
e pattern, but in picrotoxin the center of the representation did not
collapse. The GABAergic amacrine cells thought to mediate this effect
have quite narrow spread of processes, so the existence of this edge-e
nhancing effect suggests a mechanism quite different from classical la
teral inhibition, namely the delayed inhibition of a spatially expandi
ng input pattern.