Journal of Neuroscience, Vol 9, 726-735, Copyright © 1989 by Society for Neuroscience
Amacrine cell interactions underlying the response to change in the tiger salamander retina
G Maguire, P Lukasiewicz and F Werblin
Neurobiology Group, University of California, Berkeley 94720.
The neural circuitry and pharmacology underlying transient signal formation
at the bipolar-amacrine cell interface were studied. Synaptic currents were
measured with whole cell patch clamp in retinal slices. Cell types were
identified with Lucifer yellow staining. Activity was initiated with puffs
of kainate of known time course and spatial spread delivered at bipolar
dendrites. OFF bipolar cells responded to kainate with a sustained inward
current, but ON bipolar cells were silent. Two types of amacrine cell were
found: (1) narrow field cells, with processes that extended laterally less
than 200 microns, responding with a sustained inward current, and (2) wide
field cells, with processes that extended laterally by up to 1 mm,
responding with a brief transient inward current followed by a more
sustained outward current. We pharmacologically dissected the synaptic
interactions underlying the transient current in the wide field amacrine
cell. In the presence of 5-aminovaleric acid (AVA), the time course of this
transient current was increased so that it resembled the response of
bipolar cells. Because AVA is a GABAB antagonist, it appears to block an
opposing signal that truncates the sustained excitatory bipolar input,
thereby generating the transient. GABAB specificity is confirmed by (1)
block of the transient inward current by baclofen, a GABAB agonist, and (2)
block of the baclofen effect by AVA. The site of GABAB action appears to be
presynaptic to the amacrine cell membrane because neither baclofen nor AVA,
in combination with picrotoxin, had a direct effect at the amacrine cell
membrane. GABAB receptors are often found at presynaptic terminals where
they modulate calcium or potassium conductances. It has been shown that
bipolar cell terminals receive a GABAergic synaptic input (Vaughn et al.,
1981; Wu et al., 1981; Tachibana and Kaneko, 1987). The narrow field
sustained-responding amacrine cells appear to be GABAergic (Werblin et al.,
1988). This suggests that transient activity measured in wide field
amacrine cells is formed at a population of bipolar cell terminals by
GABAergic feedback from narrow field amacrine cells at GABAB receptors.
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