Dy. Xin et Sa. Bloomfield, Comparison of the responses of AII amacrine cells in the dark- and light-adapted rabbit retina, VIS NEUROSC, 16(4), 1999, pp. 653-665
We studied the light-evoked responses of AII amacrine cells in the rabbit r
etina under dark- and light-adapted conditions. In contrast to the results
of previous studies, we found that AII cells display robust responses to li
ght over a 6-7 log unit intensity range, well beyond the operating range of
rod photoreceptors. Under dark adaptation, AII cells showed an ON-center/O
FF-surround receptive-field organization. The intensity-response profile of
the center-mediated response component followed a dual-limbed sigmoidal fu
nction indicating a transition from rod to cone mediation as stimulus inten
sities were increased. Following light adaptation, the receptive-field orga
nization of An cells changed dramatically. Light-adapted AII cells showed b
oth ON- and OFF-responses to stimulation of the center receptive field, but
we found no evidence for an antagonistic surround. Interestingly, the OFF-
center response appeared first following rapid light adaptation and was the
n replaced gradually over a 1-4 min period by the emerging ON-center respon
se component. Application of the metabotropic glutamate receptor agonist AP
E, the ionotropic glutamate blocker CNQX, 8-bromo-cGMP, and the nitric oxid
e donor SNAP all showed differential effects on the various center-mediated
responses displayed by dark- and light-adapted AII cells. Taken together,
these pharmacological results indicated that different synaptic circuits ar
e responsible for the generation of the different AII cell responses. Speci
fically, the rod-driven ON-center responses are apparently derived from rod
bipolar cell synaptic inputs, whereas the cone-driven ON-center responses
arise from signals crossing the gap junctions between AII cells and ON-cent
er cone bipolar cells. Additionally, the OFF-center response of light-adapt
ed All cells reflects direct synaptic inputs from OFF-center cone bipolar c
ells to AII dendritic processes in the distal inner plexiform layer.