Comparison of the responses of AII amacrine cells in the dark- and light-adapted rabbit retina

Abstract

We studied the light-evoked responses of AII amacrine cells in the rabbit retina under dark- and light-adapted conditions. In contrast to the results of previous studies, we found that AII cells display robust responses to light 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/OFF-surround receptive-field organization. The intensity-response profile of the center-mediated response component followed a dual-limbed sigmoidal function indicating a transition from rod to cone mediation as stimulus intensities were increased. Following light adaptation, the receptive-field organization of AII cells changed dramatically. Light-adapted AII cells showed both 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 then replaced gradually over a 1-4 min period by the emerging ON-center response component. Application of the metabotropic glutamate receptor agonist APB, the ionotropic glutamate blocker CNQX, 8-bromo-cGMP, and the nitric oxide 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 are responsible for the generation of the different AII cell responses. Specifically, 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-center cone bipolar cells. Additionally, the OFF-center response of light-adapted AII cells reflects direct synaptic inputs from OFF-center cone bipolar cells to AII dendritic processes in the distal inner plexiform layer.

Deletion of Connexin45 in Mouse Retinal Neurons Disrupts the Rod/Cone Signaling Pathway between AII Amacrine and ON Cone Bipolar Cells and Leads to Impaired Visual Transmission

“…Mills and Massey (1995) showed that larger biotinylated tracers pass rather poorly through gap junctions between AII amacrine cells and bipolar cells, whereas they pass easily through homotypic gap junctions between AII amacrine cells. However, tracer coupling seems to be bidirectional between AII amacrine and ON bipolar cells in rabbit retina (Trexler et al, 2001), in agreement with physiological data from Xin and Bloomfield (1999), who demonstrated that cone signals, presumably transmitted by means of the ON bipolar/AII amacrine cell gap junctions, can be measured in AII amacrine cells. Thus physiological data neither support nor contradict conclusively the possibility that Cx36 and Cx45 form the heterotypic gap junctions between AII amacrine and ON bipolar cells.…”

Electrical synapses between AII amacrine cells in the retina: Function and modulation

“…At the EM level, the presynaptic elements are ribbon synapses here as well. Although it has not been examined extensively, electrophysiological recordings suggest that the input is mediated by iGluRs (Veruki et al, 2003; see also Xin and Bloomfield, 1999). The AII amacrine lobular appendages can also be presynaptic to the axon terminals of OFFcone bipolar cells from which they receive input and to dendrites of OFF-ganglion cells (McGuire et al, 1984;Strettoi et al, 1992Strettoi et al, , 1994Tsukamoto et al, 2001).…”

Active Roles of Electrically Coupled Bipolar Cell Network in the Adult Retina

“…It is well known that retinal gap junctions are modulated by light and dark adaptation (Dong and McReynolds, 1991;Xin and Bloomfield, 1999). Thus, we investigated the effects of light and dark adaptation on the properties of the electrically coupled Mb1-BC network.…”