Single Ganglion Cell

CENTER CENTER + SURROUND

experiments on the pharmacology of the DC component of the ERG (Katz et al., 1992) suggest that both the b-wave and the DC component (cf. Fig. 5.17) are generated primarily by the distal K+-Müller cell mechanism in response to the K+ efflux from depolarizing bipolar cells. In addition, Masland and Ames (1975) demonstrated that following a short period of anoxia, or after incubation in a low calcium medium, there was marked diminution of the b-wave with no apparent reduction in ganglion cell response (Fig. 5.23B). Comparable results were obtained after selectively poisoning the Müller cell with D,L-a-aminoadipic acid (Bonaventure et al., 1981). If the reduced b-wave seen in these studies was the result of abnormal bipolar cell function, it is puzzling to find retention of seemingly normal signal transmission from photoreceptors to ganglion cells.

The Bipolar Cell Hypothesis: Despite the previously cited findings, there is reason to believe that the b-wave may not reflect radial current flow generated by a K+-induced depolarization of Müller cells (cf. Tomita and Yanagida, 1981). For example, membrane potential measurements from amphibian Müller cells correlate poorly with the waveform and time course of the b-wave, but appear to mirror an extracellular field potential (the M-wave) recorded in the proximal retina (Karwoski and Proenza, 1977, 1978). Inconsistencies between the current sinks and sources for the b-wave (CSD analysis) and the kinetics and loci of K+ fluxes contradict the Müller cell hypothesis (Vogel and Green, 1980). In addition, a question has been raised as to whether the magnitude of the light-evoked [K+]o increase recorded in the distal retina is sufficient to generate the large transretinal b-wave, although it is generally recognized that electrode-induced damage, interference from the large distal K+ decrease, as well as other factors may dilute considerably the K+ measurements. (Karwoski et al., 1985).

Figure 5.23. A. Recordings of light-evoked responses from the toad retina superfused with a normal Ringer (control) solution or one containing 0.2 mM Ba2+; the stimulus marker is shown on the bottom trace. The uppermost traces show the extracellular ERG and the distal K+ increase; the lower pair are intracellular membrane potential recordings (Vm) from a Müller cell and rod photoreceptor. Note that the rod potential and the K+ efflux are relatively unaffected by exposure to barium, but both the Müller cell response and the ERG b-wave are substantially reduced (Wen and Oakley, 1990). (Copyright 1990 National Academy of Sciences, U.S.A., reprinted with permission.) B. Effects of anoxia (upper pair of traces) and low Ca2+ (lower traces) on the transretinal ERG, the compound action potential recorded from the optic nerve, and the spike activity of a single ganglion cell. Both anoxia and the low calcium solution reduce significantly the ERG b-wave, but have no detectable effect on the responses recorded from ganglion cells or their optic nerve bundles (Masland and Ames, 1975). (Copyright 1975 John Wiley & Sons, Inc., reprinted with permission.)

Nevertheless, a large body of evidence supports the view that the b-wave potential is predominantly a direct expression of the activities of roddriven depolarizing (ON) bipolar cells (cf. Xu and Karwoski, 1994b; Robson and Frishman, 1995; Hanitzsch etal., 1996; Green and Kapousta-Bruneau, 1999; Shiells and Falk, 1999; Lei and Perlman, 1999). The depolarizing responses of these cells reflect the opening of cGMP-activated cation channels in postsynaptic membranes, as a result of the light-induced suppression of glutamate release from photoreceptor terminals (Shiells and Falk, 1990; Nawy and Jahr, 1990,1991). Membrane depolarization and the radial orientation of the bipolar cell would be effective in creating an extracellular current path consistent with the polarity of the b-wave.

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