Ilm

Figure 5.13. The light-evoked changes in K+ recorded with an extracellular ion-selective electrode as it was advanced from the vitreal surface (ILM) to the outer limiting membrane (OLM). The retinal schematic shows the approximate locations of the photoreceptor (r), horizontal (h), bipolar (b), amacrine (a), and ganglion (g) cells. The large, prolonged efflux of K+ seen in the IPL becomes more transient and smaller as the electrode approaches the ONL. In the photoreceptor region, the fall in K+ dominates the KRG (Dowling, 1987). (Copyright 1987 Belknap Press, reprinted with permission.)

ments (Bok and Filerman, 1979). Although the pump drives K+ into the cell as the excess Na+ is removed, a passive efflux of K+ (Fig. 5.14) restores the ionic balance. However, light triggers an enzymatic cascade that leads to closure of the CNG channels and causes the photoreceptors to hyperpolar-ize, thereby reducing the passive K+ efflux. Because the activity of the Na+/ K+ pump is not immediately affected by these events, the result is a net influx of K+, and a large transient decrease in [K+]o in the region of the receptor inner segments (Matsuura et al., 1978; Oakley et al., 1979).

Figure 5.14. In darkness (left side of figure), a sustained inward current carried primarily by Na+ enters the photoreceptor outer segment through cGMP-gated channels. A Na+-K+ exchanger in the inner segment extrudes the excess Na+ and brings in K+, which then exits the cell through passive ion channels to maintain the dark level of extracellular K+. The influx of cations depolarizes the cell, and induces the release of glutamate from the photoreceptor terminal. The effect of light (shown on the right) is to trigger the sequential activation of rhodopsin (R), transducin (T), and phosphodiesterase (PDE). This enzymatic cascade leads to the hydrolysis of cGMP, channel closure, and suppression of the dark current. The resultant hypolarization reduces both the discharge of transmitter, and the passive efflux of K+. However, the inward K+ flux mediated by the Na+-K+ pump is not significantly affected, thus producing a fall in extracellular K+.

Figure 5.14. In darkness (left side of figure), a sustained inward current carried primarily by Na+ enters the photoreceptor outer segment through cGMP-gated channels. A Na+-K+ exchanger in the inner segment extrudes the excess Na+ and brings in K+, which then exits the cell through passive ion channels to maintain the dark level of extracellular K+. The influx of cations depolarizes the cell, and induces the release of glutamate from the photoreceptor terminal. The effect of light (shown on the right) is to trigger the sequential activation of rhodopsin (R), transducin (T), and phosphodiesterase (PDE). This enzymatic cascade leads to the hydrolysis of cGMP, channel closure, and suppression of the dark current. The resultant hypolarization reduces both the discharge of transmitter, and the passive efflux of K+. However, the inward K+ flux mediated by the Na+-K+ pump is not significantly affected, thus producing a fall in extracellular K+.

The [K+]o increases detected in the outer and inner plexiform layers are attributable to the activation of cells that depolarize in response to photic stimulation. In the distal retina, the principal source of the K+ efflux in the OPL is the depolarizing (ON) bipolar cell (Dick and Miller, 1978; Kline et al., 1978). The light-evoked response recorded at this locus with an ISM appears in Fig. 5.13 as a small, transient rise in K+. More proximally, in the region of the IPL, there is a larger, more sustained K+ efflux that derives primarily from the depolarizing synaptic potentials of the spikegenerating amacrine and ganglion cells. Both cell types respond to the onset and offset of illumination (Werblin and Dowling, 1969), and both exhibit center-surround antagonism (Burkhardt, 1974), features that are reflected in recordings of the K+ changes induced by these stimulus parameters (Fig. 5.15; cf. Kline et al., 1985).

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