REMOVAL OF EXTRACELLULAR CHLORIDE SUPPRESSES TRANSMITTER RELEASE FROMPHOTORECEPTOR TERMINALS IN THE MUDPUPPY RETINA

Removal of extracellular Cl- has been shown to suppress light-evoked v oltage responses of ON bipolar and horizontal cells, but not photorece ptors or OFF bipolar cells, in the amphibian retina. A substantial amo unt of experimental evidence has demonstrated that the photoreceptor t ransmitter, L-glutamate, activates cation, not Cl-, channels in these cells. The mechanism for Cl-free effects was therefore reexamined in a superfused retinal slice preparation from the mudpuppy (Necturus macu losus) using whole-cell voltage and current clamp techniques. In a Cl- free medium, light-evoked currents were maintained in rod and cone pho toreceptors but suppressed in horizontal, ON bipolar, and OFF bipolar cells. Changes in input resistance and dark current in bipolar and hor izontal cells were consistent with the hypothesis that removal of Cl- suppresses tonic glutamate release from photoreceptors. The persistenc e of light-evoked voltage responses in OFF bipolar cells, despite the suppression of light-evoked currents, is due to a compensatory increas e in input resistance. Focal application of hyperosmotic sucrose to ph otoreceptor terminals produced currents in bipolar and horizontal cell s arising from two sources: (a) evoked glutamate release and (b) direc t actions of the hyperosmotic solution on postsynaptic neurons. The in ward currents resulting from osmotically evoked release of glutamate i n OFF bipolar and horizontal cells were suppressed in a Cl-free medium . For ON bipolar cells, both the direct and evoked components of the h yperosmotic response resulted in outward currents and were thus diffic ult to separate. However, in some cells, removal of extracellular Cl- suppressed the outward current consistent with a suppression of presyn aptic glutamate release. The results of this study suggest that remova l of extracellular Cl- suppresses glutamate release from photoreceptor terminals. Thus, it is possible that control of [Cl-] in and around p hotoreceptors may regulate glutamate release from these cells.