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Glutamate is a major neurotransmitter in the retina. Glutamate is released by photoreceptors to convey the visual signal to postsynaptic bipolar and horizontal cells, and is released from bipolar cells to act on amacrine and ganglion cells. The actions of glutamate on horizontal, bipolar and ganglion cells are well understood but not much is known about its effect on photoreceptors, or its action on retinal glial cells. The first part of this thesis deals with experiments in which the whole-cell variant of the patch-clamp technique was used to study the action of glutamate on isolated cone photoreceptors from the tiger salamander retina. Glutamate is shown to bind to a kainate-type receptor and evoke a current carried by chloride ions and blocked by removal of external sodium. The glutamate-evoked current is localized to the synaptic teminal of the cone suggesting that these receptors act as autoreceptors. Next, the effect of glutamate on retinal glial (Müller) cells isolated from the rabbit retina is described. Glutamate evokes an inward membrane current by activating a high affinity uptake carrier. Uptake is strongly inhibited by depolarization, by removal of extracellular sodium or intracellular potassium, and by raising the extracellular potassium concentration. This suggests that the uptake carrier transports sodium ions into the cell and potassium ions out of the cell. Uptake of glutamate into glial cells may be important in terminating its transmitter action. Finally, the distribution of Müller cell processes around the photoreceptor output synapse is investigated by injecting tiger salamander Müller cells with horseradish peroxidase for examination in the electron microscope. Although Müller cells do not project between the processes of bipolar and horizontal cells entering the photoreceptor synaptic pedicle, they do wrap around the synaptic terminals of the photoreceptors and come within 1-3μm of the site of glutamate release.