Abstract— 1. Whereas exogenous l-glutamate enters rat brain cortex slices incubated in a glucose-physiological saline medium by both low affinity (Km= 0.7 mm) and high affinity (Km= 27−30 μM) processes, the uptake of d-glutamate occurs only by a low affinity (Km= 2mm) system. 2. d-glutamate appears to release l-glutamate from incubated rat brain cortex slices only to a very small extent, whether the tissue l-glutamate is of endogenous or exogenous origin. 3. Competitive inhibition takes place between l- and d-glutamates at the low affinity carrier. This indicates that a common carrier exists for l- and d-glutamates for the low affinity uptake process. 4. Apparently non-competitive inhibition by d-glutamate of l-glutamate uptake occurs at the high affinity carrier, but the affinity of d-glutamate for this carrier is about 0.4% of that of l-glutamate. 5. Both d-, and l-glutamate exchange freely with labelled d-glutamate taken up by preliminary incubation of the brain slices with this amino acid. Whereas l-glutamate exchanges freely with labelled l-glutamate taken up by preliminary incubation, d-glutamate shows little or no exchange. 6. The uptake of labelled d-glutamate by exchange diffusion into brain slices previously loaded with unlabelled d-glutamate proceeds by a low affinity system. Therefore, the process of exchange diffusion does not necessarily involve a high affinity uptake component. 7. Whereas ouabain suppresses both high and low affinity concentrative uptakes of l- and d-glutamate it has little apparent effect on the exchange diffusion process. 8. Sensitivity to tetrodotoxin of evoked release of l- and d-glutamates, taken up by brain slices by preliminary incubation with these amino acids, indicates that the major proportion of the uptake of exogenous l- or d-glutamate proceeds into non-neuronal structures (presumably the glia). 9. At 0°C non-carrier mediated (passive) diffusion of labelled d- and l-glutamate takes place in brain slices.