IMMATURE glia may not be able to buffer K+ions released during neuronal activity. Therefore, we investigated entorhinal-hippocampal slices of juvenile rats (ages P15–18 and P22–26) using a perfusion medium containing 2 mM BaCl2in order to block glial inward rectifying and leak potassium channels. In contrast to adult animals, rises in [K+]oin slices from juvenile animals elicited by repetitive alvear stimulation were not augmented by Ba2+. Ba2+effects on fast field potentials, slow field potentials and the applied current sink source distribution were roughly similar as in adult rats. We conclude that the capacity to buffer large quantities of K+ions by mechanisms involving Ba2+-sensitive K+channels has not yet developed in juveniles.