PURPOSE: To determine the electrophysiological pattern and propose a clinical relevance of a deficient glutamate transport in the developing brain. METHODS: (a) Surface EEG-video monitoring in freely moving pups; (b) intracortical multiple unit activity (MUA) and local field potential recordings in 5- to 7-day-old rats after pharmacological inhibition of the glutamate transporters by DL-TBOA. RESULTS: Glutamate transporters inhibition alters the background cortical electrical activity inducing a dominant and persistent pattern of bilateral recurrent paroxysmal bursts alternating with periods of hypoactivity and also partial seizures. Intracortical local field recordings show that paroxysmal bursts are associated with multiunits and gamma oscillations separated by periods of silence. This cortical activity involves the activation of ionotropic glutamate receptors and was not observed after kainate and pilocarpine administration. CONCLUSIONS: We show that a dysfunction of glutamate transporters in immature rats leads to a singular cortical activity that is reminiscent of a "suppression-burst" pattern. We propose that an early deficiency of glutamate transport may underlie some early onset epilepsies.