The histopathological sequelae of parenteral administration of kainic acid were investigated in immature rats (3-35 days of age). The brains were fixed 1-14 days after the administration of kainate and the damage evaluated by means of argyrophylic (Fink-Heimer, Gallyas or Nauta-Gygax) and Nissl stains. In animals of less than 18 days of age there was no sign of damage even after 1-2 h of severe tonico-clonic convulsions. Between 18 and 35 days after birth, there was a progressive increase in the severity of the damage, the adult pattern being reached at the latter age. As in adult animals, brain damage was most severe in structures which are part of the limbic system, i.e. the hippocampal formation, lateral septum, amygdaloid complex, claustrum, piriform cortex, etc. In addition to neuronal abnormalities, the following reactions were observed: hypertrophy and swelling of satellite oligodendroglia, proliferation of hypertrophic microglia, proliferation of astroglia and hypertrophy of endothelial cells in the capillary wall. The latter type of change, together with local coagulative necrosis, was almost exclusively restricted to the granular and molecular layers of the fascia dentata. In the hippocampal formation we found a temporal gradient of vulnerability. The earliest and most consistent neuronal alterations were largely restricted to interneurons of the hilar region and to a lesser extent to non-pyramidal neurons of strata oriens and radiatum. The severe necrotic destruction of the pyramidal layer of CA3 is conspicuous at a later age (postnatal day 30-35) and with longer survival times. Our results suggest that: (1) the neurotoxin only induces brain damage once it also causes limbic motor seizures and its associated metabolic activations, notably in the amygdala; (2) the earliest pathological sequelae occur in interneurons of the hilar region and (3) sclerosis of the vulnerable region of the Ammon's horn--the CA3 region--is only obtained once the dentate granules and their mossy fibres are fully operational, thereby reflecting the crucial role of this axonal connection in eliciting hippocampal damage.