The mechanism of afterdischarge termination in the various hippocampal
regions was examined in the rat. Stimulation of the perforant path or
the commissural system was used to elicit afterdischarges. Combinatio
n of multiple site recordings with silicon probes, current source dens
ity analysis, and unit recordings in the awake animal allowed for a hi
gh spatial resolution of the field events, Interpretation of the field
observations was aided by intracellular recordings from anesthetized
rats. Irrespective of the evoking conditions, afterdischarges always t
erminated first in the CA1 region. Termination of the afterdischarge w
as heralded by a large DC shift initiated in dendritic layers associat
ed with a low amplitude ''after discharge termination oscillation'' (A
TO) at 40 to 80 Hz in the cell body layer. ATOs were also observed in
the CA3 region and the dentate gyrus. The DC shift spread at the same
velocity (0.1-0.2 mm/ sec) in all directions and could cross the hippo
campal fissure. All but 1 of the 25 putative interneurons in the CAI a
nd dentate regions ceased to fire before the onset of ATO. Intracellul
arly, ATO and the emerging DC potential were associated with fast depo
larizing potentials and firing of pyramidal cells and depolarization b
lock of spike initiation, respectively. Both field ATO and the intrace
llular depolarization shift were replicated by focal microinjection of
potassium. We hypothesize that [K+](o) lost by the intensely discharg
ing neurons during the afterdischarge triggers propagating waves of de
polarization in the astrocytic network. In turn, astrocytes release po
tassium, which induces a depolarization block of spike generation in n
eurons, resulting in ''postictal depression'' of the EEG.