The dentate gyrus in rat hippocampal slices produces spontaneous, prolonged bursts of population spikes (i.e. prolonged field bursts) when [Ca2+](0) is lowered (0-0.5mM) and [K+](0) is concurrently elevated (9-11 mM). In this investigation we examined whether the dentate gyrus could also generate spontaneous field bursts in relatively ''normal'' (i.e. nominal 1.3 mM) or only moderately decreased [Ca2+](0) (i.e. nominal 0.9mM). In 1.3 mM [Ca2+](0), no prolonged field bursts occurred spontaneously in the dentate gyrus when [K+](0) was raised as high as 12 mM. Prolonged held bursts were generated, however, when [K+](0) was further increased to 13-15 mM. Similar bursts could be generated at [K+](0) within the ''physiological ceiling level'' observed in vivo during seizure activity (i.e. 11-12 mM) if: (i) the bath [Ca2+] was reduced to 0.9 mM; or (ii) the GABA type A-receptor antagonist bicuculline was added in the presence of ''normal'' (1.3 mM) [Ca2+](0). Adding both the N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor antagonists, (+/-)-2-amino-5-phosphonopentanoic acid (50-100 mu M) and 6,7-dinitroquinoxaline-2,3-dione (50-100 mu M), respectively, did not block the occurrence of the field bursts. The bursts generated in 1.3 mM [Ca2+](0), 12 mM [K+](0),, bicuculline, (+/-)-2-amino-5-phosphonopentanoic acid and 6,7-dinitroquinoxaline-2,3-dione could, however, be reversibly depressed or blocked if [Ca2+](0) was raised to 2.0 mM. These data suggest that: (i) the dentate gyrus (like CA1) can produce prolonged field bursts in ''normal'' [Ca2+](0), when [K+](0) is elevated, although the [K+](0) threshold is higher; (ii) the dentate gyrus can generate prolonged held bursts in response to [K+](0) elevations within the physiological ceiling, provided [Ca2+](0) is moderately lowered (i.e. 0.9 mM) or GABA type A-transmission is blacked; and (iii) antagonists of excitatory amino acid-mediated neurotransmission do not block the prolonged field bursts produced under any of these conditions.