J. Bear et Ew. Lothman, AN INVITRO STUDY OF FOCAL EPILEPTOGENESIS IN COMBINED HIPPOCAMPAL-PARAHIPPOCAMPAL SLICES, Epilepsy research, 14(3), 1993, pp. 183-193
Brain slices from adult rats that included ventral hippocampus and adj
acent parahippocampal areas were studied at various sites for the appe
arance of epileptiform discharges as extracellular potassium ([K+]o) w
as systematically varied over the range of 3 mM to 10 mM. The developm
ent of evoked epileptiform discharges (EEDs) and spontaneous epileptif
orm discharges (SEDs) was monitored in areas CA1, CA3, the hilus of th
e dentate gyrus (dentate hilus), the granule cell layer of the dentate
gyrus (dentate gyrus), subiculum and entorhinal cortex. Increasing [K
+]o elicited EEDs in a concentration-dependent manner. The entorhinal
cortex and CA1 areas were most susceptible to this effect; the dentate
gyrus was least susceptible. Increasing [K+]o also caused an increase
in SEDs in all hippocampal areas. Separating entorhinal cortex from t
he rest of the slice by transections did not abolish discharges in any
location. Lesions of the Schaeffer collaterals abolished discharges i
n CA1 but not in CA3. These findings demonstrate that changes in the e
xtracellular milieu that are associated with epileptiform discharges i
n vivo are capable of eliciting paroxysmal discharges at multiple loci
in the hippocampus and adjacent regions. Further, these findings demo
nstrate for the first time the intrinsic capacity of the entorhinal co
rtex to generate epileptiform discharges under in vitro ionic conditio
ns known to occur in the intact brain during seizures.